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This is an early online draft of this embryology and histology textbook.
This is an early online draft of this embryology and histology textbook.


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{{Orban1944 TOC}}
{{Historic Disclaimer}}
{{Historic Disclaimer}}
=Oral Histology and Embryology=
=Oral Histology and Embryology=
Oral Histology And Embryology
Oralihstology
Am)
Embryology
Edited By
Edited By


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Loyola University, School of Dentistry, Chicago, Illinois
Loyola University, School of Dentistry, Chicago, Illinois


THIRD EDITION
Third Edition


WITH 263 TEXT lLI.L'SI'RATIO.\'S
With 263 Text Illustrations
INCLUDING 4 COLOR PLATES


ST. LOUIS
Including 4 Color Plates


THE C. V. MOSBY COMPANY
St. Louis
1953
COPYRIGHT, 1944, 19:9, 1953, BY THE C. V’. Mossy COMPANY
(All rights reserved)


second Edition Reprinted
The C. V. Mosby Company
June. 1950


Printed in the
Copyright, 1944
United States or America
{|
 
|
Press of
==Contributors==
The C. 7. Mosby Company
St. Louie
CONTRIBUTORS


Myron S. Aisenberg, D.D-S.
Myron S. Aisenberg, D.D-S.
Line 83: Line 67:
San Francisco
San Francisco


Donald A. Kerr, A.B., D.D.S., ‘MS.
Donald A. Kerr, A.B., D.D.S., MS.


School of Dentistry
School of Dentistry
Line 94: Line 78:
Columbus
Columbus


Edgar B. Manley, l\v£.Sc., B.D.S., F.D.S.R.C.S. (Eng.)
Edgar B. Manley, M.Sc., B.D.S., F.D.S.R.C.S. (Eng.)


Department of Dental Pathology Medical School
Department of Dental Pathology Medical School
Line 100: Line 84:
Birmingham, England
Birmingham, England


Balint Orban, l\l.D., D-D.S.
Balint Orban, M.D., D-D.S.


School of Dentistry
School of Dentistry
Line 129: Line 113:
Boston
Boston


B. O. A. Thomas, B.A., D.D.S., l\rI.S., Ph.D.
B. O. A. Thomas, B.A., D.D.S., M.S., Ph.D.


School of Dentistry
School of Dentistry
Line 141: Line 125:


Chicago
Chicago
| valign=top|
==Contents==
* Chapter I [[Book - Oral Histology and Embryology (1944) 1|Development of the Face and Oral Cavity]]
* Chapter II [[Book - Oral Histology and Embryology (1944) 2|Development and Growth of Teeth]]
* Chapter III [[Book - Oral Histology and Embryology (1944) 3|Enamel]]
* Chapter IV [[Book - Oral Histology and Embryology (1944) 4|The Dentin]]
* Chapter V [[Book - Oral Histology and Embryology (1944) 5|Pulp]]
* Chapter VI [[Book - Oral Histology and Embryology (1944) 6|Cementum]]
* Chapter VII [[Book - Oral Histology and Embryology (1944) 7|Periodontal Membrane]]
* Chapter VIII [[Book - Oral Histology and Embryology (1944) 8|Maxilla and Mandible (Alveolar Process)]]
* Chapter IX [[Book - Oral Histology and Embryology (1944) 9|The Oral Mucous Membrane]]
* Chapter X [[Book - Oral Histology and Embryology (1944) 10|Glands of the Oral Cavity]]
* Chapter XI [[Book - Oral Histology and Embryology (1944) 11|Eruption Of The Teeth]]
* Chapter XII [[Book - Oral Histology and Embryology (1944) 12|Shedding of the Deciduous Teeth]]
* Chapter XIII [[Book - Oral Histology and Embryology (1944) 13|Temporomandibular Joint]]
* Chapter XIV [[Book - Oral Histology and Embryology (1944) 14|The Maxillary Sinus]]
* Chapter XV [[Book - Oral Histology and Embryology (1944) 15|Technical Remarks]]
|}


PREFACE TO THIRD EDITION
==Preface To Third Edition==


As we continue to revise this book. some of our practices are becoming
As we continue to revise this book. some of our practices are becoming
Line 153: Line 156:
would have aided us most.
would have aided us most.


“'9 have new men with us—neW as contributors to this book, but well
“I have new men with us—new as contributors to this book, but well
known as research men and teachers. \Ve happily welcome them. The
known as research men and teachers. We happily welcome them. The
changes that have been made in this third edition are mainly due to their
changes that have been made in this third edition are mainly due to their
eiforts.
eiforts.
Line 160: Line 163:
Many changes have been made in the chapter on "Enamel," with
Many changes have been made in the chapter on "Enamel," with
numerous new illustrations. The chapter on the “Glands of the Oral
numerous new illustrations. The chapter on the “Glands of the Oral
C‘avit)"" was reduced and simplified, eliminating some of the rather cumber-
Cavity" was reduced and simplified, eliminating some of the rather cumbersome details. It was our aim in this revision to eliminate throughout
some details. It was our aim in this revision to eliminate throughout
the book statements that could be misinterpreted or cause some confusion.
the book statements that could be misinterpreted or cause some confusion.
Twelve new illustrations, some of them composite. are replacing old ones-
Twelve new illustrations, some of them composite. are replacing old ones
We are grateful to our critics who have pointed out the weak spots
in our text and invite all our students and their teachers to make suggestions which will improve this book. It is our hope that this material
will remain a basic tool in creating better and better dentists.


\\'e are grateful to our critics who have pointed out the weak spots
Balint Orban
in our text and invite all our students and their teachers to make sug-
gestions which will improve this book. It is our hope that this material
will remain a basic tool in creating better and better dentists.


BALINT 033,0:
Chicago
Chicago
PREFACE TO FIRST EDITION
 
==Preface To First Edition==


Oral histology and embryology have rapidly advanced during the last
Oral histology and embryology have rapidly advanced during the last
Line 190: Line 192:
several times, according to the suggestions made by the collaborators.
several times, according to the suggestions made by the collaborators.


Whfle it is true that the co-workers cannot accept every detail pre-
Whfle it is true that the co-workers cannot accept every detail presented in this book, the major difierences in concept were successively
sented in this book, the major difierences in concept were successively
eliminated. We pooled our resources, selected the best illustrations from
eliminated. We pooled our resources, selected the best illustrations from
our material, and we believe that the result presents a sincere effort in
our material, and we believe that the result presents a sincere effort in
Line 203: Line 204:
We hope that this textbook will be of help, not only to undergraduate
We hope that this textbook will be of help, not only to undergraduate
students, but also to those who work for graduate degrees, and to the
students, but also to those who work for graduate degrees, and to the
practicing dentist. Every chapter contains remarks on the clinical appli-
practicing dentist. Every chapter contains remarks on the clinical application of the basic biologic principles.
cation of the basic biologic principles.
 
\‘\'e dedicate this book to those who recognize that clinical procedure


is based on the knowledge of normal structure.
We dedicate this book to those who recognize that clinical procedure is based on the knowledge of normal structure.
BALINT ORBAN
Chicago
CONTENTS


CHAPTER I


DEVELOPMENT or THE FACE AND ORAL Cavxrr _
Balint Orban


Introduction. 13; Development of the Face. 13: Development of the Sec-
Chicago
ondary Palate. 18; Development of the Tongue. 23: Clinical Considerations,
26; Some Malformations of the Face. 26.
 
CHAPTER II
 
DEVELOPMENT AND GROWTH or TEETH _
 
Introduction, 29; Developmental Stages. 29: Dental Lamina and Bud Stage,
3:2; Cap Stage, 34: Bell Stage, 36: Hertwig's Epithelial Root Sheath and
Root Formation, -12: Histophysiology and Clinical Considerations, -153.
 
CHAPTER III
ENAMEL
 
Histology, 50: Physical Characteristics. 50; Chemical Properties, 51;
Structure. 53; Age Changes. 71; Submicroscopic Structure, 73; Clinical
Considerations, 75; Development, S1; Enamel Organ, 81; Life Cycle of
the Ameloblasts. S5; Amelogenesis, S9: Formation of the Enamel Matrix,
S9; Maturation of Enamel lfatrix (Calcification and Crystallization), 93;
Clinical Considerations, 98.
 
CHAPTER IV
 
THE D1-:.\"rm' -
 
Physical Properties. 101; Chemical Composition. 101; Morphology, 102;
Innervation, 114; Age and Functional Changes, 115: Development, 121;
Clinical Considerations, 123.
 
CHAPTER V
 
PULP_____-__-_-_____-_..___..
 
Function, 127: Anaton1_\'. 128; Development, 134: Structural Elements, 135;
Regressive Changes, 148; Clinical Considerations, 151.
 
CHAPTER VI
 
CEMENTUM
Definition, 154; Physical Characteristics, 15-1; Chemical Composition, 15-};
Cementogenesis, 154; Morphology, 159: Cemento-enamel Junction, 16-1;
Cemento-dentinal Junction, 166; Function, 167; 1'-Iypercementosis, 168;
Clinical Considerations, 172.
 
CHAPTER VII
 
PERIODONTAL M.I::~mm.\:n
 
Definition, 176; Function, 176; Development, 176; Structural Elements,
177; Physiologic Changes, 187; Clinical Considerations, 190.
 
9
 
PAGE
13
 
29
 
50
 
101
 
127
 
154
 
176
10 C0.\'TE.\'TS
 
CHAPTER VI II PAGE
 
.\I.\.\‘:l.L.\ .\.\'1- .\I.x.\'xn:m.E .-\L\'l~ZDl..‘\R Priovfiss» - _ - _ _ — — — — — — 194
 
lievciopment of Maxilla an-l Man-lilnle. 194-: Development of the Alveolar
Process. 197: -\'trus.-ture of the Alveolar Process. 197: Physiologic Changes
in the Alveolar PrLIL‘e.\S. 2113: Internal Reconstruction of Bone, 205; Clin-
ical Coxisitlerations. 2607.
 
CHAPTER IX
 
Tm: 0l‘..\I. .\I1'cr-vs .\IEI\lBf‘«-\.\'E - - _ - - — _ _ - — _ - — — - 211
General L'haracteri.<tics. 211: '[‘ran.-ition Between Skin and Mucous Mem-
hraiie. 214: Sulniivisions of the Oral Mucosn, 215; Masticatory Mucosa,
‘.115; Gingiva, 216; Epithelial Attachment and Gingival Sulcus, 227; Hard
Palate. 244: Lining Mucosa. 247: Lip and Cheek, 247; Vestibular Fornix
and Alveolar Mueosa. 25H: Mucous Membrane of the Inferior Surface of
the Tongue and of the Floor of the Oral Cavity, 251; Soft Palate, 253;
Specialized ‘_\Iueosa or Dorsal Lingual Mucosa, 254; Clinical Considera-
 
tions, 259.
CHAPTER X
GLANDSOFTHEOPALCAVITY- - - - _ _ - - _ - _ - - - - - 263
 
Introduction. 263; Histogenesis, 266; Classification of the Salivary Glands,
 
267; Classification of the Oral Glands According to Location, 267; Secretory
Cells of the Salivary Glands. 268; llyoepithelial Cells, 271; Duct Elements,
 
273; Interstitial Conne--tive Tissue: Blood. L_vmpl1 and Nerve Supply, 274;
Major Salivary Glands, 274: Minor Salivary Glands, 280; Clinical Con-
siderations, 283.
 
CHAPTER XI
ERFPTIONOI-‘THETEETH.. - - _ _ - - _ _ _ - - _ _ _ _ _ 237
Introduction, BS7; Histology of Eruption, 287; Jeehanism of Eruption, 297;
Clinical Considerations, 302.
 
CHAPTER XII
 
.’\'HF.xmx:~:u or Tm: Dr.c11-rors TEETH _ - _ _ _ _ _ _ _ _ _ _ _ _ 307
Introduction and Definition. IIHT; Prure.~.< of Shedding, 307; Clinical Cou-
siderations. 31$.
 
CHAPTER XIII
 
TE.\lT‘0R0)-[A.‘€blBl‘L.\R Jo1.\"r _ - - - _ _ _ - _ _ - _ _ _ _ _ 334
Anatomic Remarks. 3:’.-1: Histology. 325: Clinical Considerationr, 331.
 
CHAPT ER X IV
 
THE .\.IAX1l.LARY Sl.\IL‘S_ _ - _ _ _ _ _ _ _ _ _ _ _ _ _ _ 333
 
Introduction, 333: Development.  Anatomic Remarks, 333; Function,
33?; Histology, 337: Clinic-:«1l Consiale-rations. 337.
 
CHAPTER XV
 
'1‘!-:cu:~:1cm.R1~:1r.uzKs_-__-_____________3.;1
 
Introduction. 341: Preparation of Histologic ‘Specimens, 341; Preparation
of Ground Sections, 3-1-7; Preparation ct‘ Organic Structures in the Enamel,
3-LS: Photomierograph_v_. 3-I9.
COLOR PLATES
 
1-‘IG. PAGE
2. Development of the human fave .. _ _ _ .. _ _ ._ _ _ _ _ _ _ 1-1
95. Argyrophilie K01-fi"s fibers become transformeul into the collagenous ground
 
substance of the dentin _ _ _ .. _ - - _ _ - - _ _ _ _ 12-1
 
151. Reconstruction of the skull of a human embryo - - - _ - _ - - _ 194
209. Salivary glands of major secretion _ - _ - - _ _ _ _ _ _ _ 268
 
11
 
ORAL HISTOLOGY AND
EMBRYOLOGY
 
CHAPTER I
 
DEVELOPMENT OF THE FACE
AND ORAL CAVITY
 
1. DTTRODUGTION
 
2. DEVELOPMENT OF THE FACE
 
a. Early Development—Pacia.l Processes
b. Formation of the Primary Palate
 
c. Development of the Mandibular Arch
d. Later Development
 
3. DEVELOPMENT 01‘ THE PALATE
 
a. Formation of the Palatine Processes
1:. Formation and Closure of the Secondary Palate
c. Development of Oral Vestihulum and Alveolar Ridge
 
4. DEVELOPMENT 01‘ THIS TONGUE
 
a. Visceral Aches
1:. Development of the Tongue
 
5. GI:IN'IOA.I; CONSIDERATIONS
 
some Malformations of the race
:2. Introductory Remarks
 
b. Earelip
 
c. Cleft Palate
 
d. Oblique Facial Cleft
 
1. INTRODUCTION
 
Knowledge of the embryology of an organ is essential for an under-
standing of its structure; it is also an important source of information in
the field of malformations. This chapter deals with the development of the
face, the palate, and the tongue.
 
2. DEVELOPMENT OF THE FACE
 
In the human embryo, 3 millimeters in length (3 weeks old), the
rounded prominence formed by the forebrain (proseneephalon. the anterior
of the three primary brain vesicles) constitutes the greater part of the face.
It is covered by the ectoderm and a thin layer of mesoderm (Fig. 1).
 
First draft submitted by Harry Sicher.
l3
 
Early Develop-
ment, racial
Processes
1-1 ORAL HISTOLOGY AND EMBRYOLOGY
 
Below this rounded prominence there is a deep groove, the primary oral
groove or stomatodenm. Its caudal boundary is the first branchial arch
or mandibular arch. Its lateral boundaries are formed by the maxillary
processes which arise from the posterolateral ends of the mandibular
arch. and are directed upward and slightly anteriorly. In early stages,
the mandibular arch consists of three parts. On either side a smooth
bulge protrudes on the lateral and anterior surfaces of the embryonic
head. They are ‘united at the midline by the copula (Fig. 2. -1).
 
The oral groove lined by ectoderin extends inwards to meet the blind
cranial end of the foregut. Here, the entoderinal gut and ectodermal oral
groove are separated by a double layer of epithelium, the buccopharyngeal
membrane (Fig. 1). Anterior to the cranial end of this membrane the
primordium of the anterior lobe of the hypophysis develops as a shallow
ectodermal pouch: Rathke's pouch. Rupture of the buccopharyngeal
membrane, which occurs when the eu1br_vo is about 3 millimeters long,
establishes the communication between the oral cavity and the foregut.
 
 
 
Fore brain
 
Rathke's pouch
 
Oral groove
 
Buccopharyngeal ———_:_.________
membrane — Foregut
Mandibular
arch
Notochord
Heart
 
\
 
l
 
1
 
t
\
.l
I
I
I
I
I
I
 
Fig. 1.—Dia.gi-am of a. median section through the head of a human embryo of 3 mm.
Oraingxlxvboriengemrated from foregut by a double layer of epithelium, the bucco-
 
T.he  Significant change in the development of the face is caused by
rapid proliferation of the mesoderni which covers the anterior end of the
brain, and a broad prommence is formed between the two maxillary proc-
esses (Fig. 2, it). This prominence constitutes the middle part of the up-
per face and is known as the frontonasal process. The next stage is the
formation of shallow and ever deepening oval grooves, olfactorv (nasal)
pits, which divide the caudal part of the frontonasal process into a single
middle and two smaller lateral nasal processes (Fig. 2, C). The lateral
nasal processes are adjacent to the ll1aXlllaI‘_\' processes, and are separated
from them by shallow furrows, running upward and laterallv. These flu-_
rows, the nasomaxillary groove, was formerly called the nasolacrimal
groove, but it is now known that this groove has no relation to the de.
 
Fig. 2.—Deve1opme.nt of the human face.
 
A and B. Embryo 3 mm. long, 3rd week: Frontonasal process (blue) undivided.
Caudal to mandibular arch (yellow), the hyoid arch and the third branchial arch.
Depression on top of figure is neuropore.
 
C. Embryo 6.5 mm. long. 4th week: Nasal Difs divide the frontonasal process into
medial nasal process (blue) and lateral nasal processes (red).
 
D. Embryo 9 mm. long, 5th week: Fusion of medial nasal and maxillary processes
has narrowed entrance into nasal pit.
 
E. Embryo 9.2 mm. long. 6th week: Fusion of medial and lateral nasal processes
 
has further narrowed the nostrils. Medial nasal process reduced in relative width. Eyes
at lateral edges of face.
Medial nasal
process
 
Lateral
nasal
process
 
Maxillary
process
 
Mandibular
arch
 
F. Embryo 14.5 mm. long, 7th week: Nasal area slightly prominent. Nasal septum
further reduced in relative width. Eyes on anterior surface of face.
 
G and H. Embryo 18 mm. long, Sth week: Lidless eyes an anterior surface of face.
Their distance relatively reduced, mandible short.
 
1 and .1. Embryo 60 mm. long, 12th week: Lids closed. Nostrils closed by epithelial
proliferation. Relation of mandible to maxilla normal.
 
K. Adult face: the derivatives of medial nasal process (blue), lateral nasal processes
(red). maxillary processes (green). and mandibular arch (yellow). Modified after
Sicher and 'l‘and1er.1°
 
DEVELOPMENT or men .a..\1> ORAL curry 15
 
velopment of the nasolacriinal duct. The nasolacrimal duct begins its
development with the forniation of an epithelial ingrowth. along a line
parallel with, but medial to the nasoinaxillary groove (Fig. 3 .7
 
The medial nasal process grows downward more rapidly than the lateral
nasal processes. its rounded and prominent infer-olateral corners
are known as the globular processes (Fig. ‘2, C and D}. Later, the globular
processes come in contact with the maxillary processes on both sides. There-
fore, the lateral nasal processes do not take part in bounding the entrance
 
into the oral cavity.
 
Maxillary
process
 
Mandibular
arch
 
I-Iyoid arch
Eye
Nasomaxillary
groove
Nasolacrinial
groove
 
 
Fig. 3.—Photograph of human embryo of 10 mm. length. I\'asomaxilIa.ry and nasolacrimal
grooves. (Courtesy Dr. P. Gruenwald.)
 
The subsequent changes are only partly due to fusion of primarily
separated “processes.” A fusion takes place only during formation of the
primary palate and, to some extent, during the development of the
mandible. In all other regions the grooves separating the facial processes
gradually become shallow by proliferation of the mesoderm, and finally
disappear. The primary palate is a horseshoe-shaped rounded structure
that will give rise to the upper lip and the anterior part of the upper
alveolar process. The term “primary palate" for this tissue has been
chosen because in the embryo it separates nasal duct from oral cavity
and because a small anterior part of the palate is derived from the same
tissue.
 
The formation of the so-called primary palate (Fig. 4) and the primary
choana begins with a deepening of the nasal or olfactory pit (Fig. 4,
A and A’). Here, an actual fusion takes place, beginning at the inferior
border of the nasal groove. At first the lateral border of the medial nasal
process fuses with the adjacent part of the maxillary process. (Fig. 4, B);
 
Formation of
 
Pnmary
Palate
16 ORAL I-IISTOLOGY AND EMBRYOLOGY
 
Medial nasal
 
PfO!l5|
 
Nasal pi‘!-
 
Lad’: ml nasal
Plocus
 
Man‘ II Ai’L_.[
P1-test.
 
Mau:1i'He
 
Fig. 4.—Six smges in the development of the primary palate (diagrams).
 
A and .—l'.—Face of a. human embryo of 6.5 mm. length (compare Fig. 2, 0). The zig-
zag line on the inferior border of the nasal pit marks the line or later fusion of medial
ntasal procezs to maxillary and lateral nasal processes. The broken line marks the plane
0 section .
 
B and B’.-—-Human embryo of 9 mm. length (compare Fig. 2, D). The medial nasal
process has fused with the maxillary process. By this tuslon _a.n epithelial wall has been
formed which is visible in section B’. The nasal pit is closed in its interior part to form
a short blind olfactory sac.
 
6‘ and b".—Human embryo, 9.5 mm. in length (compare Fig. 2, E). The medial nasal
process is now fused to maxillary and lateral nasal processes. The epithelial wall has
lengthened (0'). The arrow in 0' points to the area in which the epithelial wall sepa-
rates olfactory san from oral cavity.
 
D.—Huxnan embryo of 12 mm. length. The plane or section is as in Figs. A’, B’, and
C". The mesoderm has broken through the superior part of the epithelial _wa1l thus
strengthening the primarily epithelial fusion of medial nasal process to maxillary and
lateral nasal processes. The interior part of the epithelial wall has thinned out (arrow).
 
_E.-—_Human embryo of 14 mm. length. The destruction of the superior part or the
epithelial wall by proliferating mesoderm (crosses) has advanced. The interior part of
the epithelial wall is thinned out to form the nasobuccal membrane (arrow).
 
F.—Human embryo of 15 mm. length. The nasobuccal membrane has disappeared.
Nasal cavity communicates with oral cavity through the primary choana (arrow): The
superior part of the epithelial wall is entirely replaced by proliferating mesoderm form-
ing the primary palate between nasal and oral cavities
m'«:vr:Lo1>.\1E.\"r or race .a..\1) ORAL CAVITY 17
 
later, the medial nasal process fuses with the tip of the lateral nasal process,
and, therefore, the maxillary process does not border the outer nasal
opening or the nostril (Fig. -1, C).
 
By the fusion of the epithelial covering of the processes an epithelial
lamina, or epithelial wall, is formed, extending from the lower border
of the nostril to the blind end of the nasal groove at the anterior part
of the primitive oral cavity «Fig. -1. B and ('3. The epithelial wall is de-
stroyed by a penetration of the adjacent mesotlerm which comprises the
main body of the processes éFig. -l. D and E . Only the part close to the
oral cavity persists: it thins out and forms the only boundary between the
blind oral end of the nasal groove and the primitive oral cavity itself
(Fig. 4, D and E’). This epithelial lamella is called the bucconasal mem-
brane. When this membrane ruptures and disappears the nasal sac opens
into the primitive oral cavit_v through the primary choana «Fig. 4, F 3.
The bar of tissue between nasal duct and oral cavity at the edge between
facial and oral surfaces is the primary palate ( Fig. 4. F ,1.
 
 
Fig. 5.—Ma.ndible of a. human embryo of 6.5 mm. length (fourth week) showing the
median and lateral groovm. (Sicher and Pohl.')
 
While these changes take place in the upper region of the face the
mandible undergoes a peculiar transformation; at first it is an undivided
arch. In embryos, approximately 5 to 6 millimeters in length, furrows
appear on the mandible (Fig. 5): one, in the median plane, divides the
mandible into halves. On either side of this sharp median groove,
parallel to and not far from it, another furrow develops. The median
groove disappears by coalescence of the medial prominenees. The lateral
grooves, first reduced to rather deep pits, are eventually closed by fusion of
their epithelial lining. These grooves and pits close and disappear simul-
taneously with the fusion of nasal and maxillary processes in the upper
face; this occurs in embryos about 10 millimeters long (6 to 7 weeks).
 
Further development can be explained briefly by difierential growth of
the regions of the embryonic face (Fig. 2). The most important change
is caused by the fact that the derivatives of the medial nasal process grow
 
more slowly in breadth than those of the lateral nasal and maxillary
processes. On the other hand, the middle region of the face between the
 
Median groove
 
. Lateral groove
 
Development
of Mandibu-
lar Arch
 
Later Develop-
ment
18 OR.-\L IIISTOLOGY .-\.\'D IBAIBRYOLOGY
 
eyes increases in an anterior direction and, thus, bulges over the surface of
the face. Thereby. tl1e external nose is formed and, at the same time, the
eyes, fiI’S't situated on the lateral surface of the head. come to lie on the
anterior surface Fig. 2. E’, F, and G). The outer nasal openings are tem-
porarily closed by proliferating epithelium. as are the openings of the eyes
after development of the lids (Fig. 2, I and J).
 
The nose, even in a newborn infant, is not yet fully developed. This is
illustrated by the fact that all children are born with a deeply saddled
snub nose. Only at the time of puberty does the nose develop to its in-
herited size and shape.
 
The growtli of the mandible follows a peculiar curve. At first it is small
as compared with the maxilla: the growth in length and width shows a spurt
coinciding with a certain stage in the development of the palate. Later,
the mandible again lags in growth behind the maxilla (Fig. 2, G and H).
A t'etns of ‘2 to 3 months still shows a physiological mierognathism which
disappears before birth. The oral opening is, at first, very wide. In the
lateral area the upper and lower lips fuse to form the cheeks and, thereby,
the width of the mouth is considerably narrowed.
 
3. DEVELOP]!/EEINT OF THE SECONDARY PALATE
 
D°"1°Pm°11* When the primary palate is formed the primary nasal cavity is a short
 
e duet leading from the nostril into the primitive oral cavity. Its outer
 
and inner openings (primary choanae) are separated by the primary
palate (Fig. 4), which develops into the upper lip, the anterior part of
the alveolar process, and the premaxillary part of the secondary palate.
 
" Nasal
 
 
 
 
_ septum
Upper lip Inferiolr;
. COIXC 8.
T°°t“l "age Palatine
process
Pharyngeal . . ‘ .Eustachia.n
1'00! tube
 
Pig. 6.-—Reconst1-uction of the root‘ of the primitive oral and pharyngeal cavities of a
human embryo of 23 mm. length (8th week). Primary palate and internal surface of
maxillary process form a. horseshoeshaped and incomplete root of the oral cavity. In
the center the oral cavity communicates with the nasal cavity. At the edges of maxillary
proceses the palatme processes develop. (Sieher and Tandlerl“)
 
When the primitive oral cavity increases in height, the tissue separating
the two primitive ehoanae grows back and down to form the future nasal
septum. At this stage, the oral cavity communicates freely with the nasal
cavities. The oral cavity has an incomplete horseshoe—shapcd roof formed
DE\'ELOP.\lE.\'T OF I-‘AC1-I AND ORAL C.\\'I'l"1'
 
anteriorly by the primary palate and laterally by the inner horizontal
surface of the maxillary processes ‘Fig. 6 . In the middle the oral cavity
communicates with the nasal cavities to the left and right of the nasal
septum (Fig. T).
 
Folds develop where the lateral part of the oral roof bends sharply
into the vertical lateral wall of the nasal cavity. They grow downward al-
most vertically and lie to each side of the tongue which, in cross section, is
high and touches the inferior edge of the nasal septum (Fig. 7). This
vertical process, the posterior end of which can be traced to the lateral
walls of the pharynx, is the palatine process (Figs. 6 and '7).
 
 
 
.\
 
Nasal cavity
 
Nasal septum
 
Palatine process V —- -'
 
~‘ "Hr,
 
Meckel’s cartilage
 
Fig. 7.—-—Frontal section through the head of a human embryo of 24 mm. length (8th
week). Tongue high and narrow between the vertical palatine processes. (Courtesy Dr.
P. Gruenwald.)
 
The secondary palate which separates oral and nasal cavities is formed
by a fusion of the palatine processes. after they have changed from a ver-
tical to a horizontal position (Fig. 8). The anterior parts of the palatine
processes fuse not only with each other but also with the inferior edge of
the nasal septum (Fig. 9 ). In this area the hard palate develops. The
posterior parts of the palatine processes which form soft palate and uvula
have no relation to the nasal septum.
 
The transposition of the palatine processes can occur only when the
tongue has moved down and. thereby has evacuated the space between these
processes. This is made possible by a sudden growth of the mandibular
arch in length and width, at this time. The growth of the mandible is
 
Formation and
closure of
 
Secondary
Palate
Nasal septum
 
Inferior concha
 
J Palatine process
 
I  Tectal ridge
' . §
. p _ «_
 
Fig. 8.——F‘ronta1 section through the head of a. human embryo of 30 mm. length (9th
week). Tongue has evacuated the space between the palatine processes and lies flat and
 
wide_wlthin the mandibular arch. The palatine processes have assumed a. horizontal
POSHIOD. (Courtesy Dr. P. Gruenwald.)
 
Interior concha
 
Palatine process
 
_ — —— MeckeI's
\' ca.rtila.ge
 
Fig. 9.~—-Frontal section through the head or a human embryo slightly older than that
in Fig. 8. The honzontal palatine processes have fused with each other and with the
nasal septum. Secondary palate separates nasal from oral cavitl
DE\'ELOP1IE.\'T OF FACE AND ORAL CAVITY
 
accelerated to such an extent that a mandibular protrusion can be ob-
served. The tongue drops into the wide arch of the mandible and as-
sumes its natural shape, with its transverse diameter larger than its
vertical (compare Fig. 7 with Figs. 8 and 9}. The transposition of the
palatine processes is brought about by difierential growth. The meso-
dermal cells are densely grouped on the oral (lateral) surface of the
vertical palatine processes, especially at the angle between the process
itself and the lateral part of the oral roof 4‘Fig. '7). The dense arrange-
ment of the cells and the presence of mitoses prove this area to be one
of rapid proliferation. In other words, the oral surface of the fold grows
more rapidly than the nasal; this, necessarily. leads to a rapid change in
the position of the fold away from the faster growing side. Thus, the
palatine processes turn into horizontal position immediately after the
tongue has evacuated the space between them.
 
Upper up Tegmen oris
 
Tectal ridge
 
 
ggitngjlate ‘ l » nuszacman tube
roof 3 Um“
 
Fig. 10.—Reconstruction of palate or a. human embryo or 28.5 mm. length. The pala-
tine processes fused in the area of the hard palate. The fusion has not reached the soft
palate and uvula. (Sicher and Tandlen”)
 
When the palatine processes have assumed their horizontal position,
they touch the lower border of the nasal septum, but are still separated
from each other by a median cleft (Fig. 8) which widens posteriorly.
The cleft closes gradually in an anterior-posterior direction. At first an
epithelial suture can be observed between the palatine processes and
between those and the nasal septum (Fig. 9). Later, this epithelial wall
is perforated and broken up by growing mesoderm; remnants of the
epithelium may persist as epithelial pearls. The epithelium remains only
at the anterior end where the palatine processes fuse with and partly
overgrow the primitive palate on its oral side. Here, the epithelium
forms two strands, beginning in the nasal cavity and uniting below the
septum to connect with the oral epithelium. They are the primordium of
the nasopalatine ducts, vestigial in man (see chapter on Oral Mucous
Membrane).
Tuberculum of upper llp
 
Papma palafina I Tectolabial frenulum
 
 
   
 
 
’ /:1‘ Pars villosa. 3
’ , of upper lip
 
Alveolar ridge Pars glabm _
 
J
 
Pseudo-alveolar ridge — .... __
 
—— Tuberculum of upper lip
 
— Tectolabial frenulum
 
/T Pars villosa;
 
 
Papilla. palatina of upper lip
 
- ——— Pars glabra.
 
Pseudo-alveolar — ,‘ .;’
ridge '
 
Tuberculum of upper lip
Upper labial trenulum
 
Pars villosa. 1
 
Papilla or upper lip
pa.Ia.- Pars glabra
tina.
—— Lateral frenulum
- I
Alveolar _
 
Pseudo- -4
alveolar K
ridge '
 
.3’;
 
W 1;’ v
 
 
w-————
 
0.
Fig. 11.—-Advanced ta ‘ th d I
3 months old. 3. I-Iumzn gin: 4 1'1e1on§l‘;§ %Il’g.len(§. °Htut£:nh:‘e.‘ViVbI:)al.‘Il1atieIlfalAl-1E. Human fetus’
 
Note the changes in th 1 t‘ h‘ f ' '
between the alveolar ridge eanxcle :sle‘l’xr¢|is;:I-l21l)l\':3)olal:'a‘r£l‘v.E1?¢:3. p(a§il::Il;a'era:;l1dtr.l‘ea:lIEg1l1<;nn1°§'nd those
nx«:vELornE.\'r or I-‘ACE A.\'D om}. CAVITY 23
 
It has to be stressed that the entire palate does not develop from the
palatine processes. They give rise only to the soft palate and the central
part of the hard palate. This portion of the hard palate. termed the teg—
men oris, is surrounded by a horseshoe-shaped prominence. the tectal ridge
(Fig. 10).
 
The palate is separated from the lip by a shallow sulcus. From its
depth two epithelial laminae arise: an outer vestibular and an inner
 
dental lamina. Later, the alveolar process forms from the mesoderm be-
tween these laminae.
 
The palatine papilla develops very early as a round prominence in the
anterior part of the palate. Irregular transverse folds. the palatine rugae.
cross the palate in its anterior part. At this stage the lips show a definite
division into an outer smooth zone, pars glahra, and an inner zone, beset
with fine villi, pars villosa. In the upper lip the middle part of this inner
zone is prominent, forming the tubercle of the upper lip. A fold con-
nects the palatiue papilla with this tubercle: the tectolabial frenulnm
(Fig. 11, .4 and B).
 
When, in later stages, the growing alveolar process bulges between
palate and lip the tectolabial frennlum is separated from the palatine
papilla and persists as the upper labial frenulum. connecting the 'anterior
surface of the alveolar ridge with the upper lip (Fig. 11. C’).
 
The development of the maxillary alveolar ridges is complicated by the
appearance of a bulge in the molar region which may be easily confused
with the alveolar process. It has been called the pseudo-alveolar ridge and
disappears gradually when the alveolar process expands posteriorly
(Fig. 11).
 
The development of the alveolar ridge in the mandible is simple. No
pseudo-alveolar ridge is present and the alveolar process bulges gradually
into the oral cavity, inside the labial sulcus. The labial sulci open up
and form the oral vestibule which extends posteriorl_v into the region of
the checks.
 
4. DEVELOPMENT OF THE TONGUE
 
Before describing the development of the tongue a few words should
he said about the development of the branchial arches (Fig. 2). A prom-
inence similar to the mandibular or first branchial arch develops parallel
and caudal to it. This, the second or l1_void arch, is separated from the
first by a sharp and deep furrow. Caudal to the second branchial arch
a third, fourth, and fifth develop, each smaller and less prominent than
the preceding. The last three arches do not reach the surface at the
midline but are confined to the lateral region of the neck.
 
The furrows which separate the arches on the outer surface are the
branchial grooves. Corresponding deep furrows develop as lateral
pockets on the pharyngeal wall; these are the pharyngeal pouches
(Fig. 12, A).
 
Development
of Oral
Vestibule
and Alveolar
Ridge
 
Brannhial
24: ORAL HISTOLOGY AND EJIBRYOLOGY
 
The epithelium of the pharyngeal pouches gives rise by complicated
processes to a variety of organs. From the first pouch are derived the
auditory tube and the cavities of the middle car. In the region of the
second pouch the palatine tonsil is laid down. The third gives rise to one
parathyroid gland and the thymus; the fourth to the second parathyroid
 
and the ultimo-branchial body.
 
Lateral tubercule —-—-——:-_‘_"__. L
 
Tuberculum impa: ———- ‘— ' '  *”,v.w_“§‘
. 4 - u .. I
 
     
 
 
Copula of 2nd and
 
 
3rd branchial arch 3rd arches
4th branchial arch j
* L
A.
Lateral t“b°1'¢“1°" V. 7 I‘ T. - ‘ — Tuberculum impar
 
It bronchial arch-
L
 
 
id branchial ar<~.h—  lg?
 
rd bx-anchial arch
 
' __ Epiglottis
 
eav1i«‘ti§.sJé§;;—t13.er\!r]elvc;;i)tntnI;elxl1.t of the tongue. Anterior wall of pharynx and floor of the 01-31
 
A. Human embryo of 3.5 mm. length (3rd week).
B. Human embryo or 6.5 mm. length (4th week).
 
On the outside the third, fourth, and fifth arches are overgrown by a.
caudal outgrowth of the second arch, the ope:-culum (Fig. 20). Thus,
third, fourth, and fifth arches are placed in a deep recess, the cervical
DEVELOPSIENT OF I-‘ACE AND ORAL CAVITY Z0
 
sinus. Later, this is closed by fusion of the operculum with the lateral
Wall of the neck. The cavity of the recess is soon obliterated although
remnants may give rise to branchial or cervical cysts.
 
Lateral tuberculum _?___ _ _
gt , . Tuberculum impar
 
lst branchial arch —£--~¢-- --
 
Znd branchial arch -1”
Apex of tongue
Body of tongue
 
Base of tongue For-amen cecum
 
Fig. 12.——Coutinued.
 
0. Human embryo of 8 mm. length (5th week).
D. Human embryo of 11 mm. length (6th week). (Sicher and Tandlerfi.)
 
The tongue is derived from the first, second, and third branchial arches. Development
The dividing line between the derivatives of the first and the more ¥,,::,
caudal arches is marked throughout life by the terminal sulcus in the
area of the vallate papillae. The body and apex of the tongue origi-
nate as three prominences on the oral aspect of the mandibular arch
(Fig. 12, A B, and C). The lateral lingual prominences are two in
number, one on each side; the third, unpaired, appears between these two
and somewhat posteriorly; it is the tuberculum impar. The base of the
tongue develops later as a bulge on the middle part (copula) of the sec-
ond and the third arches. The unpaired tubercle. prominent and large at
first, is soon reduced in relative size (Fig. 12, C) and, later, almost disap-
 
pears (Fig. 12, D).
26 ORAL HISTOLOGY .\.\'n n.\n3m'o1.oor
 
In the midline, between the derivatives of the first and Second aI‘0hCS
which contribute to the development of the tongue, the thyroid anlage
develops. This gives rise to the thyroid gland by progressive downward
growth. The beginning of the traiisitory thyroglossal dllct is 111aI'k€d
by the forameu cecum of the tongue which persists in the adult. In this
region thyroglossal duct cysts may develop.
 
The later stages of tongue development are characterized by a mush-
room-like growth of the organ, and by gradual differentiation of the
various lingual papillae (see chapter on Mucous Membrane). The skeletal
(extrinsic) muscles of the tongue grow into its mesodermal primordium;
the intrinsic muscles differentiate in situ from the mesenchyme of the
tongue.
 
The described development of the tongue explains two malformations.
A lack of fusion between the two lateral mandibular tubercles may cause
a bifid tongue. A persistence of the tuberculum impar is said to be the
cause for the rhomboid glossitis.
 
5. CLINICAL CONSIDERATIONS
Some Malformations of the Face
 
Introductory The most frequent malformations of the face are known as clefts. Clefts
mm“ of the lip, jaw, or palate may occur once in about eight hundred births.‘
The complete harelip is a cleft, lateral to the midline cutting through the
upper lip and continuing as cleft jaw or gnathoschisis through the anterior
part. of the alveolar process. It may be unilateral or bilateral. The cleft
palate may be unilateral or bilateral, complete or partial, involving the
uvula only or extending into the soft and hard palate. The oblique facial
cleft is a defect which begins in the upper lip and can be traced through
the nostril. or lateral to it, over the cheek to the eye. More or less deep
pits in the lower lip not far from the midline, on one or both sides, are
known as labial fistulae.
 
Han-.1ip, Cleft In its complete form the harelip and cleft jaw is a cleft which extends
3;; ifadme from the lower border of the nostril, lateral to the midline, through the
upper lip and upper alveolar process, to the region of the foramen in-
cisivum. In the past, the development of this malformation was attributed
to a lack of fusion of the medial nasal process with the lateral nasal, and
the maxillary process. However, recent investigations“ have revealed
that an epithelial fusion does occur in cases of harelip but that the epithe-
lial wall is not perforated by mesoderm. Therefore, the epithelial union of
these processes ruptures. This explanation is borne out by the occurrence
of thin strands of tissue which Imite, in some cases, the medial and lateral
walls of the harelip. These bridges develop if the mesoderm perforates
the epithelial wall only in a restricted area. Ilarelip and cleft jaw would
be evident at 6 to 7 weeks in utero.
 
The relation of cleft jaw to the bone and to the teeth varies considerably.
In some cases the cleft corresponds to the suture between premaxilla
DE\'ELOP.\lI-‘..\‘T or men .\.\'o ORAL CAVITY 27
and maxilla: in other cases the cleft cuts through the premaxilla itself,
dividing it into a medial and a lateral part. Frequently, the lateral in-
cisor is found medial to the cleft jaw. in some cases lateral to it. The
lateral incisor is. in some instances, medial to the harelip. and a super-
numerary lateral incisor lies lateral to it. In other cases the lateral incisor
is missing. The explanation for this variability is that the skeletal parts
appear long after fusion of the facial processes has been completed. Thus,
the bones develop in a uniform tissue and with no regard for the primary
boundaries between the processes.
 
The dental lamina, the matrix of the tooth germs, is likewise independ-
ent of the facial processes. Harelip and cleft jaw occur in the general re-
gion of the lateral incisor. I11 some cases. it may cut the matrix medially or
laterally to the prospective primordium of the lateral incisor. or it may go
right through it. In the latter cases. by a process of regeneration. each part
of the divided primordium may produce a complete lateral incisor or, on
 
the other hand, the development of the lateral incisor may be suppressed
altogether.
 
Cleft palate results from a lack of fusion of the palatine proeeses, with
each other and the nasal septum. In unilateral defects one process fuses
with the lower border of the septum so that one nasal cavity is completely
separated from the oral cavity. Palatal fusion is usually completed at
the end of the fourth month in utero.
 
The fusion of the palatine processes commences at their anterior ends and
proceeds backward. The process of fusion ma_v be interrupted at any time.
This explains the different types of cleft palate. The cleft may be limited
to the uvula, may extend through a portion of, or the entire soft palate, or
may involve parts of. or the entire hard palate.
 
Cleft palate is frequently (8-1 per cent) associated with a unilateral or
bilateral harelip. In the latter case the tissues between the two clefts
are, sometimes. protruding as a knohlike growth in the midline. whereas.
in other cases. the tissues may fail to grow. The latter results in the
formation of the so-called false median cleft of the upper lip.
 
Heredity probably is the major etiologic factor in clefts of the face,
lip, jaw, and palate. Members of one family sometimes show. in ad-
dition to, or instead of. harelip. the so-called fistula of the lower lip.
This tends to show that these fistulae develop from causes similar to
those responsible for harelip. In these cases. the pits between the medial
and lateral parts of the mandibular arch (Fig. 5) remain open and even
enlarge.
 
When the fusion between upper and lower lips remains incomplete, the
cheeks do not develop to their full extent and the mouth is abnormally wide
(macrostoma) .
 
The oblique facial cleft, extending from the upper lip to the region of
the eye, was, in the past, explained by failure of fusion between the maxil-
lary process and the nasal processes. It has been stressed that such fusion
occurs only below the nostril. The explanation for the oblique cleft
 
cleft
Palate
 
Oblique
Cleft
28 oau. HISTOLOGY .A.:<n nuemzonoer
 
between nostril and eye has been sought for in a traumatic injury to the
face of the embr_vo. Adhesions of the amnion to the face may, according
to this theory, cause this cleft by producing actual tears or cuts which
have a variable relationship to the nasolacrimal duct.
 
Dermoid or epidermoid cysts may be located at any fusion point of
the body, including those in the oral region. Median cysts are formed in
the median fissure of the palate from embryonic epithelial inclusions. In-
cisive canal (nasopalatine duct) cysts form in or at the incisive canal
from remnants of the nasopalatine ducts. Globulomaxillary cysts form
from epithelial inclusions between the globular and maxillary processes.
Branchial fistulae result most frequently from the first branchial groove
or pharyngeal pouch, and branchial cysts result from proliferation of
epithelial rests in the region of branchial clefts or the cervical sinus.“
 
References
1. Arey, L. B.: Developmental Anatomy, ed. 5, Philadelphia, 1946, W. B. Saunders
(10
 
Ex’)
 
Burket, L. W.: Nasopalatine Duct Structures and Peculiar Bony Patterns in
the Anterior Maxillary Region, Arch. Path. 23: 793, 1937.
 
Grace, L. 6%.: Frequency of Occurrence of Cleft Palate and Bare Lips, J. Dent.
Research 22: 495, 19-13.
 
Hochstetter, F.: Beitriige zur Entwicklungsgeschichte des menschlichen Gaumens
(Contributions to the Development of the Human Palate), Morphol. J ahrb.
77: 179-272, 1936.
 
Keibel, F., and Mall, F. P.: Manual of Human Embryology, Philadelphia and
London, 1910, J. B. Lippincott Co.
 
Peter, K.: Die Entwicklung des Saugetiergaumens (Development of the Mam-
malian Palate), Ergebn. d. Anat. Entwcklngsgesch. 25: 448-564, 1924.
 
7. Politzer, Gr.: Die Grenzfurche des Oberkieferfortsatzes und die Tranennasenrinne
beim Menschen (The Limiting Sulcus of the Maxillary Process and the Nasc-
gafgcrixgal Groove in Man), Ztschr. f. Anat. u. Entwcklngsgesch. 105: 329-
 
. , 1 36.
8. Robinson, H. B. G.: Classification of Cysts of the Jaws, Am. J. Orthodont. 85
Oral Surg. 31: 370, 1945.
9. Sicher, H., and Pohl, L.: Zur Entwicklung des menschlichen Unterkiefers (De-
velopment of the Human Mandible—A Contribution to the Origin of the
Fistulae of the Lower Lip), Ztschr. f. Stomatol. 32: 552-560, 1934.
10. Sicher, H., and Tandler, J.: Anatomic fur Zahniirzte (Anatomy for Dentists),
 
Vienna and Berlin, 1928, Julius Springer.
11. Veau, V., and Politzer, G.: Embryologie du bec-de-liévre; le palais primaire
(Embryology of the Harelipz The Primary Palate. Formation and Anoma-
lies), Ann. d ’ anat. path. 13: 275-326, 1936.
 
.°°S"l“f-°
CHAPTER II
 
DEVELOPMENT AND GROWTH OF TEETH
 
1. IN'1'B.0DU'C'1'ION
 
Histologic Stages and Physiologic Processes
Tooth Development
 
2. DEVELOPMENTAL STAGES
 
a. Dental Lamina and Bud Stage
 
b. Cap Stage
 
c. Bell Stage
 
d. Hertwig’s Epithelial Boot Sheath and Boot Formation
 
3. EISTOPHYSIOLOG-Y AND CLINICAL CONSIDERATIONS
 
Initiation (Dental Lamina and Bud Stage)
Proliferation (Bud and cap Stages)
Histodifierentiafion
 
Morphodifierentiation
 
Apposition
 
1. INTRODUCTION
 
This chapter deals with the development of the tooth beginning with
its initiation from the oral epithelium, up to the formation of enamel and
dentin (Fig. 13) (Table I).
 
The life history of the tooth consists of the following stages:
 
1. Growth: (:1) Initiation; (1)) Proliferation; (c) Histodiiferentiation;
(d) Morphodiiferentiation; and (e) Apposition
 
2. Calcification. 3. Eruption. 4. Attrition.
 
These stages, except for initiation, are not sharply demarcated, but
overlap considerably and many of them are concurrent for some time
(Fig. 13). Thus, one microscopic section shows the predominance of one
stage and indicates characteristics of the preceding as well as succeeding
stages.
 
The dilferent stages in the growth of the teeth will first be considered
in terms of their morphologic and histologic appearance, and will then be
discussed in terms of the physiologic processes which they represent. An
understanding of the histologic structure is greatly facilitated by an ap-
preciation of its physiologic aspects. The histologic stages in tooth de-
velopment are well defined and, while more knowledge will be added to this
field, it is probable that further advance will be largely in the direction
of histophysiology. The histologic description of the subject matter in
this chapter will, therefore, be followed by physiologic interpretation
(Table I).
 
2. DEVELOPMENTAL STAGES
 
The tooth germ develops from ectoderm and mesoderm. The ectoderm
of the oral cavity forms the epithelial enamel organ which molds the
 
First draft submitted by Isaac Schour in collaboration with Maury Hassle:-.
 
29
D  , E.
Initiation Proliferation Hiatodifferentiation Appoaition (Ir-tm-0&5-eoua) unto oralirc-avityV
(Bud. stage) (cap ataqo) (Ben atuqe) K
 
and —v
 
GROWTH CALCIFI CATION ERUPTION ATTRITION
 
Fig. 13.—DIagran1matlc illustration of the life cycle of the tooth. Stage 0 shnws active
from Schuur and Ma.-;sler.")
 
 
nxorplladlrrerentlatian as well as hlstodifferentiatlon. (Modified
31
 
DE\'I~1l.0P.\lE.\"I' AND GROWTH OF TEETH
 
i Tooth buds and
dental lamina
 
Enamel organs
 
 
 
Enamel organs
( deciduous
teeth )
 
Anlage of
permanenl
tooth
 
 
 
I’ .
 
.-tnlage of first
permanent
molar
 
1,-
 
Fig. I-l.--Diagrammatic reconstruction uf the dental lamina and enamel organs of the
niamlible. (.\Io1lified from I\'urberg.~)
 
A. 22 mm. embryo, bud stage (8th week).
B. 43 mm. embryo, cap stage (10th week).
 
6'. 163 mm. embryo. bell stage (about 4 months old). The primordia of permanent
teeth are seen as thickenings of the dental lamina. on the lingual side of each tooth germ.
Distal extension of the dental lamina with the primordium of the first molar.
Dental
Lamina
 
32 ORAL HISTOLOGY .-ma EMBRYOLOGY
 
shape of the entire tooth and gives rise to the enamel. The mesoderm
inside the enamel organ. the dental papilla. differentiates into the dental
pulp and elaborates the dentin. The mesoderm surrounding the enamel
organ, the dental sac. forms the eenientum covering the root, and the
periodontal memlzrane.
 
A. Dental Lamina and Bud Stage
 
The first sign of human tooth development is seen during the sixth week
of embr_vonic life (11 mm. e1nbr_vo). At this stage the oral epithelium
 
 
 
 
Oral cavity
 
Dental lamina %—:———.—..
 
4.2
bower jaw
 
Tongue
 
 
 
4.
4 y ‘ ’
,,—. :3. ‘ ~ -—- '-‘v — Mitotic cell
 
{ division in
 
. . : _ f 1 epithelium
Basement:-:—~ T «, .  ___ I '
membrane ~. t / u _.._ ‘% 3
x .
 
Mitosis '— " l ‘
 
Mitotic cell
 
1 division in
 
mesoderm
B. .. . ._ __ _ .
 
Fig. 15.-—Initie.tion of tooth development Human embryo 13.5 mm. long. 5th week.
(0rba.n').
 
A. Sagittal section through upper and lower jaws.
B. High magnification of thickened oral epithelium.
 
consists of a basal layer of high cells and a surface layer of flattened
cells. The rich glycogen content of their cytoplasm, which does
not stain in routine preparations, gives them an empty appearance.
The epithelium is separated from the connective tissue by a basement
membrane. Certain cells in the basal layer of the oral epithelium
begin to proliferate at a more rapid rate than do the adjacent cells. An
DE\‘ELOP.\IE.\'T AND GROWTH or TEETH 33
 
epithelial thickening arises in the region of the future dental arch and
extends along the entire free margin of the jaws (Figs. 1-1 and 15). It is
the primordium of the ectodermal portion of the teeth known as the dental
lamina. Mitotic figures are seen not only in the epithelium but also in the
subjacent mesoderm «Fig. 1.5}.
 
About the time of differentiation of the dental lamina there arise from
it and in each jaw. round or oval swellings at ten different points corre-
sponding to the future position of the deciduous teeth, the primordia of
 
Cent: * "
incisor
 
I..a.tera.l :-
incisor
 
 
"‘ d’ 1. ‘
*  3w.'.~-.
.' . Of £‘”‘c*s '*~ _‘
I . W .‘ ‘ l __
\ *1 . €‘-  .
.3’ v" 2 we  *3
&.._....—.'AI_--— 0” \ iv‘. K ' A 1
R‘ 4’ .
5? g “
£ 6- -, _~ _ ~Tooth bud
+3 : XL 3 
Lip furrow:-—--‘H-%!3:‘:"  t "" 1‘ ¥ 1‘; ‘,4’-‘.
band I  ~— t 1: . -5 4
‘ ' .,,.  '1 “iii Mesoderm
.—— x V__ ~ =
0.
 
Fig. 16.——Bud stage of tooth development (proliferation stage).
16 mm. long, 6th week (0rban5).
 
A. Wax reconstruction of the germs of the central and lateral lower incisors.
B. Sagittal section through upper and lower jaws.
0'. High magnification or the tooth germ or the lower incisor in bud stage.
 
Human embryo
 
Tooth Buds
 
(Prlmordta
of Teeth)
Outer and In-
ner Enamel
Epithelium
 
3-} ORAL HISTOLOGY .\.\‘D EMBRYOLOGY
 
their enamel organs, the tooth buds ( Fig. 16 l. Here the development of tlic
tooth germs is initiated and the cells proliferate faster than the adjacent
cells. The dental lamina is shallow. and microscopic sections often
 
show the tooth buds close to the oral epithelium.
 
B. Cap Stage
 
As the tooth b11d continues to proliferate it does not expand uniformly
into a larger sphere. Unequal growth in the different parts of the bud
leads to formation of the cap stage which is characterized by a shallow
invagination on the deep surface of the bud (Figs. 14, B and 17).
 
 
Dental lamina.
 
Vestibular lamina :' '-
 
-r.. \
 
Enamel organ
 
   
   
 
‘II
 
~  Enamel organ
-' '3 ‘v .
 
. —--- -—r?—-1 Enamel knot
 
,.
.:.‘
 
 
 
Bone of mandible ..
 
Mecl<el’s cartilage
B, L .__ for
 
Fig. 1'.'.—Cap stage of tooth development. Human embryo 31.5 mm. long. 9th week,
torhanfi)
 
A. Wax reconstruction of the enamel organ of the lower lateral incisor.
B. Labxoiingual section through the same tooth.
 
The following histologic changes seen in the cap stage are prepara-
tory to those in the subsequent bell stage:
 
The peripheral cells of the cap stage appear in two portions, the
outer enamel epithelium at the convexity consisting of a single row of
short cells, and the inner enamel epithelium at the concavity consisting
of a layer of tall cells (Figs. 17 and 18).
Di-‘.\'El.0l’.\lE.\'T .\.\'D GROWTII OF TEETH
 
The cells in the central core of the enamel organ situated between
the outer and inner enamel epithelia begin to separate by an increase
of the intercellular fluid, and arrange themselves in a network called
the stellate reticulum or enamel pulp (Figs. 20 and 21). The cells assume
a branched reticular form, resembling mesenchyme. In this reticular
network the spaces are filled with a mucoid fluid rich in albumin. giving
the enamel pulp a cushion-like consistency which, later, protects the deli-
cate enamel-forming cells.
 
 
Vestibular lamina fr" V‘ I o
 
-— Enamel organ
 
 
   
 
Vestibular .,
lamina ,2
 
Enamel organ
 
Dental papilla
 
Fig. 18.—Cap stage of tooth development Human embryo -11.5 mm. long, 10th week.
(Orban.-")
 
A. Wax reconstruction of the enamel organ of the lower central incisor.
B. Labiolingual section through the same tooth.
 
Stellate
Reticulum
(Enamel
Pulp)
Dental
Papilla.
 
Inner Enamel
 
Epithelium
 
36 ORAL HISTOLOGY AND nunnronoer
 
At first, there is no change into a stellate arrangement of the cells in
the center of the tooth germ which contains the enamel knot (Fig. 17).
The latter projects in part toward the underlying dental papilla, so that
the center of the epithelial invagination shows a slightly budlike enlarge-
ment which is bordered by the labial and lingual enamel grooves (Fig.
17). At the same time there arises in the increasingly high enamel organ
a vertical extension of the enamel knot, called the enamel cord (Fig.
20). Both are temporary structures which disappear before enamel for-
mation begins. Another temporary appearance is an indentation in the
outer enamel epithelium, next to the enamel cord, called the enamel navel.
 
Under the organizing influence of the proliferating epithelium of the
enamel organ the mesench_vme, partially enclosed by the invaginated por-
tion of the inner enamel epithelium, proliferates; it condenses to form the
dental papilla which is the formative organ of the dentin and primordium
of the pulp (Figs. 17 and 18). The changes in the dental papilla occur
concomitantly with the development of the enamel organ. While the
enamel organ exerts a dominating influence over the adjacent connective
tissue, the condensation of the latter should not be considered as a pas-
sive reaction to the crowding by proliferating epithelium. The dental
papilla shows active budding of capillaries and mitotic figures, and its
peripheral cells adjacent to the inner enamel epithelium enlarge and,
later, differentiate into the odontoblasts.
 
Concomitant with the development of the enamel organ and the dental
papilla, there is a marginal condensation in the mesenchyme surrounding
the outside of the enamel organ and dental papilla. At first this mesen-
chymal border is distinguished by a lesser number of cells. Soon, how-
ever, a denser and more fibrous layer develops which constitutes the
primitive dental sac.
 
The enamel organ, the dental papilla and dental sac constitute the
formative tissues for a11 entire tooth and its periodontal membrane, hence
collectively form a tooth germ.
 
C. Bell Stage
 
As the invagination, developed during the cap stage, deepens and its
margins continue to grow, the enamel organ assumes the bell stage of its
development (Figs. 14, C, 19, and 20). The following histologic modifica-
tions of the cap stage are significant.
 
The inner enamel epithelium consists of a single layer of cells which
differentiate prior to amelogenesis into tall columnar ameloblasts (Figs.
20 and 21). They are 4 to 5 microns in diameter and about 40 microns
high. In cross-section they assume a hexagonal shape, similar to that
seen later in transverse sections of the enamel rods.
 
There is a change in the polarity of the ameloblasts which is proved
by the fact that their nuclei are no longer next to the dental papilla but
DEVELOP.\IEN'l‘ AND GROWTH OF TEETH 37
 
are situated near the stratum intermedium {see chapter on Enamel De-
velopment).
 
The ameloblasts exert an organizing influence upon the underlying
mesenchymal cells which differentiate into odontoblasts.
 
Several layers of low squamous cells, called stratum intermedium, appear
between the inner enamel epithelium and stellate reticulum I: Fig. 21). This
layer seems to be essential to enamel formation. It is absent in that part
of the tooth germ which is not amelogenic and which outlines the root
portions of the tooth.
 
The enamel pulp nstellate Ieticulunr expands further. mainly by in-
crease of the intercellular fluid. The cells are star-shaped with long
processes which anastomose with those of adjacent cells (Fig. 21).
 
The cells of the outer enamel epithelium flatten to a low cuboidal form.
At the end of the bell stage, preparatory to and during the formation
of enamel, the formerly smooth surface of the outer enamel epithelium
is laid in folds. Between the folds the adjacent mescnchyme of the
dental sac sends in papillae which contain capillary loops and thus pro-
vide a rich nutritional supply for the intense metabolic activity of the
avascular enamel organ.
 
In all teeth excepting the permanent molars the dental lamina prolifer-
ates at its deep end to give rise to the enamel organ of the permanent
successor. while it distintegrates in the region between the enamel organ
and the oral epithelium. The enamel organ becomes gradually inde-
pendent and separated from the dental lamina at about the time when
the first dentin is formed.
 
The dental papilla is largely enclosed in the invaginated portion of the
enamel organ. Before the inner enamel epithelium begins to produce
enamel, the peripheral cells of the suhjacent mesenehymal dental papilla
( or primitive pulp: undergo histoditferentiation into odontoblasts under
the organizing influence of the epithelium. They assume a high columnar
form and acquire a specific potentiality to take part in dentin formation.
 
The basement membrane separating the enamel organ and dental pa-
pilla, at the time just preceding dentin formation is called membrana
preformatira. Between this and the incompletely difierentiated odonto-
blasts there is a clear layer.
 
In the root the histoditfercntiation of the odontoblasts from the dental
papilla takes place under the influence of the inner layer of HertWig’s
epithelial root sheath. As the primary dentin is laid down the dental
papilla becomes the dental pulp.
 
Before apposition begins the dental sac shows a circular arrangement
of its fibers and resembles a capsular structure. With the development of
the root, the fibers of the dental sac differentiate into the periodontal
fibers which become embedded in the cementum and alveolar bone.
 
During the advanced bell stage the boundary between inner enamel
epithelium and odontoblasts outlines the future dentino-enamel junction
 
Stratum
Intermedium
 
Enamel
 
Outer Enamel
Epithelium
 
Dental
 
Papilla
 
Advanced
Bell Stage
Function of
Dental
 
38 ORAL n1s'roLocr .x.\'n EMBRYOLOGY
 
L Figs. 20 and 22). In addition, the junction of the inner and outer
enamel epithelia at the basal margin of the enamel organ, in the region
of the future cemento-enamel junction, proliferates and gives rise to
the epithelial root sheath of Hertwig.
 
 
Lip furrow band
 
Enamel organ
 
Dental
lamina
 
—_ _ Enamel
organ
 
Dental
papilla
 
 
Fig. 19.——Cap stage of tooth development. Human embryo 00 mm. long, 11th week.
(Orbanfi)
A. Wax reconstruction of the enamel organ of the lower lateral incisor.
 
B. Labiolingual section through the same tooth.
 
The functional activity of the dental lamina and its chronology may
be considered in three phases: The first is concerned with the initiation
of the entire deciduous dentition which occurs during the second month
in utero (Fig. 1-1, .1 and B). The second phase deals with the initiation of
the successors of the deciduous teeth. It is preceded by the growth of the
free end of the dental lamina lsuecessional lamina), lingually to the enamel
organ of each deciduous tooth. and occurs from about the fifth month in
DEYELOPBIEXT AND GRO\\‘T.'I OF TEETH
 
utero for the central permanent inc-isors, to 10 months of age for the
second bic-uspicl eFig'. 1-1. ('1 . The thingl phase is preceded by the extension
of the dental lamina distally to the enamel organ of the second deciduous
molar whit-I1 begins in the 140 mm. emlu-_\'o Fig. 1-1:. C‘ .. The permanent
 
. Oral
epithelium
 
Dental lamina
 
 
— '——————>- Enamel organ
V t‘b 1 “ ' "lap." "
es I u at —-TV \ -
lamina «Ix _ 1 _ ‘__ .-xnlage of
' ~ permanent
tooth
 
\\ V ‘U  Dental papilla
- \ _
 
Oral
epithelium
 
Dental lamina Enamel niche
 
. D ta] 1 '
Lateral dental ' - en amma
lamina.
 
Anlage of
permanent
tooth
 
Enamel cord
 
Dental [nu [Jilla -5-
 
Fig. ‘.‘0.—Bell stage of tooth development. Human embryo 10.‘: mm. long, 14th week.
(Orbanfi)
 
A. Wax reconstruction of lower central incisor.
B. Labiolingual section of the same tooth.
Ameloblast ——-—- — ' ~‘
l&Yel' _ Ii 3'
Stratum - -
lntex-medium ? '3 57
 
Basement A ‘
membrane
 
 
 
Fig. 21.—Tl1e four layers of the e1Jlthe“1fi.1l_gl18.!§l31 organ in high magnification. Area X
0 ug. .
 
Alveolar ridge "
 
   
 
Dental lamina
 
Enamel organ
 
. _ Anlage of
‘ permanent
 
Dental papilla
 
Flg. 22.—Advanced bell stage of tooth development. Human embryo 200 mm. long, age
about 18 weeks. Lablolingual section through the flrst deciduous lower molar.
 
Stellate reticulum
 
Outer enamel
 
epithelium
DEVELOPMENT .a.\'n GROWTH or 1'1-zarn 41
 
molars arise directly from the distal extension of the dental lamina. The
time of initiation is about -1 months of fetal life «in 160 mm. embryo) for
the first permanent molar, the first year for the second permanent molar,
and the fourth to fifth year for the third permanent molar.
 
It is thus evident that the total activity of the dental lamina extends
over a period of about 5 years, while any particular portion of it func-
 
Vc ‘I53
 
  I.
.. ' ~~ ‘I ".
ii-‘\.~.~.
 
s , Nasal cavity
' 4-.‘ '
 
 
 
 
   
   
 
Lower
central .
incisor
 
Fig. .‘:3.—Sagitt.al section through the head of a human fetus 200 mm. long. age about 18
weeks. in the region of the central incisors.
 
tinns for a much briefer period, since only a relatively short time elapses
after initiation before the dental lamina begins to disintegrate at that
particular location. Thus, whereas the free and deeper end of the dental
lamina gives rise to the bud of the permanent successor, its gingival por-
tion breaks up. Similarly, the dental lamina may be still active in the
third molar region although it has disappeared elsewhere except for occa-
sional epithelial remnants.
Fate of the
Dental
Lamina
 
Vestibular
 
-1'2 ORAL IIISTOLOGY .\.\'D I-‘JIBRYOLOGY
 
During the cap stage the dental lamina maintains a broad connection
with the enamel organ but, in the bell stage, it begins to break up
by niesenehgmal invasion which first penetrates its central portion and
divides it into the lateral lamina and the dental lamina proper. The
mesenehyinal invasion is at first incomplete and does not perforate the
dental lamina (Fig. 20). The dental lamina proper proliferates only at
its deeper margin which becomes a free end situated lingually to the
enamel organ a11d forms the bud (anlage) for the permanent successor
' Fig. ‘20 s. The rest of the structure becomes more fenestrated and finally
mostly resorbed. The epithelial connection of the enamel organ with the
oral epithelium is severed by the mesoderm. The tooth germ then becomes
a free internal organ. Remnants of the dental lamina may persist as epi-
thelial pearls.
 
Labially and buccally to the dental lamina, another epithelial thicken-
ing develops independently and somewhat later. It is the Vestibular lamina
also termed the bucco-gingival lamina or lip-furrow band (Figs. 18 and
19). It subsequently hollows out and forms the oral vestibule between the
alveolar portion of the jaws and the lips and cheeks (Figs. 22 and 23).
 
D. Eertwig’s Epithelial Root Sheath and Root Formation
 
The development of the roots begins after enamel and dentin formation
has reached the future cemento-enamel junction. The epithelial enamel
organ plays an important part in root development by forming the Hert-
wig’s epithelial root sheath which initiates formation and molds the shape
of the roots. It consists only of the outer and inner enamel epithelia,
without the stratum intermedium and stellate reticulum.” The cells of
the inner layer remain short and, normally, do not produce enamel. When
these cells have induced the differentiation of connective tissue cells into
odontoblasts and the first layer of dentin has been laid down, the epi-
thelial root sheath loses its continuity and its close relation to the surface
of the tooth. Its remnants persist as epithelial rests of Malassez.
 
There is a marked difference in the development of Hertwig’s epithelial
root sheath in teeth with one root and those with two or more roots. Prior
to the beginning of root formation the root sheath forms the epithelial
diaphragm in single-rooted teeth (Fig. 2-1:). The outer and inner enamel
epithelia bend at the future cemento-enamel junction into a horizontal
plane narrowing the wide cervical opening of the tooth germ.” The plane
of the diaphragm remains relatively fixed during the development and
growth of the root‘ (see chapter on Eruption). The proliferation of the
cells of the epithelial diaphragm is accompanied by that of the connective
tissue of the pulp which occurs in the area adjacent to the diaphragm.
The free end of the diaphragm does not grow into the connective tissue
but the epithelial organ lengthens coronally to the epithelial diaphragm
(Fin. 24, B). The diiferentiation of odontoblasts and the formation of
dentin immediately succeed the lengthening of the root sheath. At the
same time the connective tissue of the dental sac surrounding the sheath
proliferates and breaks up the continuous double epithelial layer (Fig. 24,
DI-L'\'ELOP.\{E.\‘T AND GRO\\'TH OF TEETH
 
(‘i into a network of epithelial strands ~Fig. 2-}. D . The epithelium is
pushed away from the dental surI'a(~e so that ('01ill€L‘Tl\'E' tissue comes into
contact with the outer surfac-e of the dentin. Coniiec-tive tissue cells dif-
ferentiate into eementohlasts and deposit a layer of cementum onto the sur-
 
     
 
ln” ‘
 
\ Epithelial dauphrugrr'n“"‘~J
 
 
Fig. 2-l.—~Three stages in root develoinnent (diagrams).
 
A. Section through a tooth germ showing the epithelial diaphragm and proliferation
zone of pulp.
 
B. Higher magnification of the cervical region of .-1..
 
C’. "Imaginary" stage showing the elongation of Hertwig’s epithelial sheath between
diaphragm and future cemento-enamel junction. Differentiation of odontoblasts in the
elongated pulp.
 
D. In the cervical part of the root dentin has been formed. The root sheath is broken
up into epithelial rests and is separated from the dentinal surface by connective tissue.
Differentiation of cenzentoblasts.
face of the dentin. The rapid seqiience of p1'oli1'e1-atioii and destruction of
Hertwig ‘s root sheath explains the fact that it cannot be seen as a continuous
layer on the s111'Iac-e of the developing root LFig. 2-1, D }. In the last stages
 
of root development the proliferation of the epithelium in the diaphragm
‘ . '.—Three sta es in the development of a. tooth with two roots, and one with
thrfelgrogtas. Surface vigew of the epithelial djaphragm. During growth o_t the tooth germ
the simple diaphragm (4) expands eccentrlcally go that hon_zonta._1 epxthellal fla._ps are
formed (.3). Later these flaps proliferate a.n_d umte (dotted lmes 1n 0') and divlde the
single cervical opening into two or three opening .
 
 
Fig. 26.——Two stages in the development of a. two-rooted tooth. Diagrammatic mesio-
distal sections of a lower molar. A. Beginning of dentin formation at the bifurcation.
3. Formation of the two roots in progress. (Details as in Fig. 24.)
nr:vELoPi1E.\"r AND GROWTH or TEETH 45
 
lags behind that of the pulpal connective tissue. Increasingly more of
the diaphragm is bent i11to the long axis of the root, the wide apical
foramen being thus reduced first to the width of the diaphragmatic open-
ing itself and, later, further narrowed by apposition of dentin and ce-
mentum at the apex of the root.
 
The peculiar development of the diaphragm in multi-rooted teeth causes
the division of the root stock into two or three roots.‘ During the general
growth of the coronal epithelial enamel organ the expansion of its cervi-
cal opening occurs in such a way that long tongue-like extensions of the
horizontal diaphragm develop (Fig. 25'}. Two such extensions are found
in the germs of lower molars, three in the germs of upper molars. Before
the formation of the root begins. the free ends of these horizontal epi-
thelial flaps grow toward each other and fuse. The single cervical open-
ing of the coronal enamel organ is then divided into two or three openings.
On the pulpal surface of the dividing bridges dentin formation starts
(Fig. 26, A), and on the periphery of each opening root development fol-
lows in the same Way as described for single-rooted teeth (Fig. 26, B).
 
If cells of the epithelial root sheath remain adherent to the dentin
surface they may differentiate into fully functioning ameloblasts and
produce enamel. Such droplets of enamel, called enamel pearls, are some-
times found in the area of bifurcation of the roots of permanent molars.
If the continuity of Hertwig’s root sheath is broken or is not established
prior to dentin formation, a defect in the dcntinal wall of the pulp ensues.
Such defects are found in the pulpal floor corresponding to the bifurcation
if the fusion of the horizontal extensions of the diaphragm remains incom-
plete, or on any point of the root itself. This accounts for the development
of accessory root canals opening on the periodontal surface of the root
(see chapter on Pulp).
 
3. EISTOPEYSIOLOG-Y AND CLINICAL CONSIDERATIONS
 
A number of physiologic growth processes participate in the progres-
sive development of the teeth (Table I). Except for initiation which is
a momentary event, these processes overlap considerably and many are
continuous over several histologic stages. Nevertheless, each tends to
predominate in one stage more than in another.
 
TABLE I
 
Sraens IS Toorn Gaowrn
 
 
JIOEPHOLOGIC‘ STAGES: rntsronoatc 1>3.oc1:ss£s:
Dental Lamina %—- -—————> Initiation
 
Bud Stage . ‘
 
Cap Stage (early) ? ’ Proliferation
 
Gap Stage (advanced) '] I
 
Bell Stage (early) ‘ L—————-—Histodifiei-entiation
Bell Stage (advanced) J‘ ) -——-—-—Morphodifierent‘iation
Formation of Enamel and - -
 
Dentin Matrix } "‘PP°‘“‘°”
Initiation
 
Proliferation
 
Histod.ifieren-
tiation
 
46 012.41. IIISTOLOGY .L\'D anenvotocr
 
For example, the process of histodifiercntiation characterizes the bell
stage in which the cells of the inner enamel epithelium differentiate into
functional amelohlasts. However, proliferation still progresses at the
deeper portion of the enamel organ where Hertwig’s epithelial root sheath
is forming.
 
The dental lamina and tooth buds represent that part of the oral epi-
thelium which has potencies for tooth formation. Specific cells contain
the entire growth potential of certain teeth and respond to those factors
which initiate tooth development. Ditferent teeth are initiated at definite
times. Initiation is set off by unknown chemical factors, as the growth
potential of the ovum is set off by the fertilizing spermatozoon.
 
Teeth may develop in abnormal locations such as the ovary (dermoid
tumors or cysts) or the hypophysis. In such instances the tooth under-
goes similar stages of development as in the jaws.
 
A lack of initiation results in the absence of teeth. This may occur in
isolated areas, most frequently in the permanent upper lateral incisors,
third molars and lower second hicuspids; or there may be a complete
lack of teeth (anodontia). On the other hand, abnormal initiation may
result in the development of single or multiple supernumerary teeth.
 
Marked proliferative activity ensues at the points of initiation, and
results successively in the bud, cap and bell stages of the odontogenic
organ. Proliferative growth is the result of cellular division and is.
therefore, multiplicative in character. It is marked by changes in the
size and proportions of the growing tooth germ (Figs. 15 and 19).
 
During the stage of proliferation the tooth germ has the potentiality
to progress to more advanced development. This is illustrated by the
fact that explants of these early stages continue to develop in tissue cul-
ture through the subsequent stages of histodiffercntiation and apposi-
tional growth. A disturbance or experimental interference has entirely
diiferent effects, according to the time of occurrence and the stage of
development which it attects. Aberrations in tooth development can,
therefore, be classified according to the stage of development at which
they occur. If aberrations occur during the stage of proliferative growth,
new parts may be differentiated (supernumerary cusps or roots); twin-
ning may result; or a complete suppression of parts may occur (loss of
cusps. roots or the entire tooth).
 
Histodilferentiation succeeds the prolit'erative stage The formative
cells of the tooth germs developing during the proliferative stage undergo
definite histologic as well as chemical changes and acquire their func-
tional assignment (the appositional growth potential). The cells become
restricted in their potencies; they give up their capacity to multiply as
they assume their new function (a law which governs all differentiating
cells). This phase reaches its highest development in the bell stage of
 
the enamel organ, just preceding the beginning of apposition of dentin and
enamel (Fig. 20).
DE\'ELOP.\l.E.\'T AND IEROWTII OI‘ TEETH
 
The organizing influence of the epithelial cells on the mesenchymc is
evident in the bell stage. The ditt'erentiation of the inner layer of the
enamel organ into ameloblasts has been shoxm to be an essential pre-
liminary step to the difi'erentiation of the adjacent cells of the dental
papilla into odontoblasts. With the formation of dentin. the ameloblasts
are stimulated to appositional function and enamel matrix is formed op-
posite the dentin. Enamel does not form in the absence of dentin as
demonstrated by transplanted ameloblasts failing to form enamel when no
dentin is present. Dentin formation therefore precedes and is essential
to enamel formation. The differentiation. and prestnnably the chemical
influence, of the epithelial cells precede and are essential to the difi'ercnti-
ation of the odontoblasts and the initiation of dentin 1'o1'u1ation.
 
If differentiation does not occur, the nonspecific. unorganized growth
energy expresses itself in the continued unhampered proliferation of cells.
A tumor is, therefore, characterized by unorganized proliferation and
incomplete dilferentiation of the cells. The degree of nondifferentiation
of the cells is an index to the rate of proliferation and, therefore, to the
malignancy of the tumor.
 
In dentinogenesis imperfecta {hereditary opalescent dentin) the odou-
toblasts fail to difierentiate completely. The result is formation of dentin
groimd substance, with an absence or disarrangement of the dentinal
tubules, resembling irregular secondary dentin. The shape of the tooth
and the quality of the enamel are normal.
 
In vitamin A deficiency the ameloblasts fail to ditferentiate properly.
In consequence, their organizing influence upon the adjacent mesenchymal
cells is distributed and atypical dentin formation results. This dentin
is known as osteodentin since it resembles bone.
 
The morphologic pattern or basic form and relative size of the future
tooth is established by morphodifferentiation. The advanced bell stage
marks not only active histodifferentiation but also an important stage
of morphodifferentiation of the crown. by outlining the future dentino-
enamel junction (Figs. 20 and 22}.
 
The dentino-enamel and dentino-cemental junctions which are diflfercnt
and characteristic for each type of tooth act as a blueprint pattern. Onto
this area the ameloblasts. odontoblasts and cementoblasts deposit enamel.
dentin matrix and cementum. and thus give the completed tooth its
characteristic form and size. For example. the size and form of the
cuspal portion of the crown of the first permanent molar are established
at birth, prior to appositional growth.
 
The frequent statement in the literature that endocrine disturbances
affect the size or form of the crown of teeth is not tenable unless such
effects occur during morphodil’ferentiation. that is, in utero or in the first
year of life. Size and shape of the root. however, may be altered by
disturbances in later periods. Clinical examination shows that the re-
 
Morphodif-
ferentiataon
Apposition
 
48 mm. HISTOLOGY AND EMBRYOLOGY
 
tarded eruption which occurs in hypopituitary and hypothyroid cases
results in a small clinical crown which is often mistaken for a small
anatomical crown (see section on Epithelial Attachment).
 
Disturbances in morphodifferentiation may affect the form and size of
the tooth without impairing the function of the ameloblasts or odonto-
blasts. The result is a peg or malformed tooth (e.g., Hutchinson ’s incisor)
with enamel and dentin that may be normal in structure.’ The ultimate
shape of the crown may be disturbed even in the presence of a normal
bell stage if the enamel formation is insufficient, as in enamel hypoplasia.
 
Apposition is the deposition of the matrix of the hard dental struc-
tures; it will be described in separate chapters on the formation of
 
enamel, dentin and cementum. This chapter deals with certain aspects
of apposition, in order to complete the discussion of the physiologic proc-
esses concerned in the growth of teeth.
 
Appositional growth of enamel and dentin is a layer-like deposition of
an extracellular matrix. This type of growth is, therefore, additive.
It is the fulfillment of the plans outlined at the stages of histo- and
morphoditferentiation. Appositional growth is characterized by regular
and rhythmic deposition of the extracellular material, periods of activity
and rest alternating at definite intervals, and by the fact that the de-
posited material is of itself incapable of further growth.
 
The matrix is deposited by the cells along the site outlined by the
formative cells at the end of morphodilferentiation (the future dentino-
enamel and dentino—cemental junctions), and according to a definite pat-
tern of cellular activity which is common to all types and forms of teeth.
The growth potential acquired by the formative cells at the histodiffer-
entiation stage is, therefore, expressed according to definite and universal
laws of growth. These laws, for the most part, have been elucidated in
growth studies of various other organs and organisms.
 
The process of appositional growth may be compared with the construc-
tion of a house. The blueprints (the dentino-enamel and dentino-cemental
junctions) outline the form and size of the structure and are different for
each class of tooth. However, the workers (cells), the materials used
(nutritive elements), the materials elaborated (enamel and dentin), and
 
the methods of construction (the pattern of cellular activity) are common
to all classes and forms of teeth.
 
Appositional growth proceeds according to a definite pattern. It be-
gins at a given site, at the dentinal cusps, termed the growth center, and
at a. given time, and proceeds in definite directions at definite rates which
follow gradients of time, locus and anteroposterior direction. The amount
of growth is definitely set by the rate of work (averaging 4 microns per
day in man) and the functional lifespan of the formative cells. The result
is an incremental pattern which is a summation of gnomonic curves super-
posed on the morphogenetic pattern (dentino-enamel junction).
DE\'ELOP.\IE.\'T AND GRO\\'TH OI‘ TEETH
 
References
 
1. Brunn, A. v.: Ueber die Ausdehnung des Sehmelzoz-genes und seine Bedeutung
fur die Zahnbildung (Concerning the Extent of the Enamel Organ and Its
Significance in Tooth Development_., Arch. 1-‘. mikr. Anat. 29: 367-353, 1537.
 
2. Diamond, LL, and Applebaum, B.: The Epithelial Sheath, J. Dent. Research 21:
403 19-12.
 
3. Xorberg, ’ 0.: Untersuehungen fiber das «lento-gingivale Epithelleistensystenz
im intrauterinen Leben des Menschen {Investigations of the Dentino-Gin-
gival Epithelium in Human Intranfterine Lifej, Stockholm, 1929, A. B.
Fahlcrantz’ Boktryckeri.
 
4. Orban, B.: Growth and Movement of the Tooth Germs and Teeth, J. A. D. A.
15: 1004-1016. 1928.
 
5. O1-ban, B.: Dental Histology and Embryology, Philadelphia, 1929, P. Blakiston
Son & Co.
 
6. Orban, B., and Mueller, E.: The Development of the Bifurcation of Multirooted
Teeth, J. A. D. A. 16: 297-319, 1929.
 
7. Sarnat, B. 0., Sehour, I.. and Heupel. B.: Roentgenographic Diagnosis of Con-
genital Syphilis in Unerupted Permanent Teeth, J. A. 11. A. 116: 2745-2747,
1941.
 
S. Schour, I., and Massler, )I.: Studies in Tooth Development: The Growth Pat-
tern of Human Teeth, J. A. D. A. 27: 1175-1793 (Z\'ov.); 1918-1931 (Dec.);
1940.
 
9. Sicher, 11.: Tooth Eruption: Axial Movement of Teeth With Limited Growth,
J. Dent. Research 21: 395--102, 1942.
CHAPTER 111
 
ENAMEL
 
A. HIS'1‘OLOGY*
 
1. Physical Characteristics
2. chemical Properties
 
3. Structure
 
-1. Age Changes
 
5. Submicroscopic Structure
6. Clinical Considerations
 
B. DEVELOPMENT
 
1. Enamel Organ
2. Life Cycle of Ameloblasts
3. Amelogenesis
 
:1. Formation of Enamel
 
b. Maturation of Enamel
4. Clinical Considerations
 
A. EISTOLOGY
1. Physical Characteristics
 
Human enamel forms a protective covering of variable thickness over
the entire surface of the crown. On the cusps of human molars and
bicuspids it attains a maximum thickness of about 2 to 2.5 mm., thinning
down to almost a knife edge at the cervix or neck of the tooth. The shape
and contour of the cusps receive their final modeling in the enamel.
 
The enamel is the hardest calcified tissue in the human body. This is
due to the high content of mineral salts and their crystalline arrange-
ment. The specific function of the enamel is to form a resistant covering
of the teeth. rendering them suitable for mastication.
 
The enamel varies in hardness from apatite, which is fifth in the scale
of Mohsi used to determine this physical quality, to topaz, which is
eighth. The specific structure and hardness of the enamel render it
brittle, which is particularly apparent when the enamel loses its founda-
tion of sound dentin. In cases of a fracture or in cavity preparation it
breaks with a concoidal surface. The specific density of enamel is 2.8.
 
The color of the ename1—covered crown ranges from yellowish White
to grayish-white. It has been suggested that the color is determined by
differences in the transluc-ency of enamel, yellowish teeth having a thin
translucent enamel through which the yellow color of the dentin is
visible. grayish teeth having a more opaque enamel (Fig. 26).‘ The
translucency may be due to variations in the degree of calcification and
homogeneity of the enamel. Grayish teeth frequently show a slightly
yellowish color at the cervical areas presumably because the thinness
 
‘First draft submitted by Charles F. Bodecker. Revised for 3rd Ed. by Reidar F.
Sognnaes.
 
tln this scale hardness is compared to that of 10 different minerals: (1) talc;
(E) gypsum; (3) calcite; (4) fluorite; (5) apatite; (6) orthoclase (feldspar);
(A) quartz; (8) topaz; (9) sapphire (corundum); (10) diamond.
 
50
The enamel consists mainly of inorg
 
2. Chemical Properties
anic material (96 per cent) and
only a small amount of organic substance and water (4 per cent)
 
Fig. 27.-—Influence of thickness and calcification 0!.’ enamel upon the color of the tooth.
.-1. Thin, well-calcified translucent enamel giving the tooth a yellowish appearance (Y).
3. Thick, less calcifieyl opaque enamel givi
 
cervical area enamel thm, color yelloxv 1)’).
 
ng the tooth a. Wrayish appearance G). In
s_Bodecker.‘) :5 (
 
of the enamel permits the light to stx-ik
and be reflected.
edge consists only
 
.:_  _l
 
A.
 
I
I
 
e the underlvin
Incisal areas may have a b ui.~ g
 
1
of :1 double layer of enamel.
 
"h tin
 
yellmv dentin
e where the thin
 
E.\‘A1.U-IL
5'7 ORAL I-IISTOLOGY AND EMBRYOLOGY
 
..
 
The inorganic material of the enamel is similar to apatite. Table II“
shows the most reliable data on the chemical contents of_ enamel. Some
values for dentin and compact bone are added for comparlson.
 
The figures shown in the table represent dry weights. A comparison
of the relative volume of the orgamc framework and m111eI'a1 Contents Of
 
the enamel shows that these are almost equal. Fig. 28 illustrates this
by comparing a stone and a sponge of approximately equal volume: the
former represents the mineral content, and the latter the organic frame-
work of the enamel. Although their volume is almost equal their Weights
are vastly different: the stone is more than one hundred times heavier than
the sponge or, expressed in percentage, the weight of the sponge is less than
one per cent of that of the stone.
 
TABLE II
CHEMICAL Coxrsxrs or ENAMEL, DENTIN, CEMENTUM AND Bonn
 
 
 
- CEMENTUM
m“mEI‘ DENT“ (‘OMPACT BONE
 
Water 3.3 % 13-2 % 32 %
Organic Matter 17 17.5 22
 
Ash 96.0 59-3 46
 
In 100 g. of Ash: _
 
Calcium 36.1 g 33.3 g. 35.5 g.
Phosphorus 17.3 17.1 17-1
Carbon dioxide 3.0 4-0 4-4
Magnesium 0.5 1.2 0.9
Sodium 0.2 0.2 1.1
Potassium 0.3 0-07 0-1
Chloride 0.3 0-03 0-1
Fluorine 0.016 0.017 0.015
Sulfur 0.1 0.2 0.6
Copper 0.01
 
Silicon 0.003 0.04
Iron 0.0025 0-09
Zinc 0.016 0.018
 
WHOLE TEETH BONE
Lead 0.0071 to 0.037 0.002 to 0.02
 
 
Small amounts of: Ce, La, Pr, Ne,
Ag, Sr, Ba, 01-, Sn, Mn, Ti, N1, V, Al, B, Cu,
 
Li, Se,
 
 
The nature of the organic elements of enamel is incompletely under-
stood. In development and histologic staining reactions, the enamel
matrix resembles hornifying epidermis. Recently more specific methods
have revealed sulfhydryl groups and other reactions suggestive of
keratin.“' Sinlilarly. lrvdrolysates of mature enamel matrix have shown
a ratio of aminoacids (histidine 1: lysine 3: arginine 10) indicative of an
eul:eratin.2- 3" In addition, histochemical reactions have suggested that the
enamel forming cells of developing teeth also contain a carbohydrate
protein,“ and that an acid mucopolysaccharide enters the enamel itself at
 
‘The editor is indebted to Dr. Harold C. Hodge, University of Rochester, School of
Medicine and Dentistry, Rochester, New York, for compiling this table.
 
The chemical_ constituents of ash are here given as elements, while they are in
reality present in difierent compound: e.g., phosphorus as phosphate. The neglect of
these other elements, e.g., oxygen, hydrogen. nitrogen, accounts for the difference be-
tween 100 and the actual grams.
E.\IA.\IEL 53
 
the time when calcification becomes a prominent feature:"" Tracer studies
have indicated that the enamel of erupted teeth of rhesus monkeys can
transmit and exchange radioactive isotopes originating from the saliva
and the pulp.“ Considerable investigation is still required to determine
the normal pltysiologécal characteristics and the age changes that occur
in the enamel.
 
 
Fig. 2S.——-A sponge (.1) and a stone (B1 are comparable to the organic and mineral
elements of enamel. Their volumes are approximately equal but their weights differ
greatly. (Bodecke1-.4)
 
3. Structure
 
The enamel is composed of enamel rods or prisms. possibly rod sheaths,
and a cementing inter-prismatic substance. The number of enamel rods has
been estimated”' 13 as ranging between five millions in lower lateral
incisors. and twelve millions in the upper first molars. From the dentino-
enamel junction the rods proceed outward to the surface of the tooth.
The length of most rods is greater than the thickness of the enamel,
because of the oblique direction and wavy course of the rods. The
rods located in the cusps, the thickest part of the enamel, are naturally
much longer than those at the cervical areas of the teeth. It is gener-
ally stated that the diameter of the rods averages four microns, but
this measurement, necessarily, varies since the outer surface of the
enamel is greater than the dentin surface where the rods originate. It is
claimed“ 33- *9 that the diameter of the rods increases from the dentino-
enamel junction toward the surface of the enamel at a ratio of about 1:2.
 
The enamel rods were first described by Retzius“ in 1‘35. They are
tall columns or prisms, passing through the entire thickness of the enamel.
Normally, they have a clear crystalline appearance, permitting the light
to pass through them freely. In cross section the enamel rods appear.
occasionally. hexagonal: sometimes they are round or oval. Many rods
resemble fish scales in cross sections of human enamel (Fig. 29.1). An
explanation for this peculiar shape has been attempted by the following
hypothesis: The manner in which calcification takes place seems to exert
a marked influence upon the shape of the rods. The calcification of each
rod begins close to its surface and proceeds toward the center. In human
enamel calcification of the rods does not occur on the entire circumfer-
ence of the red at the same time. but begins on one side. Consequently,
one side of each rod hardens sooner than the other and, in the process
of calcification which seems to be accompanied by increased pressure, the
Bod. sheaths
 
striations
 
5; ORAL HISTOLOGY AND EMBRYOLOGY
 
harder side presses into the softer side of the adjacent rods, compressing
it and leaving a permanent impression.*''' The calcified portions of the
enamel rods are lost in the preparation and appear as clear white spaces.
The dark areas, located excentrically within the sheaths, are interpreted
as uncalcified organic substances in the rods. This may indicate that
the calcification of human enamel rods begins at. the periphery of each
rod. and the calcification sets in earlier on one side than on the other.
 
Fig. 29.—Decalified section of enamel of a human tooth germ. Rods cut transversely
appear like fish scales.
 
A thin peripheral layer of each rod shows a different refractory index,
stains darker than the rod, and is relatively acid resistant. It may be
concluded that it is less calcified and contains more organic substance
than the rod itself. This layer is the rod sheath‘! *“ (Fig. 29).
 
Each enamel rod is built up of segments, separated by dark lines which
give it a striated appearance (Fig. 30). These transverse striations marl:
the margins of the rod segment which become more visible by the action
of mild acids. The striations are more marked in enamel which is insuffi-
ciently calcified. The rods are segmented because the enamel matrix is
formed in a distinctly rhythmic manner. In man these segments seem to
be of uniform length of about four microns.“
nterpfismatic
Substance
 
E.\'.\_\IEL 55
 
Enamel rods are not in direct contact with each other hut 212-e c-emc-ntetl
together by the intel-prismatic substance \\'l1l(‘l1 has :3 slightly l1ighe1' re-
tractlve mclex than the rods.*''’ Discussion is still active c-oiic-ex-niug the
 
o
«-
 
Fig. 30.—Ground section through enamel. Rods cut longitudinally. Cross striation of
 
rods.
 
structure of the iiitei-p1-ismzitic siibstanee «Fig. 31:. The interpi-ismatie
substance appears to be at a minimum in human teeth. In some an-
imals (dog, pig) the teeth show a C‘011SlLlE'I’21l)l€ amount of interprismatic
substance in the enamel.
 
Lately, new methods have been devised to study ground sections of hard
tissues. The principle is to take impressions of the surface after etching
56 ORAL l-IISTOLOGY AND EMBRYOLOGY
 
it with dilute acids?“ ‘*1 An improvement of this method has been achieved
 
bx‘ blowing vaporized metals onto the microcast at an acute angle, thus
duplicating shadows thrown by projections of the cast.“
 
The studv of shadowed replicas of cross sections of the enamel seems to
indicate that the enamel rod is not homogeneous. The rod sheath seems
to be the least completely calcified structure of the enamel. The 1nterpr1s-
matic substance appears to have a lower content of mineral salts than the
 
rod itself (Figs. 32.4., 32B).
 
Rod sheath
 
Intraprismatic
substance
 
 
Fig. 31,-Decalcifled section of enamel. Rods, rod sheaths. and interprismatic substance
are well difierentiated. (Photographed with ultra-violet light.) (Bodeckerfl)
 
WW9“ 0‘ Generally, the rods are oriented at right angles to the dentin surface.
In the cervical and central parts of the crown of a deciduous tooth“
they are approximately horizontal (Fig. 33, A); near the incisal edge
or tip of the cusps they change gradually to an increasingly oblique
direction, until they are almost vertical in the region of the edge or tip of
the cusps. The arrangement of the rods in permanent teeth is similar
in the occlusal two-thirds of the crown. In the cervical region, however,
the rods deviate from the horizontal in an apical direction (Fig. 33, B).
 
The rods are rarely, if ever, straight throughout; they follow a wavy
course from the dentin to the enamel surface. The most significant devia-
tions from a straight radial course can be described as follows: If the
middle part of the crown is divided into thin horizontal discs, the rods
in the adjacent discs bend in opposite directions. For instance, in one
disc the rods start from the dentin in an oblique direction and bend more
or less sharply to the left side (Fig. 34, A). In the outer third of the
enamel they change often to an almost straight radial course. In the
E.\'A\IEL 0'!
 
Fig. 32.1.—Transverse section through enamel etched 5 seconds with 0.1 X I-IC1 (shad-
owed replicab. (X15t.*I).) (Courtesy Scott and \\’yckoff.“)
 
Fig. 32B.—Cross section of demineralized enamel of a. developing canine from a
monkey fetus. Note rods. rod sheaths. and interprismatic substance. ()<T,200.)
After Sog-nnaes, Scott, Ussing and \l.’yckoff.‘=
'8 ORAL IIISTOLOGY AND EMBRYOLOGY
 
E.
 
Fig. 33.—DiagnJ.ms indicating the general direction of enamel rods. .4. Deciduous tooth.
B. Pemianent tooth.
 
  ‘E
‘ " Hypocalciiied
 
1
Hynooaicmea T €335 °‘ “‘
 
rods of a
 
 
 
. --~"'=~ Dentino-en-
amel junction
F Dentin
 
Fig. 3~i.—-Horizontal ground section through enamel near dentino-enamel junction.
4 and 3 show change in the direction of rods in two adjacent layers of enamel,
ENAMEL 59
 
adjacent disc the rods bend toward the right -Fig. 34. B ,. This alter-
nating clockwise and counter-clockwise deviation of the rods from the
radial direction can be observed at all levels of the crown if the discs
are cut in the planes of the general rod direction I Fig.
 
If the discs are cut in an oblique plane. especially near the dentin
in the region of the cusps or incisal edges. the rod arrangemeiit appears
to be further complicated. the bundles of rods seem to intertwinc more
irregularly; this appearance of enamel is called gnarled enamel.
 
The enamel rods forming the developmental grooves and pits, as on the
occlusal surface of molars and premolars, converge in their outward course.
 
1
 
5
 
Fig. 35——Long'ituAlinel grcunri section through enamel pliotograpl:e-'1 by reflected light.
Hunter-Schreger bands.
 
Fig. 36.-—DecaIcific-«I enamel. pliotogrnphed by reflectevl
 
light showing Hunter-
Schregei-'s bands. tsognnaes“ J. Dent. Research, 1949.)
 
The more or lcss regular change in the direction of rods may be re-
garded as a functional adaptation, minimizing the risk of cleavage in the
axial direction under the influence of occlusal masticatory stresses. The
change in the direction of rods is responsible for the appearance of
the Htlnter-°a(-hreger bands. These are alternating dark and light
stripes of varyiiig width (Figs. 35 and 369 which can best be seen in
a. longitudinal ground section under oblique reflected light. They origi-
 
Hunter-
Schreger
60 ORAL HISTOLOGY AND EMBRYOLOGY
 
nate at the dentino~enamel border and P335 Ouf-Ward: ending at s_°me
distance from the outer enamel surface. This Phenomenon is explamed
as follows: In a longitudinal section the rods are, generally, cut obliquely.
If the bundles of rods are traced from the surface of Such 3» Section into
the depth, it will be observed that the)’ F1111 0b1iq11€1.V', in 0119 disc to the
right, in the next disc to the left. If such a section is illuminated from
the right side, the rays pass, without being reflected, through the rods
 
Fig. 37.—Three photomicrographs or the same area. of a.
of enamel. A and B by reflected light. The change in the direction of light (180')
caused a reversal of the Hunter—schx-eg-er
 
bands. The dark band in A marked by a
particle of dust (X) appears light In B.
 
C’, The same area photographed by transmitted light.
(The particle of dust lies on the specimen under the coverglass.)
 
longitudinal ground section
Incremental
Lines of
 
E.\'.L\lEL 61
 
which the rods run in the opposite direction appear light because the rays
which run in the same direction; such discs appear dark. The discs in
are reflected from the lateral surfaces of the rods. This explanation is
borne out by the fact that a 180 degree rotation of the slide reverses the
phenomenon; the stripes which were dark in the first position appear
light; those which were light appear dark Fig. 373. Some investiga-
tors" 9’ 37 claim that there are variations in calcification of the enamel
which coincide with the distribution of the bands of Hunter-Sehreger.
Careful decalcification and staining of the enamel have provided further
evidence that these structures may not solely he the result of an optical
phenomenon, but are composed of alternate zones hating a sIightl_\' in-
creased permeability and a higher content of organic n1aterial.“'*°- 5”
 
,1, B.
 
Fig. 38.—Inc1-emental lines of Retzlus in longitudinal ground sections.
 
A. Cuspal region.
B. Cervical region (X).
 
The incremental lines of Retzius appear as brownish bands in ground
sections of the enamel. They illustrate the successive apposition of layers
of enamel matrix during formation of the crown (incremental pattern of
the enamel). In longitudinal sections they surround the tip of the dentin
6?. ORAL HISTOLOGY .-‘l.\'D EMBRYOLOGY
 
(Fig. 38, Al. In the cervical parts of the crown they run obliquely; from
the dentiiio-enamel junction to the surface they deviate occlusally (Fig.
38, B L In transverse sections of a tooth the iiicremeiital lines of Retzius
appear as concentric circles (Figs. 39.1, B). They may be compared to the
growth rings in the cross section of a tree. The term “incremental lines”
designates these structures appropriately, for they do, in fact, show the
advance of growth of the enamel matrix. The incremental lines are an
expression of the rhythmically recurrent variation in the formation of
 
 
Fig. 39.=l..—Increx-nental lines of Retzius in transverse ground section, arranged con-
centrically.
 
Laniella.
 
Retzius lines
 
Neonatal line
 
 
Dentin
 
Fig. 39B.-—Decalc-ified paraffin section of enfoliated deciduous molar. (X20.) Heavy
dark lamella. runs from darkly stained dentin to surface in an irregular course inde-
pendent of developmental pattern. Roughly parallel to dentin surface are seen a. number
it incremental lines. one of which, the neonatal line, is accentuated. (sognnaesfi J.
Dent. Research. 1949.)
Fig. -41.—Shadowed replica of the
second molar showing the perik
 
ENAMEL
 
63
 
surface of intact enamel (buccal surface of upper left
ymata. (X15004 (Courtesy Scott and \\'yckoff."’}
64 ORAL HISTOLOGY AND E.-WIBRYOLOGY
 
the enamel matrix. The cross striation of the single rod (Fig. 30) is
the result of an underlying shorter rhythm in the matrix formation (see
section Development of Enamel). The variation in the formation of the
enamel matrix causes secondary variations in the degree of calcification.
The incremental lines and cross striations are areas of diminished cal-
 
cification.
 
\\'herever the lines of Retzius reach the surface there is a shallow fur-
row. the imbrieation line of Pickerill; this is caused by an overlap of a
younger layer of enamel over an older layer. The furrows are more
numerous and closer together at the cervical part of the crown. The dis-
tances between adjacent furrows increase toward the occlusal part of the
crown. They are missing entirely close to the iiicisal edge or tip of the
cusps. The slight elevations between two furrows are known as periky—
mata (Figs. 40 and 41).
 
 
Fig. 4‘_’.—Ca.refu1ly decalcifled section tl Ii 1. Thick ‘ ' - -
stance (say in p3§€z‘l§s fi'£%;‘° tsoaeckiiffig °‘ ‘‘‘° ‘““’‘’°‘’ 3””
 
The incremental lines of Retzius, if present in moderate intensity, are
not considered pathologic. However, the rhythmic alternation of periods
of enamel matrix formation and of rest can be upset by metabolic dis-
turbances, causing the rest periods to be unduly prolonged and close
together. Such an abnormal condition is responsible for the broadening
of the incremental lines of Retzius, rendering them more prominent. At
the mcreinental lines of Retzius the iiiterprismatic substance seems to be
thickened at the expense of the rods (Figs. 39B, 42).
 
The enamel of the deciduous teeth develops partly before, and partly
after birth. The boundary between the two portions of ename1 in the
deciduous teeth is marked by an accentuated incremental line of Retzins,
mum. 65
 
the neonatal line or neonatal ring.“ This appears to be the result of the
abrupt change in the enfironment and nutrition of the newborn. The
prenatal enamel is, usually, better developed than the postnatal (Fig.
43). This is explained by the fact that the fetus develops in a Well-
protected environment, with an adequate supply of all the essential ma-
 
. :_Q__
. \
. .‘4
 
N eonatal '
line in "
dentin
 
Neonatal
line in -3
enamel e;
 
Postnatal
enamel
 
; .
5}
“is
if _
 
Fig. 43.—-Neonatal line in the enamel. Longitudinal ground section of a deciduous cuspid.
(Schom-.3’)
 
terials, even at the expense of the mother. Because of the undisturbed and
even development of the enamel prior to birth, perikymata are absent in the
occlusal parts of the deciduous teeth, whereas they are present in the post-
natal cervical parts. The diagram in Fig. -14 shows the amount of enamel
formed during prenatal and postnatal periods.
Enamel
cuticle
 
66 ORAL HISTOLOGY AND EMBRYOLOGY
 
A delicate membrane covers the entire crown of the newly erupted
tooth. This membrane was long described as Nasmyth’s membrane,"
after its first investigator. When the ameloblasts have produced the
enamel rods they produce a thin continuous pellicle termed the primary
enamel cuticle which covers the entire surface of the enamel (Fig. 5).
This cuticle is largely organic and, being more resistant to acid than the
enamel itself, can be floated off in acid. It is worn ofl early from all
exposed surfaces.
 
During the emergence of the tooth, the reduced enamel epithelium cover-
ing the crown, produces a keratinous secondary cuticle on the surface of the
primary. If a thin ground section of enamel is decalcified in acid cel-
 
C:r.tra.l Lateral Deciduous First Second First
zciducus deciduous cuspid deciduous deciduous permanent
1nCi50!' incisor molar molar molar
 
 
Semidiagrammatic tracin 5 showing the enamel and dentin
 
of the deciduous teet and first Permanent molar at
ond after birth
 
Prenatal enamel
Prenatal dentin
 
|::| Postnatal formation
 
“““ “ Neonatal line in
enamel and dentin
 
Fig. 44.—Ena.mel and dentin of deciduous teeth and flrst permanent molar at and after
birth. (Schoui-37)
 
 
loidin*- 7 the outer or secondary cuticle will resist acid and show marked
birefringence in polarized light. This indicates a structurally oriented
fibrous protein, presumably keratin“! 2‘ In specimens stained with
hematoxylin and eosin the secondary cuticle stains bright yellowish-red.
It varies in thickness from 2 to 10 microns, is homogenous in character,
and seems to be brittle (see section on Epithelial Attachment).
 
Mastication wears away the enamel cuticles on the incisal edges,
occlusal surfaces, and contact areas of the teeth. On other exposed sur-
faces, they may be worn oif by mechanical influences, e.g., brushing of
teeth. In protected areas (proximal surfaces and gingival sulcus) they
may remain intact throughout life.
i:.\'.u1EL 67
 
I-lnamel lamellae are thin leaflike structures which extend ironi the
enamel surface toward the dentino enamel junction ll-‘i,qs_ 46. .1, B».
They may extend to, and sometimes penetrate into. the dentin Hlentinal
part of lamellal. They consist of organic material. with but little min-
eral content. In ground sections these structures may be confused with
cracks caused by grinding of the specimen (Fig. 39, -14. Careful de-
 
" ll‘
‘- of I ' V
it ‘ L  ’
_ A -; ‘
0? A‘.
~ 1
3 ! 3
£3’ at
. "4:
.5 i.‘
2 ‘—- l>‘ \
:s- C
5
L
 
Enamel (lost in
decalciflcation)
 
‘Q9
.1..
,.
-.._
O
"' ‘:"s«.
__,.h
,.
 
Primary enamel
cuticle
 
 
Enamel epithelium
 
— .
 
Fig. -15.-—Decalcifled section through the crown of an unerupted human tooth.
Enamel lost in decalciflcation. Primary enamel cuticle in connection with the united
 
enamel epithelium. At (X) a cell of the epithelium is lost thus making the cuticle
more visible.
 
calcification of the enamel makes possible the distinction between cracks
and enamel lamellae: the former disappear while the latter persist (Figs.
39, B, 47).
 
Lamellae develop in planes of tension. Where rods cross such a plane.
a short segment of the rod may not fully ealcify. If the disturbance is
more severe a crack may develop which is filled either by surrounding
cells it the crack occurred in the unerupted tooth, or by organic sub-
 
Enamel
Lameuae
53 ORAL HISTOLOGY AND EMBRYOLOGY
 
stances from the oral cavity if the crack developed after eruption. Three
types of lamellae can thus be differentiated. Type A» 131391139 composed
of 1,001.1‘. calcified rod segments; Type B, lamellae consisting of degen-
erated cells- Type C those arising in erupted teeth Where the cracks are
filled with organic matter, presumably originating from s.al1vZ.“‘
last type (Fig. -17) may be more common than formerly believe . B E
lamellae of Type A are restricted to the enamel, those of Types an
 
C may reach into the dentin. If cells from the enamel Organ fin 3 Crack
in the enamel, those in the depth degenerate, whereas those close ‘to the
surface may remain vital for a time and produce a hormfied secondary
cuticle in the cleft.“ In such cases (Fifi 49) the greater inner Parts of
the lamella consist of an organic cell detritus, the outer parts of a double
 
uf'"'' , .
 
 
46.4. 463
 
Fig. 46A.-——Decalcifled incisor afiected with moderately severe mottled enamel (from
 
material obtained in Texas). Numerous lamellae can be observed. (x8.) (Sognnaesfl
J. Dent Research, 1950.)
 
Fig. 46B,—Ma.xiIlary first permanent molar of caries-free, two-year-old rhesus mon-
key._ Numerous cracks revealed themselves as bands of organic matter (lamellae) once
specimens had been decalcified. (x8.) (Sognnaes“ J. Dent. Research, 1950.)
 
H-3:-an-9.
 
layer of the secondary cuticle. If connective tissue invades a crack in
the enamel, cementum may be formed. In such cases lamellae consist
entirely or partly of cementum.3“
 
Lamellae extend in the longitudinal and radial direction of the tooth,
from the tip of the crown toward the cervical region (Figs. 46, A, B).
This arrangement explains why they can be observed better in horizontal
sections. Enamel lamellae may be a source of weakness in a tooth inas-
much as they may form a road of entry for bacteria which initiate
caries." 1“ ‘3 On the other hand, it has been suggested“ that the organic
matter which fills in enamel cracks occurring during fimction of the
teeth, may serve a crude “reparative” function, possibly as a nucleus
for secondary mineral deposition.
nxannz. 69
 
Enamel tufts (Fig. 50) arise at the dentino-enamel junction and reach
into the enamel to about one—fifth to one—third of its thickness. They were
so termed because they resemble tufts of grass when viewed in ground
sections. It has been proved“ 32 that this conception is erroneous. An
enamel tuft does not spring from a single small area but is a narrow,
ribbon-like structure the inner end of which arises at the dentin. The
impression of a tuft of grass is created by examining such structures in
 
Fig. 4T.—Parafiin section of decalcifled enamel of human molar showing the relation
between Iamella. and surrounding organic framework between the enamel prisms. H. &
E. stain. (X10004 tsognnaes“ J. Dent. Research, 1950.)
 
thick sections under low magnification. Under these circumstances the
imperfections, lying in different planes and curving in different direc-
tions (Fig. 3-1), are projected into one plane (Fig. 50).
 
Tufts consist of hypocalcified enamel rods and interprismatic sub-
stance. Like the lamellae they extend in the direction of the long axis of
the crown; therefore, they are abundantly seen in horizontal, and rarely in
longitudinal sections. Their presence and their development is a conse-
quence of, or an adaptation to, the spatial conditions in the enamel.
 
Enamel Tufts
Dent:i.no-
Junction
 
Odantoblastic
 
and Enamel
spindles
 
70 oau. msronoev AND EMBRYOLOGY
 
In microscopic sections the dentino-e11an1el junction is not 21 straight line
but appears scalloped 1 Figs. 50 and 51). The convexities of the scallops are
 
directed toward the dentin. This line is already pre-formed in the ar-
rangement of the aiueloblasts and the basement membrane of the dental
papilla, prior to the development of hard substances. This arrangement
 
"—'; Lamella.
 
Tufts
 
Dentino-enamel
junction
 
Dentinal part of
lamella
 
Fig. 48.-—'l‘ransverse ground section through a lamella reaclfng from the
Surface into the dentin. The dentinal part of the lamella is surroundedlby transparent
 
contributes to the firm attaelnnent of the enamel to the dentin and pre-
sumably to the structural pattern of the enamel as refleeted in the ar-
rangement of the tufts and the Hunter-Schreger bands.
 
Occasionally odontoblast processes pass across the dentino-enamel junc-
tion into the enamel. Some terminate there as finely pointed fibers; others
are thickened at their end (Fig. 52‘) and are termed enamel spindles. They
ENAMEL 71
 
seem to originate from processes of odontoblasts which extended into the
enamel epithelium before hard substances were formed. The direction of
the odontoblastic processes and spindles in the enamel corresponds to the
original direction of the ameloblasts. i.e., at right angles to the surface of
the dentin. Since the enamel rods are formed at an angle to the axis of the
 
 
 
- ...  ‘ 3
, ‘r’ '52
Hornifled part ‘ ' ‘'5 ~ ’ Secondary
or Iamena  év enamel cuticle
.4  i :r,, t’  ’ N; _‘‘''K.'‘‘
d ' 5 . Oxiganifi part of
» _~ «‘ ame a
.-:- .~-,_ I , if
Kr
’ .3.
D%la1.!tli‘l:fiIa part at ......4._. _‘ Enamel lost in
“* decalcification
—"""- ...-
* " ‘ ' Dentin
 
Hornifled part of lamella.
 
Organic part of lamella
 
 
3 Dentinal part of lamella
Dentin
 
. Fig. 49.-Decalcifled transverse section through a tooth. Enamel is lost. in decaiciflca-
tron; lamella of Type B collapsed. Diagram showing the relationship prior to decalciflwr
tion. Secondary enamel cuticle is hornified. Horniflcation extends into the outer part or
 
the Iamella. torban.-”=)
 
arneloblasts, the direction of spindles and rods is divergent. In ground
sections of dried teeth the organic contents of the spindles disintegrate
and are replaced by air; then-etore, the spaces appear dark.
 
4. Age Changes
 
The organic nuitrix of the enamel and the enamel surface appear to
undergo changes with age, but this change is not well understood. It
72 ORAL HISTOLOGY AND EMBRYOLOGY
 
has been suggested that the surface change is due to accretion of salivary
or bacterial products. As a result of these age changes in the organic
portion of enamel, the teeth may become darker and their resistance to
 
 
=r~w<:s»:.._ _ _ _ _
 
Fig. 5D.—-Transverse ground section through a tooth under low magnification Numerous
tufts extending from the dentino-enamel junction into the enamel.
 
i Dentino-enamel junction
 
Fig‘ 51"I‘°"3it“dim1 87011115 39¢fi0n- Swlloped deutino-enamel junction.
ENAMEI: 73
 
decay may be increased? Suggestive of the aging change is the greatly
reduced permeability of older teeth to fluids.“ There is insufiicient evi-
dence to show that enamel becomes harder with age.“
 
The most evident age change in enamel is attrition or wear of the
occlusal surfaces and proximal contact points as a result of mastication.
Histologically, the results of attrition are most prominent in the tissues
below the enamel, the dentin. pulp, and periodontium.
 
 
 
*7 ., L..Lb"Odontoblastic
. process in
: g 4 enamel
‘' I hi”.
 
Dentlnal tubule:  -e-Dentin
 
'2'.
 
A  I I I 7:
.i. l-i'...__._._‘._._. ‘  e‘ 4’! 1/
 
Fig. 52.—Ground section. Odontoblastic process extending into the enamel. and an
enamel spindle.
 
Dentlno-enamel -' ' ‘
Junction ‘I ' '*‘ y
 
5. Submicroscopic Structure
 
By means of studies in polarized light“ 9" it has been shown that com-
pletely calcified enamel consists of submicroscopic units, hexagonal in
shape and arranged with their long axes approximately parallel with the
long dimensions of the rods. There may be a deviation of as much as
twenty degrees from parallel in this relationship in human enamel (Fig.
53.4). In dog enamel the parallel relationship is common.
 
Fig. 53B is a eelloidin model of the submicroscopic crystal which is the
calcification unit of enamel and dentin. The two different axial planes
are represented by sheets of celloidin placed inside the hollow hexagonal
form. On these planes the velocity of the passage of light rays in each
is indicated by wave-like lines. A line with few waves symbolizes a more
rapid rate of travel and lower index of refraction, while one with many
waves shows a slower rate and a higher index of refraction. The light
ray vibrating in the plane parallel to the long axis is known as the ex-
traordinary, while the ray vibrating in the plane at right angles to the
long axis is the ordinary ray. In the case of this particular crystal the
birefringence is of a negative type because the so-called ordinary ray is
the one with the higher index of refraction.
-7.; ORAL. HISTOLOGY AND EMBRYOLOGY
 
This difference in indices of refraction causes a double refraction,
known as birefringence, when the enamel is viewed with crossed nicols
in any aspect except that of looking down on the ends of enamel rods.
The greatest birefringence occurs when viewing the rods at right angles
 
to their long axis.
 
f/ex¢::3ana/ Cysials
 
   
 
Lon-17 9:15 of fnamel Pod
 
K
 
Snommc enhancement or
SIIBMICROSCOPIC CRLCIHCRTIOYI
 
CRYSTALS In Hllmfifl enema ROD
ILIHEH DEVELOPMENT IS COITIPLETS.
 
Fig. 53.-1.-—Submicroscoplc, hexagonal crystals (highly magnified) in their relation to the
longitudinal axis or a. human enamel rod.
 
The use of the electron microscope has made it possible to photograph
the submicroscopic crystals of the enamel“ (Fig. 54). Recent advances
in electron microscopy of ultrathin sections of deealcified enamel“ have
revealed that a submicroscopie organic network permeates both between
 
and within the enamel prisms, presumably enveloping the crystallites
(Fig. 55).
E.\‘A.\IEL 75
 
6. Clinical Considerations
 
To know the course of the enamel rods is of importance in cavity prepa-
rations. Straight enamel cleaves more readily than bundles of enamel
prisms which take a wavy course. The cement or interprismatie sub-
stance is apparently weaker than the body of the rods, so that the line
of cleavage usually follows this substance. It can 1-eaclily be understood
that, in enamel where the bundles of rods do not lie parallel to each
other, cleavage does not occur so easily. for the stronger bodies of the
 
Fig. 53b‘.—Cel1oidin model of the submicroscopic crystal in the enamel. The _ordinar,\'
ray (horizontal plane) has a slower rate 0.‘. travel and higher index of refraction than
the extraordinary ray (vertical plane).
 
intertwined rods make a clean, straight fracture impossible. Inter-twining
rods present a greater resistance to dental instruments. The operator-‘s
choice of instruments depends upon the location of the cavity in the
tooth. Genei-all_v, the rods run at a right angle to the underlying dentin
or tooth surface. Close to the cemento-enamel junction the rods run in
a. more horizontal direction «Ficr. 33. B1. In preparing cavities it is im-
portant. that unsupported enamel rods do not remain at the cavity mar-
gins. These would soon break and produce a leakage. Bacteria would
75 out. I-IISTOLOGY AND EMBRYOLOGY
 
Fig. 54.—Submicroscopic crystals of guinea pig enamel,‘ photographed ‘th the electron
microscope. (X23000.) (Boyle. Hillier. and Davidson.
E.\'A1IEIi 77
 
lodge in these spaces. inducing early dental caries. Enamel is brittle and
does not Withstand forces in thin layers. nor Where it is not supported
by the underlying dentin (Fig. 56:1}.
 
Deep enamel fissures are predisposing to caries. Although these deep
clefts between adjoining cusps cannot be regarded as pathologic, they
afford areas for retention of caries—producing agents. Caries penetrates
the floor of fissures rapidly because the enamel is very thin in these
areas“ (Fig. 56B). As the destructive process reaches the dentin. it mush-
rooms out along the dentino-enamel junction undermining the enamel,
leaving only a small opening to the cavity. An extensive area of dentin
becomes carious without giving any warning to the patient because the
 
>:' ’  §.\‘>: I    $-
      -in tie ‘*1
 
   
     
 
 
~v“\:\vi _‘.‘|—'--.._‘ "., E; ‘, ‘;.'_\g.\.,..-.-1-
 
 
   
 
 
 
‘ac
 
Fig. 55.-—Electi-on-micrograph ()<10.000) 0! cross section of clegnineraliaed enamel of
an adult human molar. showing one prism and part or two adjoining prisinsflwith the
submicroscopic organic framework within and between the prisms. (Scott et al J. Dent.
Research. 1952.)
 
entrance to the cavity is minute. A most careful examination by the
dentist is necessary to discover this condition. Even so, the base of most
enamel fissures is more minute than a single toothbrush bristle and
cannot be detected with the dental probe.
 
Enamel lamellae may also be predisposing locations for caries. The
abundant organic material in the enamel lamellae may present an excel-
lent medium for bacterial growth. If protein tends to fill cracks in the
enamel of erupted teeth, then the resulting lamellae may Well be prefer-
able to the open cracks. The bacteria may penetrate, along cracks and
lamellae, from the surface to the dentino-enamel junction, and into the den-
tin. In some instances caries in the dentin may occur without gross clinical
73 ORAL HISTOLOGY AND EMBRYOLOGY
 
Fig. 56.-1.——Diagrammatic illustratioii of the course of en2_:.meI rods in a molgr in rela-
tion to cavity preparation. I and 3 indicate wrong preparation of cavity margms; 3 and
4 indicate correct preparation.
 
 
‘r
 
Fig. 56B.—Diagramma.tic illustration of development of a deep enamel fissure. Note the
thin enamel layer forming the floor of the fissure. (K1-on1'eld.=')
E.\'A.\IEL 79
 
destruction of the enamel surface. thereby undermining the enamel itself.
Hornification of the enamel cuticle. at the entrance of the laxnellae s.Ficr.
49), may prevent the bacteria from penetrating. It has been suggested
that a proper impregnation of the organic matter in the enamel may he
a prophylactic measure against this type of caries.“
 
The surface of the enamel in the cervical region should be kept smooth
a11d well polished by proper home care and by regular prophylactic treat-
ment by the dentist. If the surface of the cervical enamel becomes
decalcified, or otherwise roughened. food debris. bacterial plaques, etc..
accumulate on this surface. The gingival tissues in contact with this
roughened, debris-covered enamel surface undergo inflammatory changes
 
(gingivitis) which, unless pronlptly treated. lead to more serious perio-
dontal disease.
 
References
 
(Histology of Enamel)
 
1. Beust, T.: Morphology and Biology of the Enamel Tufts With Remarks on
Their Relation to Caries. J. A. 1). A. 19: 455, 1932.
 
2. Block, R. J., Hornitt, M. K.. and Bolling, D.: Comparative Protein Chemistry.
The Composition of the Proteins of Human Enamel and Fish Scales, J. Dent.
Research 28: 513, 1949.
 
3. Bibby, B. G., and Van Huysen. G.: Changes in the Enamel Surfaces; A Possible
Defense Against Caries, J. A. D. A. 20: S28, 1933.
 
4. Bodecker, C. F.: Enamel of the Teeth Decalcified by the Celloidin DeCal(.‘if_\'-
ing Method and Examined by Ultraviolet Light, Dental Review 20: 317,
 
1906.
5. Bodecker, C. F.: Nutrition of the Dental Tissues, Am. J. Dis. Child. 43: -£16,
 
1932.
6. Bodecker, C. F.: The Color of the Teeth as an Index of Their Resistance to
I
 
. Bodecker, C. F .: The Cake-Kitchin Modification of the Celloidin Decaleifying
Decay, Int. J. Orthodontia 19: 356, 1933.
Method for Dental Enamel, J. Dent. Research 16: 143, 1937.
. Bodecker, C. F.: Concerning the "\’italit_x"' of the Calcified Dental Tissues.
I\'é Vital Staining of Human Dental Enamel, J. Dent. Research 20: 377-
3S . 1941.
Bodecker, C. F'., and Lefkowitz, ‘\\‘.: Concerning the "Vitality" of the Calcilled
Dental Tissues, J. Dent. Research 16: -L63, 1937.
 
10. Boyle, P. E., Hillier, J., and Davidson. )7. B.: Preliminary Observations of the
Enamel of Human and Guinea Pig Teeth Using the Electron Microscope,
J. Dent. Research 25: 156. 19-16.
 
11. Cape. A. ’1'., and Kitchin. P. C.: Histologic Phenomena of Tooth Tissues as Ob-
served Under Polarized Light; With a Note on the Roentgen Ray Spectra
of Enamel and Dentin, J. A. D. A. 17: 193, 1931).
 
1:}. Chase, S. Y\'.: The Absence of Supplementary Prisms in Human Enamel, Aunt.
Rec. 28: 79. 19:24.
 
13. Chase, S. W.: The Number of Enamel Prisms in Human Teeth, J. A. D. A. 1-1:
1921. 1927.
 
1-1. Engel, 11. B.: Glycogen and Carboh_\'drat&Protein Complex in Developing
Teeth of the Rat. J. D. Res. 27: 4581. 19-18.
 
15. Fish, E. \V.: An Experimental Investigation of Enamel. Dentin and the Dental
Pulp, London, 1932. John Bale Sons 8: Dauielsson. Ltd.
 
16. Gottlieb, B.: lftersuehungcn iiher die organische Substanz im Schmelz mensch-
licher Ziihne (Investigation of Organic Substances in the Enamel 1, Oesterr.-
ungar. Vrtljschr. f. Zahnh. 31: 19, 1915. _
 
17. Gottlieb, B.: Aetiologie und Prophylaxe der Zahnkaries (Etiology and Prophy-
laxis of Dental Caries), Ztschr. f. Stomatol. 19: 129, 1921.
 
IS. Gottlieb, B., and Hinds, E.: some New Aspects in Pathology of Dental Caries,
J. Dent. Research 21: 317. 1942.
 
19. Gottlieb, B.: Dental Caries, Philadelphia, 1947, Lea 8: Febiger.
 
-I:
 
. -
_q
30.
31.
 
32.
33.
 
34.
35.
36.
37.
38.
 
46.
47.
48.
49.
50. Wislocki, G. B., and Sognn
51. Wolf, J.:
 
. Gruner,
 
. Gurney, B. F., and Rapp, G. W.:
 
. Gustaphson,
 
. Kitchin,
. Klein, H., and Palmer, C. E.:
 
. Scott, D. B., and Wyckofi, R. W. G.:
. Scott, D. B., and Wyckoif, R. W. G.:
. Scott, D. B., ‘Cssing,
. Skillen,
 
. Smreker,
 
ORAL I-IISTOLOGY AND EMBRYOLOGY
 
J. W'., McConnell, D., and Armstrong, W. D.: The Relationship Be-
 
tween the Crystal Structure and Chemical Composition of Enamel and
 
Dentin, J. Biol. Chem. 121: 771, 1937.
 
Technic for Observing Minute Changes in the
 
Tooth Surfaces, J. Dent. Research 25: 367, 1946. '
 
G.: The Structure of Human Dental Enamel, Odont. Tidskr.
(Supplement) 53: Elanders Boktryckeri, Griiteberg, Sweden.
 
Hodge, H., and McKay, H.: The Microhardness of Teeth, J. A. D. A. 20: 227,
1933.
 
Hollander, F., Bodecker, C. F., Applebaum, E., and Saper, E.: A Study of the
Bands of Schreger by Histological and Grenz-Ray Methods, Dental Cosmos
77: 12, 1935.
 
Karlstroem, S.: Physical, Physiologic and Pathologic Studies of Dental Enamel
With Special Reference to the Question of Its Vitality, Stockholm, 1931,
A. B. Fahlcrantz.
 
P. C.: Some Observations on Enamel Development as Shown in the
 
Mandibular Incisor of the White Rat, J. Dent. Research 13: 25, 1933.
 
The Relationship Between Post-Eruption Tooth
 
Age and Caries Attack Rate of the Lower First Permanent Molar, J‘. Dent.
 
Research 18: 283, 1939.
Kronfeld, R.: First Permanent Molar. Its Condition at Birth and Its Post-
the “Vitality” of the Cal-
 
natal Development, J. A. D. A. 22: 1131, 1935.
 
Lefkowitz, W., and Bodecker, C. F.: Concerning
cified Dental Tissues. II. Permeability of the Enamel, J. Dent. Research
17: 453, 1938.
 
Losee, F. L., and Hesse, W. C.: The Chemical Nature of the Proteins From
Human Enamel, J. Dent. Research 28: 512, 1949.
 
Nasmyth, A.: Researches on the Development, Structures and Diseases of the
Teeth, London, 1839, John Churchill.
 
Orban, B.: Histology of Enamel Lamellae and Tufts, J. A. D. A. 15: 305, 1928.
 
Pickerill, H. P.: The Prevention of Dental Caries and Oral Sepsis, ed. 3, New
York, 1924, Paul B. Hoeber, Inc., p. 340.
 
Retzius, A.: Microscopic Investigation of the Structure of the Teeth, Arch.
 
Anat. 87 Physiol. 486, 1837.
Robinson, H. B. G., Boling, L. R., and Lischer, B.: in Cowdry’s Problems of
(Manual of Bio-
 
Ageing, Baltimore, 1942, Williams & Wilkins, Chapter 13.
 
Schmidt, W. .T.: Handbuch der biologischen Arbeits Methoden
logic Working Methods), Abderhalden, Abt. 5, Teil 10, 1934, p. 435.
 
Schour, I.: The Neonatal Line in the Enamel and Dentin of the Human Decidu-
ous Teeth and First Permanent Molar, J. A. D. A. 23: 1946, 1936.
 
Schour, I., and Hoffman, M. 1312.: Studies in Tooth Development. I. The 16
Microns Rhythm in the Enamel and Dentin From Fish to Man, J. Dent.
Research 18: 91, 1939.
 
Schour, I.: Recent Advances in Oral Histology, Int. Dent. J. 2: 10, 1951.
 
Typical Structures on Replicas of Ap-
 
Intact Tooth Surfaces, Pub. Health Rep. 61: 1397, 1946.
 
shadowed Replicas of Ground Sections
 
Through Teeth, Pub. Health Rep. 62: 422, 1947.
 
M. J., Sognnaes, R. F., and Wyckofi, R. W. G.: Electron
 
Microscopy of Mature Human Enamel, J. Dent. Research 31: 74, 1952.
 
Eli’. C.: The Permeability of Enamel in Relation to Stain, J. A. D. A.
 
11: 402, 1924.
Skinner, E. W.: Science of Dental Materials, Philadelphia, 1937, W. B. Saunders
 
Co.
E.: Ueber die Form der Schmelzprisme 111‘ h Z"h
die Kittsubstanz des Schmelzes (On the Form 0? Enrlrfilrldgl :l].£.'iSe1:].S oat 1g&:ii
Teeth, and the Cement Substance of the Enamel), Arch. 1?. mikr. Anat 66'
312, 1905. ' '
Sognnaes, R. F.: The Organic Elements of th E 1. II, 111
Dent. Research 28: 549, 1949; 28: 55s,1949;%9:n2%31,e195o. ’ ’ and IV" J’
Sognnaes, R. F., and Shaw,  H.: Salivary and Pulpal Contributions to the
Radiophosphorus Uptake 111 Enamel and Dentin, J. A. D. A. 44: 489 1952.
Stiller, A. E.: A Study of the Direction of the Enamel Rods in the Deciduous
Molar-s Thesis, Northwestern University Dental School, 1937.
Williams, J. Leon: Disputed Points and Unsolved Problems in the Normal and
Pathological Histology of Enamel, J . Dent. Research 5: 27, 1923.
Am J.éAnat' 87: 239, f3;,lR. F.: Histochemical Reactions of Normal Teeth,
lastische Histologie der Zahn eweb Pl t‘ His 1
Tissues), Deutsche Zahn-, Mund- und Kgieferlfeil(kuiifidc7: 26g(,)1)9gy4i).0f Dental
 
parently
ENAMEL 81
 
B. DEVELOPMENT
 
1. Enamel Organ
 
The early development of the enamel organ and its differentiation have
been discussed in the chapter on Tooth Development. At the stage pre-
ceding the formation of hard structures (dentin and enamel) the enamel
organ, originating from the stratified epithelium of the primitive oral
cavity, consists of four distinct layers: the outer enamel epithelium,
 
   
 
     
 
L'3te"’.-1 dent’-‘J .- y 7 V_ . Enamel niche
lamina , - _
 
epithelium
 
Stellate reticulum Anlage of the
 
permanent tooth
 
Inner enamel , _ _ . , , ~- ‘.
epithelium , ,_ — - , , ' x
(amelo- . = '
 
Dental papilla‘-r%.
g ._l“
 
Fig. 5'.'.——'1'ooth gem: (lower incisor) or human embryo (105 mm., 4th month). Four
Iayers of the enamel organ. X. See Fig. 59.
 
stellate reticulum, stratum intermedium, and inner enamel epithelium
(ameloblastic layer) (Fig. 57). The borderline between the inner enamel
epithelium and the connective tissue of the dental papilla is the subse-
quent dentino-enamel junction; thus, its outline determines the pattern
of the occlusal or ineisal part of the crown. At the border of the wide
basal opening of the enamel organ the inner enamel epithelium reflects
into the outer enamel epithelium; this is the cervical loop.“ The inner
Oute: Enamel
Epithelium
 
S2 mun HISTOLOGY AND EMBRYOLOGY
 
and outer enamel epithelium are separated from each other by a large
mass of cells differentiated into two distinct layers. One, which is close
to the inner enamel epithelium and consists of two to three rows of flat
polyhedral cells, is the stratum intermedium; the other layer, which is more
loosely arranged, constitutes the stellate reticulum.
 
The different layers of epithelial cells of the enamel organ are named
according to their morphology, function, or anatomic location. Of the
four layers only the stellate reticulum derives its term from the morphol-
ogy of its cells; the outer enamel epithelium and stratum intermedium
are so named because of their location; the fourth, on the basis of ana-
tomic relation, is called inner enamel epithelium or, on the basis of
function, ameloblastic layer.
 
 
 
Capillary
it =9. I
 
Outer enamel
 
epithelium  _~ . V
a , A  l
 
I.‘ 
 
I§;i‘iiii']a.etrid ’ §.,;:'’' ‘ [
 
i.
if
 
Fig‘. 58.-—-Capillaries in contact with the outer enamel epithelium. Basement membrane
separates outer enamel epithelium from connective tissue.
 
In the early stages of development of the enamel organ the outer
enamel epithehum consists of a single layer of cuhoiclal cells, separated
from the surrounding connective tissue of the dental sac by a delicate base-
 
ment membrane (Fig. 58). Prior to the formation of hard structures this
regular arrangement of the outer enamel epithelium is more prominent in
the cervical parts of the enamel organ. At the highest convexity of the or-
E.\'A)IEL 83
 
gan (Fig. .37) the cells of the outer enamel epithelium hccome irregular in
shape and cannot be easily distinguished front the outer portion of the
stellate reticulum. The vascularized connective tissue surrounding the
enamel organ on its convexity is in close contact with the outer enamel epi-
 
thelium. The capillaries are prolific in this area and protrude toward the
enamel organ (Fig. 58). Immediately before enamel formation com-
 
mences, capillaries may even invade the stellate reticulum.‘-‘° This in-
creased vascularity insures a rich metabolism of the avascular enamel
organ during the formation of hard structures when a rich influx of
substances from the blood stream to the inner enamel epithelium is
required.
 
epithelium
( ame.lo-
blasts)
 
Fig. 59.—Region of the cervical loop (higher magnification of X in Fig. 5?). Transition
of the outer into the inner enamel epithelium.
 
The stellate reticulum, which forms the middle part of the enamel
 
organ, corresponds to the middle layer of the surface epithelium. Here,
 
the neighboring cells are connected by intercellular bridges spanning the
 
minute intercellular spaces. The features which characterize the stellate
reticulum are primarily due to the great increase of the gelatinous inter-
 
     
 
stellate
Reticu
84 ORAL HISTOLOGY mo EMBRYOLOGY
 
cellular substance. It separates the cells without breaking the inter-
cellular connections, and causes each cell to become stellate, or star-
shaped, with long processes reaching in all directions from a central
body and anastomosing with similar processes of neighboring cells (Figs.
58 and 59). The origin of the stellate reticulum, from the central por-
tion of a stratified epithelium, explains further the fact that the cells
are connected, by inter-cellular bridges, with the cells of the outer
enamel epithelium and the stratum intermedium.
 
- - Dental lamina
 
 
   
 
 
 
Outer enamel" .
epithelium ' _'..
 
W” A1118-ge ot Derma-
 
Dentin and enamel' “ .1 nent enamel organ
 
formation
 
Stellate reticulum ‘
 
Dental pulp’
 
Cervical loop
 
F18. 60.——Tooth germ (lower incisor) or a. human fetus (5th month). Beginning of
 
t<_iheil(1:;‘i1!l1e;’a.sI.1d §_na.rsneeel Ifggriggon. The stellate reticulum at the tip or the crown reduced in
 
The structure of the stellate reticulum renders it resistant and elastic;
theretore, it seems probable that it has a supporting and protecting func-
fmn {11 Preserving the shape of the inner enamel epithelium, as well as
msurmg undisturbed development until the time when the hard struc-
tures have acquired adequate resistance. It seems to permit only a
axannn 85
 
limited flow of nutritional elements from the outlying blood vessels to the
formative cells. Indicative of this is the fact that the stellate reticulum
is noticeably reduced in thickness when the first layers of dentin are laid
down and the inner enamel epithelium is thereby cut ofi from the dental
papilla, its original source of supply tFig. 60 ,1.
 
The cells of the stratum intermedium are situated between the stellate
reticulum and inner enamel epithelium. They are flat to cuboid in shape,
and are arranged in one to three layers. They are connected with each
other, and with the neighboring cells of the stellate reticulum and inner
enamel epithelium, by intercellular bridges. They may play an impor-
tant role in the development of the enamel.“ It is possible that they take
an active part in the calcium metabolism of the inner enamel epithelium.
That they are rich in phosphatase, would tend to support the theory that
they are actively involved in the process of calcification.“-'= *5 The cells
of the stratum intermedium show mitotic division. and are active in this
regard even after the cells of the inner enamel epithelium cease to divide.
 
The cells of the inner enamel epithelium which lie in contact with the
dental papilla assume a columnar form before enamel formation begins
and come to be known as ameloblasts. Like the outer enamel epithelium.
the cells of the inner enamel epithelium are derived from the basal cell
layer of the oral epithelium. Their basal end is in contact with the con-
nective tissue; the peripheral end is in contact with the stratum inter-
medium. The cells are separated by narrow intcrcellular spaces which
are crossed by intercellular bridges and contain a cementing substance.
Terminal bars, which are condensations of the intercellular substance
sealing the intercellular spaces, are found on both the basal and
peripheral ends of the cells. The ameloblasts undergo changes in shape
and structure which will be described as the life cycle of the ameloblasts.
 
At the free border of the enamel organ, where the outer and inner
enamel epithelial layers are continuous and reflected into one another, is
formed the portion known as the cervical loop” (Figs. 57 and 59l. Here
is a zone of transition between the cuboidal cells of the outer enamel
epithelium and columnar cells of the inner enamel epithelium in which
the cuboidal cells gradually gain in length. This zone of transition is
found in the cervical parts of the outer enamel epithelium. When the
enamel organ of the crown is fomied the cells of this portion give rise to
Hertwig’s epithelial root sheath (see chapter on Tooth Development).
 
2. Life cycle of the Ameloblasts
 
The cells of the inner enamel epithelium differentiate into ameloblasts.
which produce the enamel matrix. However, the cells of the inner enamel
epithelium may be termed ameloblasts even before they actually begin
to produce enamel.
 
According to its function the life span of an ameloblast can be divided
into several stages. The differentiation of ameloblasts is most advanced
in the region of the incisal edge or tips of the cusps; least advanced in
 
Stratum
Intermedium
 
Inner Enamel
Epithelium
 
cervical
Ameloblasts (long)—:p""'—E j""’
D »
 
       
 
 
,—— ..‘—" Pulp cells and amelo-
\ " blasts in contact
 
 
Stellate reticulum "
 
i
F
 
Cell-tree zone
 
Cell-free zone
 
Ameloblasts (short)
 
I-‘ig. 6L—-(For legend see opposite page.)
E.\'.\.\il-IL E7
the region of the cervical loop. Thus. all at‘ some stages of the develop-
ing ameloblast can be observed in one tooth germ. Because these cells
enter into this ditferentiation process successively the manner in which
enamel formation takes place maybe referred to as a stagger system.
 
Before the ameloblasts reach their full differentiation. and produce the
enamel, they play an important part in fixiiig the morphologic shape of the
crown (dentino-enamel junction) (Fig. 60?, During this morphogenetic
stage the cells are short columnar. with a large oval nucleus which almost
fills the cell body. The ameloblastic layer is separated from the connec-
tive tissue of the dental papilla by a delicate basement membrane. The
adjacent pulpal layer is a cell-free, narrow, light zone containing fine
 
argyrophile fibers and the cytoplasmic processes of the superficial cells
of the pulp (Fig. 61).”
 
In the organizing stage of development the ameloblasts seem to exert
an influence upon the adjacent connective tissue cells which causes them
to differentiate into odontoblastsf-’ This stage is characterized by a
change in the appearance of the ameloblasts whereby they become longer
and the nucleus-free zone. at the basal end of the cells. becomes almost
as long as the peripheral part containing the nucleus (Fig. 613. In prepa-
ration for this development a reversal of functional polarity of these cells
takes place becoming apparent by the migration of the central bodies"
and the Golgi apparatus.‘ from the periphery of the cell into the basal
end (Fig. 62). Moreover. the cytoplasm shows difierences in staining
reaction, in the region peripherally and basally to the nucleus. The nar-
row peripheral part stains red in hematoxylin eosin preparations. and the
wide basal part slightly pink.” Special staining methods reveal the pres-
ence of fine acidophile granules in the peripheral part of the cell.” At
the same time, the clear cell-free zone between the ameloblast layer and
dental papilla disappears (Fig. 61), probably due to elongation of the
ameloblasts toward the papilla.” By this process the ameloblasts come
into close contact with the connective tissue cells of the pulp, which are
stimulated to differentiate into odontoblasts. During the terminal phase
of the organizing stage of the ameloblasts the formation of the dentin by
the dental pulp begins, and this is accompanied by a slight shortening of
the elongated ameloblasts (Fig. 61).
 
The first appearance of dentin seems to be a critical phase in the life
cycle of the ameloblasts. As long as they are in contact with the con-
nective tissue of the dental papilla. they are nourished by the blood ves-
sels of this tissue. When dentin forms. however, it cuts ofi the amelo-
blasts from their original source of nourishment and, from then on, they
have to be supplied by the capillaries which surround and may penetrate
 
Fig. 61.——High magnification of ameloblasts, from (X) in Fig. 60. In the cervical
region the ameloblasts are short and the outermost layer at the pulp is cell-tree.
Occlusally the ameloblasts are long and the cell-tree zone of the pulp has disappeared.
aye amelolggasts are again shorter where dentin formation has set in. (Diamond and
 
einmann.
 
Morphogenetlc
stage
 
Orsazuxinx
stage
Founative
Stage
 
Maturation
Stage
 
88 ORAL HISTOLOGY AND EMBRYOLOGY
 
the outer enamel epithelium. This reversal of nutritional source is char-
acterized by proliferation of capillaries of the dental sac, and by reduc-
tion and gradual disappearance of the stellate reticulum (Fig. 60). Thus,
the distance between the capillaries and ameloblast layer is shortened.
Experiments with vital stains demonstrate this reversal of the nutritional
stream.“
 
The ameloblasts enter their formative stage only when the first layer
of dentin has already been formed. The presence of dentin seems to be
necessary to induce the beginning of enamel matrix formation just as it was
necessary for the ameloblasts to come into close contact with the connec-
tive tissue of the pulp to induce dilferentiation of the odontoblasts and
the beginning of dentin formation. This mutual action of one group of
cells upon another is one of the fundamental laws of organogenesis and
histodiiferentiationfif "
 
   
 
o_-.. ' . I‘ ‘ _ E:-.
 
;- M ‘:5. tr.
1.
 
.,. ca. it "'55" -ff;
 
.»'_
 
-. ' ‘.-i51r' .3 .’ v‘‘‘‘ 2.,‘
"35 I-—* .
' ' ‘wad’
 
'_‘.._  r‘¢i,'-::‘;- Tfi
T
 
 
Fig. 62.—Migx-ation of the centrioles from the peripheral (A) into the basal part (B) of
the ameloblasts indicating reversed functional polarity. D : Dentin. (Renyifl)
 
During formation of the enamel matrix the ameloblasts retain, approxi-
mately, the same length and arrangement. The minute changes in the
cell bodies are related to the formation of enamel matrix.
 
Enamel maturation occurs after the entire thickness of the enamel
matrix has been formed in the occlusal or incisalarea.’ In the cervical
parts of the crown, enamel matrix formation is, at this time. still pro-
gressing. During enamel maturation the ameloblasts are slightly reduced
in length and are closely attached to the enamel matrix. The cells of the
stratum intermedium lose their cuboidal shape and regular arrangement
2:x.un~:L 89
 
and assume spindle-shape. It is probable that the ameloblasts also play a
part in the maturation of the enamel: ultimately they produce the primary
cuticle.
 
When the enamel has completely developed and matured {calcified}
the ameloblasts cease to be arranged in a well-defined layer, and can no
longer be dificrentiated from the cells of the stratum intermedium and
outer enamel epithelium. These cell layers then form a stratified epi-
thelial covering of the enamel, the so-called reduced enamel epithelium.
The function of the reduced enamel epithelium is that of protecting the
mature enamel by separating it from the connective tissue until the tooth
erupts. If connective tissue comes in contact with the enamel. anomalies
may develop. Under such conditions the enamel may be either resorbed or
covered by a layer of cementum.“ '
 
The reduced enamel epithelium seems also to induce atrophy of the con-
nective tissue separating it from the oral epithelium. so that fusion of the
two epithelia can occur (see chapter on Oral Mucous Membrane). It is
probable that the epithelial cells elaborate an enzyme that is able to destro_v
connective tissue fibers by desmolysis. Premature degeneration of the
reduced enamel epithelium may prevent the eruption of a tooth?’
 
3. Amelogenesis
 
Development of enamel takes place in two distinct phases, i.e., for-
mation of enamel matrix and maturation of enamel matrix. The fully
developed enamel matrix is structurally identical to the mature enamel in
that it is formed by enamel rods and interprismatic substance. Chemi-
cally and physically, however, it differs from the mature enamel. The
fully developed matrix contains approximately 25 to 30 per cent mineral
salts in solution, the rest is organic material and water.“ The process by
which the matrix is transformed into the finished enamel, containing 96
per cent mineral salts and 4 per cent organic substance and water, is
called maturation of the enamel. In the process of maturation more
mineral salts are deposited and cr_vstall.ize in the matrix, and water is
eliminated.
 
The chemical and physical differences between enamel matrix and
mature enamel can be summarized as follows: {1} the enamel matrix has
the consistency of cartilage whereas mature enamel is the hardest substance
of the body: {'2} the enamel matrix is less radiopaque than the mature
enamel; and (3" the enamel matrix is not birefringent; the mature enamel
is birefringent when viewed in polarized light at right angles to the long
axis of the rods?‘ ‘"-
 
A. Formation of the Enamel Matrix.-
 
The formation of the enamel matrix is a very intricate process in its
morphogenesis as well as in its chemistry. In analyzing this process the
following stages can be distinguished:
 
(a) Formation of dentino-enamel membrane
 
Protective
Stage
 
Desmolytic
Stage
90 ORAL Hisronoor AND EMBRYOLOGY
 
(b) Development of Tomes’ processes
 
(c) Horuogenization of Tomes’ processes
 
((1) Formation of pre-enamel rods
 
(e) Influx of mineral salts in solution into the matrix
 
Dgnuno. It has been shown that, prior to the formation of dentin, the connective
‘figfiglmne tissue of the dental papilla is separated from the inner enamel epithelium
 
by a basement membrane (Fig. 63). On the connective tissue side fibers
 
.»  :-*5 "’  *3
‘4
i
4
3
 
Basement membrane  I5’ -C-,1”;
( Dentino-enamel 1 "
membrane) « _ ;,"
 
Basement membrane - - -‘
 
Eh
 
.;t"v,.
.‘§''’:.._’ “‘ -
 
Fig. 63.—Basement membrane of the dental papilla can be followed on the outer surface
of the dentin, forming the dentino-enamel membrane. (Orban, Sicher and Weinmannfi‘)
 
of the pulp are attached to this membrane fomuing the fibrous precursor of
the dentin. When a thin layer of dentin has been laid down the antelo-
blasts begin their amelogenetie activity by forming a. continuous thin
menlbrnne on the enamel side of the basement membrane;“’ it has been
termed dentinoenamel membrane.” In later stages of amelogenesis it is
found to be continuous with the interprismatic substance. Its presence ac-
E.\‘A.\:EL 91
 
counts for the fact that the dentinal ends of the rods are not in direct
contact with the dentin «Fig. 64?. The dentinna:-name} membrane cal-
cifies soon after its formation. similar to the interprismatic stthstanne.
After formation of the dentino-enamel membrane the ameloblasts pro-
duce short proeesses at their basal end which are known as Tomes’ proc-
esses (Fig. 65). These are hexagonal prismatic in shape and are a con-
tinuation of the ameloblasts. Synchronized with the appearance of
Tomes’ processes the terminal bars appear at the basal end of the antelo-
 
 
blasts. They denote the boundary between the cell body and Tomes’
I
it
i ‘ (Z1
Enamel rods —— - — I V,
" w
, I
{FEVE-
Dentino- p
r?ear:1heriane  “r '__’ ‘V '3_
Den:in' ‘ ‘ “ ‘ ‘i
 
Fig. 64.-—Dentino-enanzel membrane separates the rods from dentin.
 
processes. Structurally, they are condensations of the intereellular sub-
stance and appear, in a surface view, as more or less regular hexagons
which can be compared to a honeycomb -.'_Fig. 66'. The Tomes’ processes
are separated from each other by thin extensions of the terminal bars.
They retain their approximate length throughout the entire formation of
the enamel rods. The Tomes’ processes are continuously transfomied into
 
enamel rod substance at their dentinal end, and rebuilt at their 3.111810-
blastic end.”
 
The portion of the ameloblast designated as Tomes’ process is granular
during amelogenesis. The first indication of formation of the enamel rod
is a homogenization in the dentinal end of the Tomes’ process; the chemi-
 
Development.
of Tomes’
Processes
and Termi-
nal Bars
 
Homogenizar
tion of
Tomes’
?rocesses
92 om. HISTOLOGY .a.\'n EIIBRYOLOGY
 
cal nature of this change is unknown; the homogenized Tomes’ process is
slightly basophil in reaction (Fig. 67:1).
rounation or At the time this change is occurring, the lateral parts of the homoge-
gfggnamel nized processes are transformed into a diiferent chemical substance,
denser in structure and strongly basophil in character (Fig. 67A). This
substance does not contain calcium salts; it can be regarded as pre-
enamel. The transformation of the homogenized Tomes’ processes into
pre-enamel proceeds rhythmically by the formation of the so-called
globules or segments (Fig. 6713). The transformation of each segment pro-
ceeds excentrically, starting from one lateral surface, thus giving a
picket-fence-like appearance to the pre-enamel. The developing rods are
at an angle to the axis of the ameloblast and Tomes’ processes”! 2“ The
primary segmentation of the rods remains visible as a cross-striation
of the mature rods (Fig. 30). The outer layer of each rod shows a
slightly different staining reaction and is known as the rod sheath.
 
 
Ameloblasts
 
 
 
' — Terminal bars
.
 
Tomes’ processes
 
Dentin
 
Fig. 65.—For-matlon of Tomes’ processes and terminal bars, as the first step in enamel
rod formation Rat incisor. (Orban. sicher and Weinmannfi)
 
The interprismatic substance, which is continuous with the exten-
sions of the terminal bars between the Tomes’ processes, can be dis-
tinguished between the forming rods. The thickening of the terminal
bars at the basal end of the ameloblasts can be explained, therefore, by
their role in the production of the interred substance.
 
Mull! gi11é11l- When the pre-enamel rod attains a length of about 20 microns, calcium
salts in solution are deposited into its substance. The calcification begins
at the dentinal end of each rod and involves first the outer layers of each
rod, its core being the last part to calcify. However, because more pre-
enamel is forming all the while, the layer of pre-enamel remains approxi-
ENAJIEL 93
 
mately of equal width. The calcium salts are transported into the pre-
enamel from the blood vessels surrounding the enamel organ, by way of
the stratum intermedium, ameloblasts and Tomes’ processes. This influx
of mineral salts is accompanied by a chemical change in the pre—ename1.
It becomes more acidophilic.‘*"’ This acidophil layer might be termed
young enamel matrix. It forms a layer about 30 microns thick and
remains visible as a distinctly stained zone of the enamel matrix, until
maturation starts. The last stage of matrix formation is characterized
by a gradual reversal of the acidophilic nature of the young matrix into
a slightly basophilic state (Fig. 68]. The formation of the matrix follows
an incremental pattern (bands of Retzius).
 
~—, , u .. W?-‘-_r__“, t
T _ . A ‘ T
3",?‘ ‘ J  )3 f‘
r V‘ 0, vs l‘- '
 
Amelublasts
 
Terminal bar
apparatus
 
 
Fig. 66.—Terminal bar apparatus of the ameloblass in surface view. (Orban. Sicher and
W'einmann.")
 
B. Maturation of Enamel Matrix (Calcification and Crystallization).-
 
The maturation of the enamel matrix is characterized by the gradual
influx of almost three quarters of the ultimate contents of mineral salts
94 om. HIS’l‘0I.0GY AND I-2.\lBR\'0LOG'Y
 
Ameloblasts
 
Tenninal bars
Tomes’ processes
 
Homogenized
Tomes’ processes
Pre-enamel matrix
 
 
"s‘r:,‘.{"
 
 
Fig. 67A.—Homogenization of the dentinal ends of Tomes’ processes and their trar
formation into pre-enamel matrix in a picket fence arrangement. The rods are at
angle to the ameloblasts and Tomes’ processes. (orban. Sicher and We1nmann.")
 
Ameloblasts
 
Terminal bars
Tomes’ processes
 
Homogenlzed
 
Tomes’ processes
’ Preenamel
matrix
 
 
 
 
Ins. $7B.—Devdopment of rod segments during formation of pre-enamel matrix, The
alternating appearance or segmented and n ted rods is due to the honeycomb
an-anzernmt of the hexagonal prismatic rods. ( rba . Sicher and Weinmannfi)
nxman 95
 
present in the mature enamel, by crystallization of the mineral salts, and
by the simultaneous disappearance of water. The protein content of the
enamel matrix remains, in all probability, unchanged. It begins after the
enamel matrix has reached its final thicknes in the occlusal parts of the
crown. It can be assumed that the ameloblasts play an important part in
this transformation. The chemical changes in maturation are gradual.
 
 
:YGlEEIIAlE.Ifl'&
 
 
Fig. 68.——Diagramma.tic illustration of enamel matrix formation. Tomes’ processes
remain approximately the same in length during enamel matrix formation. Their
dentinal end is homogenized and then transformed into pre-enamel. Pre-enamel changes
into young enamel matrix and later into fully developed enamel matrix. The interred
substance is a continuation of the terminal bar apparatus. (Orban. Sicher and Wein-
 
mann:-")
 
The protein of the enamel before and after maturation is acid soluble.“
The proteins lose their solubility if they are denatured, for instance by
formalin fixation.“ Before maturation the enamel matrix is easily pene-
trated by the fixing fluid, while the density of the maturing and matured
Fig. is.—Dlagra.mmatlc illu.stra.fion of enamel matrix tormatiqn and maturation.
Formation follows an incremental pattern. maturation begins at fzllfiatégngé §1;§mcrBv;I;n:§g
 
proceeds oerrkally in cross relation to the incremental pattern.
and Weinmann!)
 
Fig. 70.—-Bucco-lingual section through a deciduous molar. Maturation of the
 
enamel has started in the lingual cusp—-while it has fairly well 1) in the bu -
cal cusp. Note the gradual transltian between the enamel matrix an the fully matured
 
enamel. (Diamond-Weinmsnnf)
ENAMEL 97
 
enamel renders it almost impermeable. Routine fixation of specimens
will therefore cause denaturing of the proteins of the enamel matrix
only. Thus, the enamel matrix is preserved despite decalcification, while
 
the maturing enamel disappears after its mineral contents have reached
a critical value.
 
 
 
 
Hexagonal Clyslals T
 
£a7_7I3x:'saf[nanell?od'\.
 
Suoums Ammnsarnenr or
suemcaosconc cnncmcnnon
cnvsmus m Hlllflflfl enmI£L Roo
ounmc ueiaovmarr.
 
Fig. 71.-—Dlag:-ammatic illustration of the crystal (black) and space (white) relation
in developing enamel as observed by polarized light. Compare with Fig. 53A to note the
subsequent elimination of space during the last stages of enamel maturation.
 
The process of maturation starts in the incisal region of the crown,
or at the heights of the cusps, and proceeds toward the cervical region‘
 
(Figs. 69, 70). It does not follow the incremental pattern but proceeds in
planes at right angles to the long axis of the tooth. The pattern of
maturation is correlated with that of tooth eruption.
 
During maturation the highest content of mineral salts is found at the
tip of the cusps or on the incisal edge; the lowest content of mineral
100
 
7.
8.
9.
 
10.
11.
12.
 
13.
 
14.
15.
16.
17.
18.
19.
20.
21.
22.
 
23.
 
24.
 
25.
 
26.
27.
28.
29.
30.
31.
 
32.
33.
 
ORAL HISTOLOGY AND EMBRYOLOGY
 
Dean, H. T., and Kitchin, P. 0.: Fluorine and Dental Health, Washington, D. G.,
1942, American Association for Advances of Science.
 
Diamond, M., and Weinmann, J. P.: The Enamel of Human Teeth, New York,
1940, Columbia University Press. _ _
Diamond, M., and Weinmann, J. P.: Morphogenesis of the Amelob_lasts in Re-
 
lation to the Establishment of the Fixed Dentino-Enamel Junction, J. Dent.
 
Research 21: 403, 1942. _ _
Diamond, M., and Applebaum, E.: The Epithehal Sheath:
 
Function, J. Dent. Research 21: 403 1942.
 
Histogenesis and
 
Engel, M. B.: Glycogen and Carbohydrate—-Protein Complexes in Developing
Teeth of the Albino Rat, J. Dent. Research 27: 681, 1948. _ _
Engel, M. B., and Furuta, W.: Histochemical Studies of Phosphates: Distribu-
 
tion in Developing Teeth of Albino Rat, Proc. Soc. Exper. Biol. £5 Med. 50:
5 1942.
 
Frisbie, H. E., Nuckolls, J., and Saunders, J. B. de C. M.: Distribution of Or-
ganic Matrix of Enamel in the Human Tooth and Its Relation to Histo-
pathology of Caries, J. Am. Coll. Dent. 11: 243, 1944.
 
Glasstonc, S.: Development of Toothgerms in Vitro, J. Anat. 70: 260, 1936.
 
Gomori, G.: Calcification and Phosphatase, Am. J. Path. 19: 197, 1943.
 
Gottlieb, B.: Calcium Deposition and Enamel Hypoplasia, J. Dent. Research 20:
549 1941.
Hahn,  E.: The Capacity of Developing Tooth Germ Elements for Self-
 
Diflferentiation When Transplanted, J. Dent. Research 20: 5, 1941.
 
Hampp, E. G.: Mineral Distribution in the Developing Tooth, Anat. Rec. 77:
273 1940.
Held, H.,: Ueber die Bildung des Schmelzgewebes (On the Formation of Enamel),
 
Ztschr. f. mikr.-anat. For-sch. 5: 668, 1926.
Jump, E. B.: Vascularity of the Human Enamel Organ, J. Dent. Research 17:
505 1938.
Kitchin,’ P. 0.: Some Observations on Enamel Development as Shown on the
Mandibular Incisor of the White Rat, J. Dent. Research 13: 25, 1933.
Kotanyi, E.: Histologische Befunde an retinierten Zahnen (Histologic Findings
on Embedded Teeth), Ztschr. f. Stomatol. 22: 747, 1924.
 
Logan, W. H. G., and Kronfeld, R.: Development of the Human Jaws and Sur-
rounding Structures From Birth to the Age of Fifteen Years, J. A. D. A. 20:
379 1933.
 
Orban,  Zur Entwicklung und feinei-en Struktur des Schmelzes (On the De-
velopment and Finer Structure of the Enamel), Ztschr. f. Stomatol. 23:
599 1925.
 
Orban,  Zur Histologie des Schmelzes und der Schmelzdentingrenze (His-
tology of Enamel and Dentino-Enamel Junction), Vrtljschr. f. Zahnheilk.
42: 336, 1926.
 
Orban, B., Sicher, H., and Weinmann, J. P.: Amelogenesis (A Critique and a.
New Concept), J. Am. Coll. Dentists 10: 13, 1943.
 
Renyi, G. S. de: Central Bodies in the Cells of the Inner Enamel Epithelium,
Am. J. Anat. 53: 413, 1933.
 
Sarnat, B. G., and Schour, I.: Enamel Hypoplasia (Ghronologic Enamel Aplaaia)
in Relation to Systemic Disease, J. A. D. A. 28: 1989, 1941; 29: 67, 1942.
 
Saunders, J. B. de G. M., Nuckolls, J., and Frisbie, H. E.: Amelogenesis, J.
Am. Coll. Dentists 9: 107, 1942.
Waserman, F.: Enamel Production and Calcification: Normal and Experi-
 
mental, J. Dent. Research 20: 254, 1941.
Weinniann, J. P., Wessinger, G. D., and Reed, (3.: Correlation of Chemical and
Histological Investigations on Developing Enamel, J. Dent. Res. 21: 171,
 
1942.
Weinmann, J . P., Svoboda, J . F., and Woods, R. W.: Hereditary
Enamel Formation and Calcification, J . A. D. A. 32: 397, 1945.
Weinmann, J. P.: Developmental Disturbances of the Enamel, The Bur 43: 20,
 
1943.
 
Disturbances of
CHAPTER IV
 
THE DENTIN
 
PHYSICAL PROPERTIES
CEENIICAL COMPOSITION
MORPHOLOGY
 
ZCNNERVATION
 
AGE AND FUNCTIONAL CHANGES
DEVELOPMENT
 
CL.'CNICAIa CONSIDERATIONS
 
.‘‘.°’.‘’‘!‘‘?”!‘'’’.'‘
 
The dentin constitutes the bulk of the tooth. As a living tissue it
consists of specialized cells, the odontoblasts, and an intercellular or
ground substance. In its physicaland chemical qualities it closely re-
sembles bone. The main morphological difference between bone and
dentin is that some of the osteoblasts forming the bone are included in
the intercellular substance as osteocytes, whereas the dentin contains only
cytoplasmic processes of the odontoblasts.
 
1. PHYSICAL PROPERTIES
 
In teeth of young individuals the dentin is, usually, light yellowish in
color. Unlike enamel which is very hard and brittle, dentin is slightly
compressible and  It is somewhat harder than b_one, but
considerably softer than enamel. The smaller content of mineral salts
in dentin renders it more radiolucent than enamel. Dentin is birefrin-
gent due to the positive birefringency of the collagenous fibrils of the
ground substance and the negative birefringency of the mineral contents
which form submicroscopic apatite crystals.
 
2. CHEMICAL COMPOSITION
 
Dentin consists of 30, per cent organic matter and water, and 70 per
cent inorganic material (see Table in chapter on Enamel). The organic
substance is chiefly collagen, a substance which yields glue or gelatin
when boiled in water. The inorganic component is mostly apatite, as in
bone, cementum and enamel. Organic and inorganic substances can be
separated by decalcification or incineration. In the process of deca1ci-
fication the organic constituents can be retained as a cartilage-like mate-
rial which maintains the shape of the dentin structure. Incineration
removes the organic constituents and the inorganic substances shrink but
retain the shape of the organ and become very brittle and porous.
 
First draft submitted by Getrit iéevelander.
101
Ground Sub-
stance
 
ORAL HISTOLOGY AND EMBRYOLOGY
 
3. MORPHOLOGY
 
The dentin consists of a fibrillar calcified ground substance which
contains cytoplasmic processes of the odontolilasts (odontoblastic processes
or Tomes’ fibers) in small tubes known as dentinal tubules. The matrix
consists of fine collagenous fibrils‘ of approximately 0.3 micron in diam-
 
;/_-_~u-«~-—— ———— -
 
E. as
 
Fig. 72.—Collagcnous fibrils in the dentirml ground substance (decalclflcd longitudinal
section ; silver impregnation).
 
cter, set in a homogenous calcified cementing substance (Fig. 72). These
are the collagenous fibrils of the dentinal ground substance which are
densely packed together and which are arranged in a direction approxi-
mately at right angles to the dentinal tubules (Fig. 73). The external
layers of the dentin contain a variable amount of coarse and irregularly ar-
 
‘Fiber: "A filamentary or threadlike structure."
 
Fibril: "A small fiber or component filament of a. fiber." (Goulrl.)
DENTIN 103
ranged fibrils which give this layer a diiferent appearance under the micro-
scope; this is the so-called “mantle” dentin.” In each successively
formed layer of the dentin the fibrils cross each other at an acute angle.
It has been claimed that the arrangement of the fibrils in the ground
substance is adapted to functional stresses.” The fibrils are bound to-
gether into small bundles by the homogenous cementing substance, to
form the dentinal ground substance. The calcium salts are contained in
the cementing substance, the fibrils being uncalcified.”
 
“JIg:v  J g.f|
.1 1 9..
 
E. .$ ." .‘ '_ Q. 0 ;
i ‘ . 9
 
’ , ' ‘ 9 l ‘
 
_‘ p .__r I . s
 
(E ‘xii’? 3 ,3‘? ii
 
\ 2
""§§ ex ‘1 I; .‘
5 " ’ \
a 4 (1 ‘ m.
we‘ '0 ' ' It‘?
Kile‘-1 .' DC 0,5‘
‘ ’. .. . Q 5
 
4 ‘cg
 
' ‘ 3.!
i  Q 5 i W
.94 '3;  ‘4* we‘. is "
5, __ nu
 
Fig. 73.-—Colls.genous fibrils in the dentinal ground substance‘ (decalcifled transverse sec-
tion; Mallory-Azan). (Orbanfl)
 
The odontoblasts are arranged along the pulpal surface of the dentin
(see chapter on Pulp). Each cell sends a long cytoplasmic process (Fig.
74) throughout the entire thickness of the dentin (odontoblastic processes)
which is contained in a dentinal tubule. There is only a potential space be-
tween the fiber and Wall of the tubule. This space is frequently enlarged
 
Odontoblastic
Processes
and Denti-
nal Tubules
104 ORAL HISTOLOGY AND EMBRYOLOGY
 
during histologic preparation, due to shrinkage. The course of the dentinal
tubule is somewhat curved, resembling an S in shape (Fig. 75). Starting
at right angles from the pulpal surface the first convexity of this doubly
curved course is directed toward the apex of the tooth. In the root of the
tooth, and in the area of incisal edges and cusps, the tubules are almost
straight.
 
_ _—_" Calcifled dentin
 
' '  ' " Unealcifled dentin
(predentin)
 
" ' Odontoblastic processes
 
*_ '"— '3 '?—'—* Odontoblasts
 
Q Q
 
-  if i O
 
Fig. 74.—0dontob1a.stic processes (Tomes' fibers) lyin in dentinal tubules, extend from
the odontoblasts into the entin.
 
The processes of the odontoblasts are thickest, and the dentinal tubules
widest, near the cell body, tapering toward the outer surface. They
divide dichotomously near the end into several terminal branches (Fig.
76). Along their course they send out thin secondary processes which
seem to unite with similar processes from neighboring odontoblastic
processes (Fig. 77). They may be compared to the anastomosing processes
of osteocytes. Some terminal branches of the odontoblast processes extend
into the enamel (see chapter on Enamel). Occasionally, an odontoblast
process splits into two almost equally thick processes; the division can
occur at any distance from the pulp (Fig. 78).
DENTIN 105
 
The odontoblast processes are cytoplasmic extensions of the cells, with
a denser and slightly deeper staining outer layer. The dentinal tubules
containing the odontoblast processes are relatively wide near the pulpal
cavity (3 to 4 microns), becoming narrower at their outer end (1 micron)
(Fig. 79). Near the pulpal surface of the dentin the number of tubules in
1 square millimeter varies, according to some investigators, from 30,000 to
7 5,000.“ The pulpal surface of the dentin is about one—third to onefifth of
the outer surface of the dentin. Accordingly, the dentinal tubules are far-
 
Fig. 75.—Ground section of human incisor. Observe course of dentinal tubules.
 
ther apart in the peripheral layers of the dentin, and more closely packed
near the pulp (Figs. 79, A and B). The ratio of the number of tubules per
unit area, on the pulpal and outer surfaces, is about 4 to 1. There are more
tubules per unit area in the crown than in the root. Their fine lateral
branches contain the secondary branches of Tomes’ fibers. A thin zone of
the Wall of the tubules immediately bordering the lumen, appears dark in
hematoxylin and eosin stain. The area can be compared to the so—called
capsule of the lacunae in bone. It is said to be a layer of ground substance
Incremental
 
106 ole.-xi. HIS’i‘()I.()GY AND EMBRYOLOGY
 
devoid of fibrils“ and is known as Neun1ann’s sheath (Fig. 79). Even
studies with the electron 1nieroscope”““ have failed to decide the question
as to the nature of Neuinann ‘s sheath.
 
The formation and calcification of dentin begin at the tip of the cusps
and proceed inward by a rhythmic apposition of conic layers, one within
the other. When the dentin of the crown has been laid down, the apical
layers assume the shape of elongated, truncated cones (Fig. 80). The daily
 
_»~——»— A— Deniinal lubulo-s
 
Dentino-enamel - - - *-
Junction
 
Enamel —
 
-~ W-*—“—“‘ Dentinal tubules
 
 
 
Fig. 76.—Dentina.l tubules showing dichotomous branching close to the dentino-enamel
junction.
 
rate of apposition of the dentin in the crown varies from 4 to 8 microns in
thicl:11ess.29:“ The appositional growth is graded in such a way that the
increments become thinner as root formation progresses.“ The rhythmic
growth pattern of dentin is indicated in the completed structure by fine
lines (Fig. 81). These seem to correspond to rest periods in cellular ac-
tivity and are known as the imbrication or incremental lines of von Ebner
DENTI1\‘ 107
 
»-1
.
 
...\~ 9-t'~
1'4 ,_ma-»z,4."SL
.I _~
 
 
 
 
-‘x 1  ; x  r -
 
’ ‘Alf bf-gl  ml?
 
Fig. 77.—Seconda.ry branches of dentlnal tubules anastomosiug with those of neighboring
as well as distant tubules. (Be\'ulancler.)
 
_f_  ,‘, I 1, V1‘ . .
_;:b fit ‘ . ~ /
Enamel .  / ' ’ I ’. '-
 
 
Terminal branches "A
of dentinal tubules
 
 
Splitting of
dentinal tubules
 
 
 
 
Splitting of
dentinal tubules
 
 
Fig. ’l8.—Splitting of dentinal tubules into branches. (Bevela.nder.)
Fig. 79.—We1I-fixed decalcifled section of dentin.
A. Close to the pulp.
B. Close to the outer surface.
 
(Magnification X2000. No shrinkage between dentinal fibers a d (1 ti 1 t b I -
the entire tubule is fllle by the fiber. Note size and number o1'nden:i':1ai1atub'{l1I¢:.lse?fi
 
A and B.
 
Fig. 80.-—Diag'rammatlc illustration of the inc ta! it‘ 1 tt
¢e°i'1“°“S central incisor) 5 m.i.u. = 5 montheilhelilitezzo. ap(ps°§h$3?aan§aM§§§1ergémer
DENTIN 109
 
and Owen. They run at right angles to the dentinal tubules. Sometimes,
the incremental pattern is accentuated due to less complete calcification.
These lines, readily demonstrated in ground sections, are known as “con-
tour lines of Owen” (Fig. 82). In the deciduous teeth and first permanent
molars, where the dentin is formed partly before and partly after birth
 
i.»~  x \ . -  .
__ . .
 
.
r
I
 
.
|
is’
>‘ (
l \
\ ' '3
. v_ —
C’
. . ‘..‘ \
5 ' \
‘l‘.‘l‘ "'1 -
V ‘ K
. \
‘:-:——_I .——T_
 
Fig. 81.—Incrementa.l lines in the dentin. Imbricatlon or incremental lines of v. Ebner
and Owen. Ground section.
 
 
Fig. 82.—Accentuated incremental lines in the dentin: Contour lines of Owen.
Postnatal dentin ——~:——--————-—— v ~——--
 
Interglobular
Dentin
 
Prenatal dentin --
 
110 onnn msronooy AND EMBRYOLOGY
 
(Fig. 44), the prenatal and postnatal dentin are separated by an accentu-
ated contour line, the so-called neonatal line“ (Fig. 83). It corresponds
to the incompletely calcified dentin formed in the first two weeks after
birth; it is caused by metabolic disturbances at the time of adjustment of
the newborn to the abrupt changes of environment and nutrition.
 
Neonatal line -—
 
K’:
 
Fig. 83.—PostnataIly formed dentin is separated from the prenatally formed by an ac-
centuated lncremental line: the neonatal llne. (Sehour and Poncher."-‘)
 
Calcificatiogf the dentinal ground substance occurs by deposition
Fofrsmalflcalciuifij globules which, normally, fuse to form a seemingly
liomogenousrstrbstance (pages 122, 123). If calcification remains incom-
plete, the uncalcified or hypoealcified ground substance bounded by the
globules forms the interglobular dentin. The dentinal tubules pass unin-
terrupted through these uncalcified areas (Fig. 84). In ground sections of
dried teeth the uncalcified ground substance is shrunk or lost, and inter-
globular areas are filled with air and, therefore, appear black in trans-
mitted light (Fig. 85). Interglohular dentin is found chiefly in the
crown, near the dentino-enamel junction and arranged according to
the incremental pattern of the tooth. Minute areas of interglobular
 
dentin are, presumably, also responsible for the contour lines of Owen.
DENTIN 111
 
A thin layer of dentin adjacent to the cementum shows, in ground
sections, a granular appearance (Fig. 86) ; this is known as Tomes’ granu-
lar layer. It is a constant morphologic feature, which is limited-to the root.
Numerous minute areas of interglobular dentin are believed to give this
zone its granular appearance. The development of Tomes’ granular layer,
a zone of inadequately calcified dentin, has been attributed to the presence
of a highly vascularized tissue on the surface of the root before cementum
 
_  _ ___
 
J, J
,i '
 
 
 
6
5
 
.5
 
__ __ ._.:.'.
 
Fig. 84.—Inte1-globular dentin (decalcifled section). The dentinal tubules pass uninter-
rupted through the uncalcifled and hypocalcifled ‘areas.
 
 
is deposited. It is claimed that calcification is retarded in close proximity
to highly vaseularized areas. The absence of a granular layer in the crown
is explained by the fact that, during development, the outer area of dentin
in the crown is separated from the vascularized connective tissue by the
enamel organ.
 
The study of dentin by means of polarized light has added to the knowl-
edge of its structure. By this method it was shown that the calcification of
dentin is largely the result of calcium salt impregnation around the fibrils.“
 
Tomes’ Granu-
lar Layer
 
Submicroscopic
Structure
112 omn HISTOLOGY AND EMBRYOLOGY
 
The long axis of the crystals is parallel to fibrils” and, therefore, approxi-
mately at right angles to the direction of the dentinal tubules (Fig. 87).
 
Subsequent studies with polarized light“ have shown another arrange-
ment of inorganic salts, unique in the dentin. The polarized light reveals
 
Dentlno-enamel
junction
 
 
 
Interglobular areas
 
Fig. 85.—Interglobule.r dentin as seen in a. dry ground section. Interglobular areas are
filled with air and appear black in transmitted light. (Bevelandex-.)
 
areas of semilunar calcification in the dentin“! 19' 2° which are due to an
initial phase of calcification in spherite form, with the crystals of the calci-
 
fication units having their long axes radiating from a common center
(Fig. 87).
DENTIN 113
 
Studies of the dentin, by means of polarized light, are difficult because
the organic fibers and the inorganic salts are both birefringent, the first
optically positive and the second optically negative; the total effect is a
combination of the two. To separate them it has been necessary to work
 
.«with (1) dentin freed of the organic constituents, and (2) dentin freed
 
i
-—— Enamel
 
Dentin —~ -
 
’ Cemento-enamel junction
 
Inter-globular dentin
 
 
Cementum
 
- - Tomes’ granular layer
 
Interglobular dentin -—- -
 
. Tomes’ granular layer
 
_.—%..——_ . A J
 
Fig. 8s.—'.l.‘omes’ granular layer lies in theectperipheral zone of the root dentin. Ground
3 on.
 
from the inorganic parts. By such means it has been shown” that the
collagenous fibrils are made up of submicroscopic units with their long
axes parallel to the length of the fibrils. In calcified dentin these fibrils
are coated with apatite crystals similar to those of the enamel, and ar-
 
ranged also With their long axes parallel to the direction of the col-
lagenous fibrils.
114 omu. HISTOLOGY AND EMBRYOLOGY
 
4. INNERVATION
 
Despite the obvious clinical observation that dentin is highly sensitive
to a diversity of stimuli, the anatomic basis for this sensitivity is still
controversial. The literature contains many accounts on the presence of
nerve fibers in the denti11al tubules but these findings have repeatedly
been demonstrated as artefacts. The difficulties of histologic technique
are the cause for the lack of definitive information.2* '-’*- “S
 
   
   
 
(‘geld Pelalian lo
Enamel Poi
 
54-rrulunar ar $-/tubal
 
n./.,r...1...,. my ;. denlirjl
 
Dentn-u1I'TubuIes _ l
 
Una  jcneml
.Dir:ci/on fiamllel la d-e
ju..=:;ny o/I‘76rr'A'figl Tomes)
 
Denfi.-I.
 
8”--:°,.*,:%;i:'::8:.i°mi:L‘;:%::.“3;* aztusiesaztztaszaez :51a::*:;'a*‘%:§::°P‘° “W
 
The pulp contains numerous unmyelinated and myelinated nerve fibers.
The former end on the pulpal blood vessels, while the latter can be fol-
lowed into the subodontoblastic layer. Here they lose their myelin
sheath and can be followed into the odontoblastic layer itself. Between
the cell bodies of the odontoblast most of the fibers apparently end in
DENTIN 115
 
contact with the odontoblastic perikaryon. Occasionally part of a nerve
fiber seems to be embedded in the predentin curving back into the odonto-
blastic layer.
 
The sensitivity of the dentin must be explained by changes in the
odontoblastic processes, possibly changes of surface tension and surface
electrical charges, that in turn provide a stimulus for the nerve endings
in contact on the surface of the cell body.
 
Fig‘. 873.-—Dentin:
seconds. Electron microscope photograph X7000.
 
5. AGE AND FUNCTIONAL CHANGES
 
A discussion on the vitality of dentin is complicated by the fact that
many investigators think of dentin as consisting only of ground sub-
stance. However, dentin consists of ground substance and the odonto-
blasts with their cytoplasmic processes. If vitality is understood to be
the capacity of the tissue to react to physiologic and pathologic stimuli,
dentin should be considered a vital tissue.
 
The intercellular substance of the dentin is permeated, as any other
tissue, by tissue fluid, unnecessarily termed dental lymph.“ 3' 9’ 1”’ “- 15
The dentin owes to this tissue fluid its turgor that plays an important role
in securing the connection between dentin and enamel.
 
shadowed replica. of ground section, etched with 1/10 N HCL for 5
(Courtesy Dr. .1. Kennedy.)
 
vitality of
Dentin
secondary
Dentin
 
Irregular
Dentin
 
116 03.1.1. nrsromev AND EMBRYOLOGY
 
Under normal conditions, formation of dentin may continue throughout
life. Frequently, the dentin formed in later years of life is separated
from that previously formed by a darkly stained line. In such cases the
dentinal tubules bend more or less sharply at this line (Fig. 88). In
other cases the newly formed dentin shows irregularities of varying de-
gree; the tubules are often wavy and less numerous per unit area of the
dentin. The dentin, forming pulpward of the line of demarcation, is called
secondary dentin. This dentin is deposited on the entire pulpal surface
of the dentin. However, its formation does not proceed at an even rate
in all areas. This is best observed in bieuspids and molars where more
secondary dentin is produced on the floor and roof of the pulpal chamber
than on the side walls (see chapter on Pulp).
 
Demarcation line
 
 
 
’-- Secondary dentin
 
Fig. 88.—’l.‘he dentlnal tubules bend sharply as they pass from the primary into the
secondary dentin. Dentinal tubules are somewhat irregular in the secondary dentin.
Ground section.
 
The change in the structure from primary to secondary dentin may be
caused by the progressive crowding of the odontoblasts which finally
leads to the elimination of some and to the rearrangement of the remain-
ing odontoblasts.”
 
The pulp reacts to more severe stimuli by forming a. type of dentin
which shows still greater diiferences from primary dentin than the sec-
ondary dentin. It forms in restricted areas of the pulpal wall as a reac-
nnnrm 117
tion to extensive wear, erosion, and caries, which by the exposure of
odontoblast processes cause pulpal irritation; it is termed irregular den-
tin. Here, the course of the tubules is frequently twisted and their number
greatly reduced (Fig. 89). Some areas of irregular dentin contain few
or no tubules. Dentin forming cells are often included in the rapidly
 
 
‘lit
 
8-. £15‘
 
tlxrd‘ 3 i
1, S "' 1
‘ ' ls‘
 
Irregular dentin
 
   
 
~ 1 in A” . Demarcation line
 
 
.~ .3»;
 
I
 
Dentin
 
’.
5%’
 
A
 
.,i
4'
 
 
Fig. 89.—Irreg'ular dentin stimulated by penetration of caries into the dentin. Dentinal
tubules are irregular and less numerous than in regular dentin. Decalcifled section.
 
produced ground substance; such cells degenerate and vacate the spaces
which they formerly occupied. Frequently, irregular dentin is separated
from primary or secondary dentin by a deeply staining line.
 
Stimuli of different nature not only induce additional formation of
dentin (secondary or irregular) but lead to changes in the dentin itself.’
Calcium salts may be deposited in or around degenerating odontoblast
 
*]_3odecker' introduced the term “protective metamorphosis” for the age changes in the
dentin, characterized by decreased permeability oi.’ the dentin due to changes in the dental
 
lymph.
 
Transparent
(sclerotic)
Dentin
- Dentinal tubules
filled with air
 
v Carious dentin
 
9
 
‘I ' Transparent dentin
 
Dentinal tubules
filled with air
 
~~A~—~A ~—~— ——--~——~ Curious dentin
 
r — ‘—-—~——‘~v"’-W“-*-' ~ " Transparent dentin
 
.
 
Dentin
 
 
 
__ _ WW, — . carious dentin
9 ,' ‘.
 
 
— --“.—’..... Transparent dentin
 
Fig. 90.-—(For legend ace oppoaite page.)
Irregular
dentin
 
DENTIN 119
 
processes and may obliterate the tubules. The refractive indices of
dentin in which the tubules are occluded are equalized, and such areas
become transparent. Transparent dentin can be observed in teeth of
old people, especially in the roots. On the other hand, zones of trans-
parent dentin developed around the dentinal part of enamel lamellae of
Type B (Fig. 48) and under slowly progressing caries (Fig. 90). In
such cases the blocking of the tubules may be considered as a defensive
 
I
9
 
 
A. B.
 
Fig. 91.——Dead tracts in the dentin of a vital tooth. due to attrition and exposure or
 
a group oi.’ dentinal tubules. Corresponding to the dead _tract irregular dentin formation
11: 1:12; glib. Dead tracts appear dark in transmitted light (A) and white in reflected
g .
 
reaction of the dentin. Roentgen ray absorption tests“ a11d permeability
studies“ have shown that such areas are denser and hardness tests“ have
demonstrated that they are harder than normal dentin.“°= 3’
 
Transparent dentin is seen only in ground sections. It appears light
in transmitted (Fig. 90, A1) and dark in reflected light (Fig. 90, B) be-
 
Fig. 90.—'l‘mnsps.rent dentin under a carious area viewed by A. transmitted light,
B, reflected light. and G, Grenz rays. Normal dentinal tubules are filled with air in
dried und sections and appear dark in transmitted light (A) and white in reflected
light ( ). Transparent dentin shows the opposite behavior because the tubules are filled
with calcium salts. In a Grenz-ray picture (0 transparent dentin appears more white
because of its higher degree of radiopucity. ( renz-ray picture courtesy E. Applebaum.
Columbia. University.)
 
Irregular
dentin
Dead Tracts
 
120 omu. HISTOLOGY AND EMBRYOI.-OGY
 
cause the light passes through the transparent dentin, but is reflected
from the normal dentin. Zones of dentin, decalcified by caries, normal
dentin, and transparent dentin can be differentiated by the examination
of ground section with soft roentgen rays (grenz rays) .1
 
4:4
 
fiffl
 
Fig. 92.—Dead tracts in the dentin or a. vital tooth, due to crowding and degeneration
of odontoblasts in narrow pulpal horns. and exposure or dentinal tubules in erosion.
Well-fixed. ground section (not dry!).
 
The composition of dentin does not change with age,“ *3 though increase
 
of specific gravity of dentin with advancing age and reduction of its
strength was reported.‘ ‘
 
In dried ground sections of normal dentin the odontoblastie processes dis-
integrate, and the empty tubules are filled with air. They appear black
in transmitted and white in reflected light (Figs. 90, A and B). Disinte-
gration of odontoblastic processes may also occur in living teeth as a result
of the irritation of caries, attrition, abrasion, or ‘erosion (Figs. 91 and 92).
Degeneration of odontoblasts is frequently observed in the narrow pulpal
DENTIN 121
 
horns (Fig. 92) due to crowding of odontoblasts. Irregular dentin seals
these tubules at their pulpal end. In all these cases, dentinal tubules in
vital teeth are filled with gaseous substances; in ground sections such
groups of tubules appear black in transmitted and white in reflected
light. Dentin areas characterized by degenerated odontoblast processes
 
have been called dead tracts.“ They are areas of decreased sensitiv-
ity.14, 34
 
6. DEVELOPMENT
 
The first sign of dentin development is _a thicke_nin.«z__Q:f the basement
membrane (membrana preformativa) between the inner enamel epithe-
lium and the mesodermal primary pulp. The thickening is first visible at
the tips of cusps or incisal edges of the tooth germs, progressing in the di-
rection of the ultimate apex (Fig. 93). The basement membrane which is
derived from the mesenchyme of the pulp consists of fine intercrossing retic-
ular argyrophil fibrils. The next staggin dentin development is character-
ized by the formation of irregularl s iralin fibers ori ' atin '
$13, which merge_with the fibrils of the l')aseme.n_’_r. me.m}n_-amp. (Fig. 94).
These spiraling fibersqstainblack with silver (argyrophil fibers), a reaction
which is characteristic of precollagenous substance. At their pulpal origin
they are continuous with many fine fibrils of the pulp; they are known as
Korff’s fibers. Each consists of a large number of fine fibrils cemented
 
together to form an optically homogenous structure.
 
While the Kor1f’s fibers appear, the spindleshaped mesenchymal ggl_l§
 
closest to the asement membrane, assume a high columnar sham (see
chapter on Enamel, Fig. 61). These cells are arranged in a continuous
 
layer and are termed odontoblasts. They are linked to one another by
intercellular bridges. A protoplasmic process of the odontoblast extends
 
toward the future dentino-enamel junction; it elongates and branches as
dentin deposition takes place.
 
The formation g£_dentin sta3ts_ with a spreading _of the parts of_ l_§orE’s
Qers nearest to the baselnent membrane (Fig. 94). This spreading may
be due to an expansion or swelling of the interfibrillar cementing sub-
stance in Korfl?’s fibers. At the same time, the substance of the KorfE’s
fibers undergoes a striking E_eg1_g_Ll1apge which caus_es__ gem to pass
gain a_ precollagenous_t_Q_a collagenous sta.ge_(Fig. 95). The change is best
detected— by the reactions which this substance exhibits to certain specific
stains. The substance which was formerly argggphg '3; no longer stains
black in silver preparation, but assumes a reddish-brown glgr which is
characteristic n'F nn11ageno11s_m%w  Its collagenous nature
can also be detected by Mallory-Azan staining; in this preparation the
collagenous ground substance appears blue (Fig. 95).
 
The 2roumLsnJ_a.s_Lmce is 3'“ firS£—uI&1°ifi&<1 and» i
predentin. The dentina] fibrils seem to diflerentiate in the primarily.
homogeneous predenE'n._
Beginning dentin
 
formation
 
Enamel organ
 
122
 
ORAL HISTOLOGY AND 1«:1\1mn'0L0uY
 
_ While the apposition of a current layer of predentin is taking place, the
previous layer is undergoing calcification. The formation of predentin and
calcification follow an incremental pattern. Calcification lags behind the
formation of the ground substance in such a way that the last increment
always remains uncalcified predentin as long as formation of dentin pro-
ceeds (Fig. 74). At the same time the K01-ff’s fibers elongate and extend
farther into the areas between the receding odontoblasts.
 
Fig. 93.—'J.‘ooth germ with beginning dentin formation.
 
Silver impregnation.
lander.)
 
(Beve-
 
The transformation of the pulpal fibrils into Kortf’s fibers, the trans-
formation of the argyrophile Korff’s fibers into the collagenous predentin,
the difierentiation of the fibrils in the pi-edentin, and finally the calcifica-
tion of the cementing substance are in all probability brought about by
the enzymatic activity of the odontoblasts. Dentinogencsis is correlated
with the presence of alkaline phosphatase in the subdontoblastie region
and in the odontoblasts and their processes.‘
 
The calcification of dentin matrix follows a varied pattern. The crys-
tals of calcium salts (apatite) are deposited around the collagenous fibrils
DENTIN‘ 123
 
in the cementing substance; the fibrils thcniselves remain uncalcified. In
some cases, globules of different sizes are formed which later fuse and
give the ground substance a homogeneous appearance. In other cases, the
calcium salts are deposited in layers. Sometimes, areas can be observed
in which globular and linear calcification are combined (Fig. 96). These
 
   
 
Ameloblasts ,  _
5%,, i "E". 3”‘
‘In » Wu!»
, I ..
.»-~«; “
' . 44-.3:
‘ k  KorfE's
E‘ flbers
 
Thickening of E-
basement
membrane
 
Fig. 94.—'.l‘hickening of the basement membrane between pulp and enamel epi-
thelium. Development ot Korlfs fibers and their transrormation lnto dentin matrix-
 
Bevelander. )
 
phenomena are similar to those occurring during precipitation of crystals
in colloidal media (Liesegang’s rings). When calcified, predentin consti-
tutes the mature dentin ground substance.
 
7. CLINICAL CONSIDERATIONS
 
The vitality of dentin is dependent upon the presence of odontoblasts
and their processes, and thus upon the vitality of the pulp. The vitality
124 omu. I-IISTOLOGY AND EMBRYOLOGY
 
of the dentin constitutes the basis of defense reactions in response to
normal and pathologic stimuli (irregular dentin, transparent or sclerotic
dentin).
 
As a vital tissue, dentin should be treated with the utmost care in opera-
tive procedures."’v 257 3‘ Whenever dentin is cut or heat or drugs are ap-
plied, a reaction occurs as a result of irritation of the odontoblasts through
their processes. The exposed dentin should not be insulted by strong drugs,
undue operative trauma, unnecessary thermal changes, or irritating filling
 
Linear
calcification
 
Globular
calcification
 
Fig. 96.—Linear and globular calcification of dentin.
 
materials. Contact of exposed dentin with saliva should be avoided. It
should be borne in mind that, by exposing one square millimeter of dentin,
about 30,000 dentinal tubules are likewise exposed. The surface may be
treated with astringent drugs, such as phenol, silver nitrate,‘*"‘- ‘° to co-
agulate the protoplasm of the exposed odontoblast processes. It is ad-
visable to cover the exposed dentin surface by a nonirritating insulating
ubstance.
formed
_ Fig. 95.—Due to a chemical change the argyrophilic Korfi’s fibers become trflfls
mto the collagenous ground substance or the dentin.
 
A. Silver impregnation (Korfl's fibers, black) and hems.toxy1in—azur¢+eosi1'I
(collagenous dentin ground substance, brownish red).
 
_ B. Silver impregnation (Korffs fibers, black) and staining by Heidenhain's
non of Mallol-y’s method. (Coflagenous dentin ground substance. blue.) (Orb$
 
stalninz
 
f;x‘9dlfl(:8.-
fl. ‘)
 
DENTIN 125
 
The rapid penetration and spreading of caries in the dentin is due to
the high content of organic substances in the dentin matrix. The enamel
may be undermined at the dentino-enamel junction, even when caries in
the enamel is confined to a small area. The dentinal tubules form a
passage for invading bacteria which may, thus, reach the pulp through a
thick dentinal layer.
 
The sensitivity of the dentin varies considerably in difierent individ-
uals. In most cases, it is greater close to the outer surface of the dentin,
and diminishes in the deeper layers. The sensitivity of the dentin, there-
fore, is not a warning signal to avoid exposure of the pulp. The opera-
tions in the dentin can be rendered less painful by avoiding heat and
pressure by the use of water and sharp instruments.
 
References
 
1. Applebaum. E., Hollander, FL, and Bodecker, C. F.: Normal and Pathologital
Variations in Calcification of Teeth as Shown by the Use of Soft X-rays_
Dental Cosmos 75: 1097, 1933.
 
Berkelbach van der Sprenkel, H.: Zur Neurologie des Zahnes (The Neurology
of the Tooth), Ztschr. f. mikr.-anat. Forsch. 38: 1, 1935.
 
Bevelander, G.: The Development and Structure of the Fiber System of Dentin,
Anat. Rec. 81: 79, 1941.
 
Bevelander, G., and Johnson, P. L.: Odontoblasts and Dentinogenesis, J. Dent.
Research 25: 381, 1946.
 
Bevelander, G., and Amler, M. H.: Radioactive Phosphate Absorption by Den-
tin and Enamel, J. Dent. Research 24: 45, 1944.
 
Black, G. V.: Investigation of the Physical Characters of the Human Teeth,
D. Cosmos 37: 353, 469, 1895.
 
Bodecker, C. F.: The Soft Fiber of Tomes, a Tubular Structure: Its Relation
to Dental Caries and the Desensitization of Dentin, J. Nat. Dent. Assn. 9:
281, 1922.
 
. Bodeeker, C. F.: Dangers of Extensive Operative Procedure on Recently
 
Erupted Teeth, J. A. D. A. 28: 1598, 1941.
9. Bodecker, C. F., and Gies, Wm. J .: Concerning the Character of the Age Changes
in Enamel and Dentin and Their Relation to the Vital Dental Pulp, J. Am.
Coll. Dentists 9: 381, 1942. ‘
10. Bodecker, C. F., and Lefkowitz, W.: Concerning the “Vitality” of Calcified
Dental Tissues, J. Dent. Research 16: 463, 1937.
11. Cape, A. T., and Kitchin, P. C.: Histologic Phenomena of Tooth Tissues as Ob-
served Under Polarized Light, J. A. D. A. 17: 193, 1930.
12. Crowell, D. C., Hodge, H. C., and Line, W. 15%.: Chemical Analysis of Tooth
Samples Composed of Enamel, Dentin and Cementum, J. Dent. Research
14: 251, 1934. '
13. Ebner, V. v.: Ueber die Entwicklung der leimgebenden Fibrillen im Zahnbein
(Development of Collagenous Fibrils in the Dentin), Sitzungsb. d. k.
Akad. d. Wissensch. Vienna 115: 281, 1906; and Anat. Anz. 29: 137, 1906.
14. Fish, E. W.: An Experimental Investigation of Enamel Dentin and the Dental
Pulp, London, 1932, John Bale Sons & Danielsson.
15. Fish, E. W.: The Circulation of Lymph in Dentin and Enamel, J. A. D. A. 14:
1, 1927.
16. Gebhardt, W.: Ueber den funktionellen Bau einiger Ziihne (The Functional
Structure of Some Teeth), Arch. f. Entwcklngsmechn. d. Organ. 10: 135,
1900.
 
P’
 
°°>'S"?‘!'°‘P’
 
_17. Grurley, W. B., and Van Huysen, Gr.: Histologic Response of the Teeth of Dogs
 
to Operative Procedures, J. Dent. Research 19: 179, 1940. _
 
18. Hodge, H. C.: Microhardncss Studies of Transparent Dentine, Brit. D. J. 63:
181 1937.
 
19. Keil, A.’: Ueber Doppelbrechung und Feinbau des menschlichen Zahnbeins (On
Birefringence and the Minute Structure of Human Dentin), Ztschr. :E. Zel1-
forsch. u. Mikr. Anat. 21: 635, 1934.
126 ORAL HISTOLOGY AND EMBRYOLOGY
 
20. Keil, A.: Ueber den Feinbau der harten Zahnsubstanz nach Untersuchungen in
polar-isiertem Licht (On the Minute Structure of the Hard Tissue of the
Teeth Studied Under Polarized Light), Deuische Zaln1- Mun(l- 11. l{iefer-
heilk. 2: 741, 1935.
 
2]. K0rfl', K. v.: Wa.chstun1 der Dentingrundsulrstanz verschiedener Wirhelliorc
((z‘rroWth of the Dentin Matrix of Difi"erent Vertebrates), Ztschr. f. 1nikr.-
anat. Forsch. 22: -1-45, 1930.
 
22. Korif, K. v.: Die Entwicklung der Zahnbein Grundsubstanz der Saugetiere
(The Development of the Dentin Matrix in Mammals), Arch. f. mikr. Anat.
67: 1 1905.
 
23. LeFevre, ’1\I. L., and Hodge, H. 0.: Chemical Analysis of Tooth Samples, J.
Dent. Research 16: 279, 1937.
 
24. Lehner, J., and Plenk, H.: Die Ziihne (The Teeth), Moel1endorif’s Handb. der
Mikrosk. Anat., vol. 5, pt. 3, p. 449, 1937.
 
25. Manley, E. G.: Traumatic Effect of the Drill During Cavity Preparation Brit.
D. J. 70: 329, 1941.
 
26. Muntz, J. A., Dorfman, A., and Stephan, R. M.: In Vitro Studies on Steriliza-
tion of Carious Dentin J. A. D. A. 30: 1893, 1913.
 
27. Orban, B.: The Development of the Dentin, J. A. D. A. 16: 1547, 1929.
 
28. Schmidt, W. J.: The Elements of the Animal Body in Polarized Light, Bonn.
192-1., quoted by Kitchin, P. (3.: Beyond the Microscope, J. Dent. Research
17: 275, 1938.
 
28a. Scott, D. B., and Wycoif, R. NY. G.: Electron Microscopy of Human Enamel,
J. 1). Res. 29: 556, 1950.
 
29. Schour, I., and Hofiman, M. M.: The Rate of Apposition of Enamel and Dentin
in Man and Other Animals, J. Dent. Research 18: 161, 1939.
 
30. Schour, I., and Massler, M.: The Neonatal Line in Enamel and Dentin of the
Human Deciduous Teeth and Ifirst Permanent Molar, J. A. D. A. 23: 19-16,
1936.
 
31. Schour, I., and Massler, M.: The Growth Pattern of Human Teeth. II,
J. A. D. A. 27: 1918, 1940.
 
32. Schour, 1., and Poncher, H. G.: The Rate of Apposition of Human Enamel and
Dentin as Measured by the Efiects of Acute Fluorosis, Am. J. Dis. Child.
54: 757, 1937.
 
33. Sicher, H..- The Biology of Dentin, Bur 46: 121, 1946.
 
34. Thomas, B. O. A.: Protective Metamorphosis of the Dentin: Its Relationship
to Pain, J. A. D. A. 31: 459, 1944.
 
35. Van Huysen, G-., and Gurley, W. B.: Histologic Changes in the Teeth of Dogs
Following Preparation of Cavities at Various Depths, J. A. I). A. 26: S7,
1939.
 
36. Van Huysen, G., Hodge, H. C., Warren, S. L., and Bishop, F. W.: Quantitative
Roentgen-Ray Study of Certain Pathological Changes in Dentin, Dental
Cosmos 75: 729, 1933.
 
37. Van Huysen, Gr., Bale, W. F., and Hodge, H. C.: Comparative Study of the
Roentgen-Ray Absorption Properties of Normal and Pathological Dentin,
Dental (‘osmos 77: 14-6, 1935.
 
38. Wasserman, F.: The Innervation of Teeth, J. A. D. A. 26: 1097, 1939.
 
39. Weidenreieh, F.: Ueber den Ban und die Entwicklung des Zahnbeines in der
Reihe der Wirbeltiere (Structure and Development of the Dentin of the
Vertebrates), Ztschr. f. Anat. u. Entwcklngsgesch. 76: 218, 1925.
 
40. Zander, H. A., and Burrill, D.: Penetration of Silver Nitrate Solution Into
Dentin, J. Dent. Research 22: S5, 1943.
ormative
utritive
 
isensory
 
CHAPTER V
PULP
 
I. FUNCTION
Formative
Nutritive
Sensory
Defensive
 
II. ANATOMY
 
Pulp Chamber
Root canal
Apical Poramen
 
HI. DEVELOPMENT
 
IV. STRUCTURAL ELEMENTS
 
Fibroblasts and Fibers
Odontoblasts
Defense Cells
 
3.. Histiocytes
b. Undifferentiated Mesenchymal cells
c. Lymphocytes
Blood Vessels
 
Lymph Vessels
Nerves
 
V. REGBESSIVE CEANGES
 
Pulp Stones
Galcifications
Secondary Dentin
Fibrosis
 
VI. GLDTICAI. CONSIDERATIONS
 
I. FUNCTION
 
The dental pulp is of mesenchymal origin and contains most of the
cellular and fibrous elements which are present in connective tissue. The
primary function of the dental pulp is the production of dentin. This
function is discussed in the chapter on Dentin. The pulp furnishes nour-
ishment through the odontoblastie processes to the dentin. Nutritional
elements are contained in the tissue fluid. The pulp also contains nerves.
Some of these nerves give sensation to the tooth structures, others serve to
regulate the blood supply of the pulp itself by ending on the muscular ele—
 
ments of the vessels.
 
First draft submitted by Balint Orban.
127
Defensive
 
128 (um. HISTOLOGY AND EMBRYOLOGY
 
The pulp is well protected against external irritations as long as it is
surrounded by an intact wall of dentin. It can evolve a very effective
reaction if exposed to irritation whether it is of mechanical, thermal,
chemical or bacterial nature. The defenive reaction may be expressed
in the formation of irregular dentin (see chapter on Dentin) if the ir-
ritation is mild, or as an inflammatory reaction in cases of more severe
irritation. While the rigid dentinal wall has to be considered as a protec-
tion to the pulp it also endangers its existence under certain conditions.
During inflammation of the pulp the hyperemia and the exudate cause
increasing pressure which, by occlusion of the blood vessels, may lead
to necrosis—self-strangulation of the pulp.
 
H. ANATOMY
 
The dental pulp occupies the pulp cavity which consists of the coronal
pulp chamber and the root canals. The pulp is continuous with the
periapical tissues through the apical foramen or foramina. Roughly the
 
--:-qr’; v-,"'* "—— -
~.ws¢§§
 
 
Fig. 97.—Age changes in the pulp chamber or the first permanent molar. Decalcifled
sections; enamel lost.
 
4. Age 8 years.
B.Ase55 years.
 
Reduction of the pulp chamber in height is greater than in mesiodlsfal diameter.
Pulp stones narrowing the entrance into the root canals in B. (Kronteld, R34)
 
shape of the pulp chamber follows, in young individuals, the outline of
the tooth. The extensions into the cusps of the tooth are called pulpal
horns. At the time of eruption the pulp chamber is large, but becomes
smaller with advancing age, due to continuous deposition of dentin“
(Fig. 97). The decrease in the size of the pulp cavity in molars does not
occur at the same rate throughout the pulp chamber. Formation of dentin
PULP 129
 
progresses fastest on the floor‘ of the pulp chamber; some is formed at the
occlusal wall and, lem still, on the side walls of the pulp chamber so that the
pulp dimension is reduced in an occlusal direction. The chamber may
 
be further narrowed and its shape may become irregular by formation of
irregular dentin. The formation of pulp stones (Fig. 97, B) may also
 
reduce the size and change the shape of the formerly Wide pulp cavity,
occasionally even occluding it.
 
=_ ' ‘,“""’”'.j
 
 
Pulp
 
lEpithella.l
iiaphragm
 
Apical
foramen
 
 
Fig. 98.—Deve1opment of the apical toramen.
A. Undeveloped root end; wide apical foramen, partly limited by epithelial diaphragm
 
B. Apical foramen fully formed. Root canal straight; apical roramen surrounded by
cementum (Coolidge, E. D.’)
 
Advancing age induces similar changes in the root canals. During Root canal
root formation the apical foramen is a wide opening, limited by the
epithelial diaphragm (Fig. 98, A), the continuation of Hertwig’s root
sheath at the root end. The dentinal walls taper and the shape of the pulp
 
canal is like a wide, open tube. As growth proceeds more dentin is formed
so that, when the root of the tooth has matured, the root canal is consider-
ably narrower. In the course of root formation Hertwig’s epithelial root
sheath breaks up into epithelial rests, and cementum is laid down on the
root surface (Fig. 98, B). This cementum will influence the size and shape
of the apical foramen in the fully formed tooth. Root canals are not
 
‘The floor oi.’ the pulp chamber is the wall opposite the occlusal wall (root) regard-
less of the position of the tooth in the Jaws.
130 ORAL HISTOLOGY AND EMBRYOLOGY
 
Fig. 99.-Drawings of teeth a.1.'t_er filling or the _root canals with India. ink and clear-
_ing. (After Okumura. 1“ and Apr1le.1) A. Upper incisors. B. Upper cuspids. C‘. Lower
mcisors. D. Lower cuspids.
F. Upper molars. G. Lower premolars.
molars.
 
Fig. 99 Contd.—E. Upper premolars.
 
H. Lower
 
.3
 
PULP
 
131
132 ORAL HISTOLOGY AND nmmzvonocv
 
always straight and single but vary by the occurrence of accessory canals,
as seen in corrosion specimens“ or after filling of the root canals with
india ink and clearing (Fig. 99).
 
At any distance from the apex of the tooth (Fig. 100, A) side branches of
the root canal may be present. In multi-rooted teeth these are observed
even at, or close to, the floor of the pulp chamber (Fig. 100, B and C). A
possible explanation for the development of all side branches of the pulp
canals may be a defect in HertWig’s epithelial root sheath during develop-
ment of the root at the site of a larger supernumerary blood vessel.
 
 
 
‘ p  Accessory
 
canal
 
Fig. 100.—Accessory canals in microscopic sections.
A. Close to the apex.
B. Close to the bifurcation.
 
Apical There are variations in shape, size, and location of the apical foramen.’
Poramen A regular, straight apical opening is rare (Fig. 98, B); occasionally, the
cementum can be traced from the outer surface of the dentin into the
pulpal canal. Sometimes, the apical opening is found on the lateral side
of the apex (Fig. 101, B) although the root itself is not curved. Frequently,
there are two or more distinct apical foramina, separated by a band of
 
dentin and cementum, or cementum only.
The location and shape of the apical foramen may also undergo changes,-
due to functional influences upon the teeth.“ A tooth maybe tipped, due
Flg. 1000.—Roentgenogram or lower molar with accessory canal filled.
(H. B. J'ohnston.")
 
Fig. 101.—Varlatlons of the apical to:-amen.
 
A. sum ot the apical roramen by resorption of dentin and cementum on one surface
md apposition of cementum on the other.
 
8. Apical fornmen on the side of the apex (Coolidge. E. D’).
 
Apex
134 ORAL HISTOLOGY AND EMBRYOLOGY
 
to horizontal pressure, or may migrate mesially causing the apex to
deviate in the opposite direction. Under these conditions the tissues
entering the pulp through the apical foramen exert pressure on one
wall of the foramen, causing resorption. At the same time cementum
 
is laid down on the opposite side of the apical root canal, resulting in a
change in the relative position of the original opening (Fig. 101, A).
 
III. DEVELOPMENT
 
The development of the dental pulp begins at a very early stage of
embryonic life, about the fifty-fifth day, in the region of the incisors;
later in the other teeth. The first indication is a proliferation and con-
densation of mesenchymal elements, lmown as the dental papilla, at the
 
Oral epithelium
 
Epithelial enamel
organ
 
Basement membrane
 
 
 
._ Dental papilla
 
i Mandi bular bone
 
Fig. 102.——Development at the pulp. Dental papilla or an embryo two and one-halt
months old. The papilla contains a. rich network of tine argyrophil fibers. Basement
 
membrane between mesenchyrne and epithelium. Silver impregnation.’ (Courtesy Dr.
P. Gruenwald.) ‘ ' w A ' ‘
PULP 135
 
basal end of the enamel organ (Fig. 102). Due to the rapid development of
the epithelial elements of the tooth germ into a bell-shaped enamel organ.
the future pulp is well defined in its outline. In a silver-impregnated
section the arrangement of the fibers in‘ the embryonic dental papilla,
is clearly visible (Fig. 102). ' In the future pulp area the fibers are fine
and irregularly grouped, and much denser than in the surrounding tissue.
At the boundary toward the epithelium a basement membrane is formed,
and the fibers of the dental papilla radiate into it.
 
The fibers in the embryonic pulp are pre-collagenous, i.e., reticular or
argyrophil. There are no collagenous fibers in the embryonic pulp, ex
cept where the fibers follow the course of the blood vessels." °~ ”' As the
development of the tooth germ progresses the pulp becomes increasingly
vascular, and the cells develop into star-shaped connective tissue cells
(fibroblasts) (Fig. 103, A). The cells are more numerous in the periphery
of the pulp. Between the epithelium and the pulp cells is a cell-free layer.
This contains numerous fibers, forming the basement or limiting mem-
brane (see chapter on Development of Dentin);
 
IV. STRUCTURAL ELEMENTS
 
The pulp is a specialized loose connective tissue. It consists of cells
(fibroblasts) and the intercellular substance. The latter, in turn, con-
sists of fibers and a cementing substance. In addition, defense cells and
the cells of the dentin, the odontoblasts, are part of the dental pulp. The
fibroblasts of the pulp and the defense cells are identical to those found
elsewhere in the body. The fibers of the pulp are in part collagenous,
in part precollagenous. Elastic fibers are absent. The cementing sub-
stance of the pulp seems to be of a much higher consistency than that in
the loose connective tissue outside of the pulp.
 
‘In the course of development the relative number of cellular elements
in the dental pulp decreases, whereas the intercellular substance increases
(Fig. 103, B). With advancing age there is a progressive reduction in the
number of fibroblasts, accompanied by an increase in the number of fibers
(Fig. 103, C’). In the embryonic and immature pulp, the cellular elements
are predominant, in the mature tooth the fibrous constituents. In a
fully developed tooth the cellular elements decrease in number toward the
apical region and the fibrous elements become more numerous (Fig. 106).
 
A microscopic specimen of a mature pulp, stained with hematoxylin eosin,
does not present a complete picture of the structure of the pulp, because not
all the fibrous elements are stained by means of this method (Fig. 104, A).
A great abundance of fibers are revealed by silver impregnation (Fig.
104, B), especially, the so-called Korfl:"s fibers between the odontoblasts.
These fibers are the primary elements in forming dentin ground substance
(see chapter on Dentin).
 
Argyrophil
Fibers
B. Nine months old.
0. Adult.
 
. Newborn in1a.nt_
 
6'.
Fig. 103.—Age changes of the dental pulp. Cellu
cellular substance increases with advancing age.
 
 
 
 
epithelium
Blood vesel
P Blood vessel
‘  Blood vessel
lax elements decrease, fibrous inter-
 
136
 
ORAL HISTOLOGY AND EMBRYOLOGY
PULP 137
 
The Korff’s fibers originate from among the pulp cells as thin fibers,
thickening at the periphery of the pulp, to form relatively thick bundles
which pass between the odontoblasts. They are pre-collagenous, staining
black with silver; hence the term argyrophil fibers. The remaining part
of the pulp contains a dense irregular network of collagenous fibers.
 
 
Dentin-—
Odontobiasts —
A.
. .
n, H is
Q!" U
3: L 3:" 9:
' - s. .e' _ l "N
r:  15‘ H .
Dentin ~  V/3; . ‘ c ,_ _ _,_ _ , capillary
 
Collagenous fibers
 
Arzyrophu fibers =--‘ “
or Kori!
 
B.
 
Fig. 104.-Cellular and fibrous elements in the pulp.
.4. Cellular elements stained with hematoxylin and eosin.
 
gi Fibrous elements stained by silver impregnation. Specimms are from the same
too .
 
The most significant change in the dental pulp during development Odonfioblagtg
is that the connective tissue cells adjacent to the enamel epithelium diifer-
entiate into odontoblasts. Dentin development sets in approximately in
the fifth embryonic month and, shortly before this, the odontoblasts begin
to differentiate. The development of odontoblasts starts at the highest point
in the pulpal horn and progresses apically. T
 
Odontoblasts are highly differentiated connective tissue cells, columnar
in shape, with an oval nucleus (Fig. 105). From each cell a cytoplasmic
OR.-\L HISTOLOGY AND EMBRYOLOGY
 
process extends into a tubule in the dentin matrix. These processes are
known as Tomes’, or dentinal, fibers. The ends of the odontoblasts, ad-
jacent to the dentin, are separated from each other by intercellular eon-
densations, the so-called terminal bars. In a section the terminal bars ap-
pear as fine dots or lines. The odontoblasts are connected with each other
and with the adjacent cells of the pulp by intercellular bridges. Some
odontoblasts are long, others short, the nuclei being irregularly placed.
 
 
Odon toblasls
 
Predentin __.
 
Dentin
 
Odontoblastic ___ _
process
 
, Pulp
 
/,:\,
 
Terminal bars ___
 
Odontoblastic __ , .
process
 
Odontoblasts
 
at
 
;i.~J.: .
 
Fig. 105.——Odontobla.sts.
 
The form and arrangement of the odontoblasts are not uniform through-
out the pulp. They are more cylindrical and longer in the crown (Fig.
106, A), and become cuboid in the middle of the root (Fig. 106, B). Close
 
to the apex of an adult tooth the odontoblasts are flat and spindle-shaped,
 
and can be recognized as odontoblasts only by their processes entering
 
the dentin as odontoblastic processes. In areas close to the apical foramen
PULP
 
 
 
Odontoblaata
 
Dentin —
 
Odontob last!
 
.’
If ?
c-. g
 
Fig. 106.—Varia.tlon o! odontablasts in different regions of one tooth.
A. High columnar odontoblasts in the pulp chamber.
 
3. Low columnar odontoblasts in the root canal.
 
0. Flu odontoblasns in the apical region.
 
139
Defense
cells
 
140 om. HISTOLOGY AND EMBRYOLOGY
 
the dentin is irregular (Fig. 106, C). This change in the shape of odonto-
blasts, toward the apical foramen, may be caused by mechanical factors,
e.g., movement of the apex when the tooth is in function, or by changes
in the blood and lymph stream producing varying pressure at the narrow
apical portion of the root} canal.
 
The odontoblasts are associated with the formation of the dentin matrix
(see Chapter on Dentin) -and mediate its nutrition. Histogenetically and
biologically they have to be regarded as cells of the dentin. Whether they
play a part in the sensitivity of the dentin is still debatable.
 
 
".2s<
 
wig‘,
 
' * "“‘ “ ' ‘ "  Cell-rich zone
 
Odontoblasts
 
Predentin
 
Dentin —-—» - .g  ,
 
 
Flg. 10'I.—Ce11-tree subodontoblastic zone of Well.
 
In the crown of the pulp a cell-free layer can be found, just inside the
layer of odontoblasts (Fig. 107). This layer is known as the zone of
Weil or subodontoblastic layer and it contains nerve fibers. Most un-
myelinated nerve fibers are a continuation of the myelinated fibers of the
deeper layers and continue to their terminal arborization in the odonto-
blastic layer. The zone of Weil can be found but rarely in young teeth.
 
In addition to fibroblasts and odontoblasts there are other cellular ele-
ments in the human pulp, usually associated with small blood vessels and
PULP 141
 
Undiflerentlated --
 
 
 
mesenchymal
Capillary
B.
Endothelial cell
Capillary _ .  ~- _"f"3.Und1flerent1atad
ifilsmcbrmu
""'57-I-Iiatiocyte
ii
“  Hf" """“J;T  ‘“'*
0. . qi
Lymphoid wan- —» ~-vi‘
dering cell A
M
‘*1?
Fibroblast
Undifrerentiated — °‘“’m”’
mesenchymal
cell ,
" '7 ' "‘Histiocyte
 
Fix. 108.-Defense cells in the Pulp.
Blood
Vessels
 
142 ORAL msronocr AND EMBRYOLOGY
 
capillaries. They are important for the defense activity of the tissues,
especially in inflammatory reaction.” Several types of cells belong to
this group; they are classified partly as blood elements and partly as
belonging to the reticuloendothelial system. In the normal pulp these
 
cells are in a resting state.
 
One group of these cells is that of the histiocytes or adventitial cells
or, according to Maximow’s nomenclaturefil» 1“ the resting wandering
cells. These cells are, generally, located along the capillaries. Their
cytoplasm has a notched, irregular, branching appearance; the nuclei
are dark and oval. They may have diverse forms in the human pulp but,
usually, can be easily recognized (Fig. 108). Intravital staining methods
have revealed that histiocytes are able to store dyes. It is assumed that
they produce antibodies and, consequently, have an important relation to
immune reactions. During an inflammatory process the histiocytes with-
draw their cytoplasmic branches, assume rounded shape, migrate to the
site of inflammation, and develop into macrophages.
 
Another cell type of the reticulo-endothelial system is described by
Maximow as undifferentiated mesenchymal cells (Fig. 108). These are
also associated with capillaries, have oval elongated nuclei similar to
those of fibroblasts or endothelial cells, and long, faintly visible cyto-
plasmic bodies. They are in close proximity to the vessel wall. These cells
can be differentiated from endothelial cells only by their location outside
the vessel wall. According to Maximow, they possess multipotency which
means that, under the proper stimulus, they can develop into any type
of connective tissue element. In an inflammatory reaction they form
macrophages.
 
A third type of cell which cannot be classified as belonging strictly
to the reticulo-endothelial system, but which plays an important part in
defense reactions, is the ameboid wandering cell, or lymphoid wandering
cell (Fig. 108, 0). These cells are migrating elements which probably
originate in the blood stream. Their cytoplasm is sparse and shows
fine extensions, pseudopodia, suggesting a migratory character. The
dark nucleus fills almost the entire cell and is often kidney-shaped. In
chronic inflammatory reactions they migrate to the site of injury and,
according to Maximow, change into macrophages. They may develop
into plasma cells which are a cell type characteristic of chronic inflamma-
tion. However, their function is not as yet fully known.
 
The blood supply of the pulp is abundant. The blood vessels of the
dental pulp enter through the apical foramen. Usually, one artery and
one or two veins enter each foramen. The artery, carrying the blood
into the pulp, branches out into a rich network of blood vessels, soon
after entering the root canal. The veins gather blood from this capillary
network and carry it back through the apical foramen into larger ves-
sels (Fig. 109). The arteries are clearly identified by their straight
1=~u1,p 143
 
course and thicker walls, whereas the thin-walled veins are wider and,
frequently, have an outline similar to a row of beads. The capillaries
form loops close to the odontoblasts, near the surface of the pulp, and
may even reach into the odontoblast layer.
 
Vein _.. ’.
 
Artery _ _T_f_,___.
 
   
 
,itA__.--__
 
Fig. 109.-—-Blood vessels or the pulp.
A. La.rger vessels in the center of the pulp.
 
B. Dense 111 tw rk in the periphery or the pulp. Arteries narrow, with thick
walls and ev3pou?:l11'1y1eI:evel2:s wide with thin walls and irregular outline.
 
The larger vessels in the pulp, especially the arteries, have a typical
circular muscular coating (Fig. 110). These muscular elements can be
traced to the finer branches. Along the capillaries are found branching
Lymph
Vessels
 
144 ORAL HISTOLOGY AND EMBRYOLOGY
 
cells, the pericytes (R0uget’s cells). It has been claimed that they are
modified muscular eleinents.“
 
Occasionally, it is difiicult to differentiate between pericytes and un-
differentiated mesenehymal cells. However, some specimens show both
types of cells and, thereby, it is possible to identify them (Fig. 11111).
The nuclei of the pericytes can be distinguished as round or slightly oval
bodies outside the endothelial wall of the capillary. A very thin cyto-
plasm can be seen between the nuclei and the outside of the endothelium.
 
,
E .,
.
 
Circular muscle
coating
 
Circular muscle
coating '
 
 
 
 
1
‘ ' I-Iistlocyte
 
Fig. 110.—Branching artery in the pulp; circular muscle coating.
 
The endothelial cells can be recognized in the continuation of the vessel
wall. The undiflerentiated mesenchymal cells lie outside the pericytes,
and have finger-like projections. If no pericytes are present the undif-
ferentiated mesenchymal cells are in close proximity to the endothelial
wall (Fig. 108).
 
It has been repeatedly stated that lymph vessels are present in the
dental pulp. Special methods are required to render them visible; the
PULP 145
 
common histological technique does not reveal them. The presence of
 
lymph vessels has been demonstrated by the application of dyes into the
 
pulp1°’ 21' 22 which are carried into the regional lymph nodes. Injection
methods have also been tried successfully.” 2’
 
' The nerve supply of the dental pulp is abundant. Thick nerve bundles mm.
enter the apical foramen and pass into the crown portion of the pulp
 
where they split into numerous fiber groups and, ultimately, into single
 
fibers and branches (Fig. 112). Usually, the nerve bundles follow the
 
blood vessels into the root canal; the finer branches can be seen following
 
the smaller vessels and capillaries.
 
 
 
Undlflerentlated
mesenchymal
cell
 
,..,..;...
 
pay A...
 
Undifferentiated
» mtlalsenchymal
 
Fig. 111.—Perlcyte.s of capillaries in the pulp. Note the differences in location and
nuclear shape between endothellal cells, pez-Icytes and undifferentiated mesenchymal
 
Most nerve elements which enter the pulp are of the myelinated type;
but, there are also unmyelinated elements. These unmyelinated nerve
fibers are of the sympathetic nervous system and are the nerves of the
blood vessels, regulating their contraction and dilation.
 
The bundles of myelinated fibers follow closely the arteries, dividing
coronally into-smaller and smaller branches. Individual fibers form a
146 ORAL HISTOLOGY AND EMBRYOLOGY
 
layer beneath the subodontoblastic zone of Wei], the parietal layer.
From there the individual fibers pass through the subotlontoblastic zone
and, losing their myelin sheath, begin to branch. Their te1'1ni11al ar-
borization occurs in the odontoblastic layer (See chapter on Dentin).
 
 
   
 
Histlocyte .- -
 
.4 far-Af ‘ ‘
 
Blood vessel v._
 
Fig. 112.—Nerves in the pulp.
 
It is a peculiar feature that, whatever stimulus reaches the pulp, it
will always elicit only pain sensation. There is no possibility in the pulp
to differentiate between heat, cold, touch, pressure, chemicals, and so
forth; the result is always pain. The cause of this behavior is the fact
PULP 147
 
that only one type of nerve endings, free nerve endings, are found in
the P111P- The free nerve endings are specific for the reception of pain.
The nerves do not have the faculty of localizing the stimulus.
 
_.ié____ _
2
 
'4
 
_~/‘ *
 
     
 
*1
 
 
”=:“""* ‘ "" ‘  True denticle
 
False denticle
 
False dentlcle
 
‘ Difluse
calciflcations
 
"** Dentln
 
Fig. 113.—Denticles (pulp stones).
A. True denticle.
 
B. False denticle.
 
0. Diflluse calciflcations.
Pulp stones
 
148 omu. HISTOLOGY AND EMBRYOLOGY
 
V. REGRESSIVE CHANGES
 
Certain formations in the dental pulp, such as pulp stones or denticles,
are on the borderline of pathologic conditions. Their discussion in this
chapter is justified only by their frequent occurrence. Pulp stones are
often found in teeth which appear to be quite normal in all other re-
 
spects. They have been found not only in functioning teeth but also in
embedded teeth.
 
' '4
'¢.c-1-hp:-nu
=1 . E .
 
     
 
 
'5».
 
s
 
i ‘ Free dentlcle
 
Adherent dentlcle
 
 
’ Embedded dentlcle
 
Fig. 114.—Free, attached, and embedded denticles.
 
Pulp stones are classified, according to their structure, as true denticles,
false denticles, and diffuse calcifications (Fig. 113). True denticles
consist of dentin, showing traces of dentinal tubuli and odontoblasts
(Fig. 113, A). They are comparatively rare and are usually found
close to the apical foramen. A theory has been advanced“ that the
development of this type of pulp stones is caused by remnants of Hert-
wig’s epithelial root sheath, which become enclosed in the pulp, due to some
local disturbance during development. These epithelial remnants may in-
PULP 149
 
duce cells of the pulp to form true denticles. This explanation is based
upon frequent observation of true denticles, close to the apical foramen,
and also the frequent presence of epithelial rests in this region. It is an
accepted fact that epithelial cells (enamel epithelium) are necessary for
the differentiation of odontoblasts and the onset of dentin formation.‘
False clenticles are calcified formations in the pulp Which do not show
the structure of true dentin. They consist of concentric layers of calcified
 
Pulp stone ""' ' *‘ if
 
 
Nerve
 
1?‘ ”"‘ —’ Pulp stone
 
‘. ,Z'l:*'A‘§
 
Fig. 115p-Pulp stones in close proximity to a nerve.
 
tissue (Fig. 113, B). In the center of these concentric calcified structures
there are usually remnants of necrotic and calcified cells. Calcification of
thrombi in blood vessels (phlebolite) may also be the starting point for
false denticles. Once calcification has begun, more layers of calcified tissue
are laid down on the surface of the pulp stones, thereby increasing their
size continuously. The surrounding pulp tissue may be quite normal (Fig.
113, B); no pathologic changes can be detected in the cells or intercellular
Calcification:
 
Secondary
Dentin
 
fibrous
 
150 ORAL n1s'ro1.ocY AND nmnmronocr
 
fibrous matrix. Sometimes, pulp stones of this character fill the pulp cham-
ber almost completely. They increase in number and size with advancing
age. Overdoses of vitamin D may cause formation of numerous denticles.‘
 
Diffuse calcifications (Fig. 113, C‘) are irregular calcific deposits in the
pulp tissue, usually following collagenous fiber bundles or blood vessels.
Sometimes, they develop into large bodies; at other times they persist as
fine spicules. They are amorphous, having no specific structure, and are
usually the final outcome of a hyalin degeneration of the pulp tissue. The
pulp, in its coronal portion, may be quite normal without any sign of
inflammation or other pathologic changes. These diffuse calcifications
are, usually, located in the root canal, seldom in the pulp chamber; ad-
vancing age favors their development.
 
Pulp stones are classified, not only according to their structure, but
also according to their location in relation to the dentiual wall. Free,
attached, and embedded denticles can be distinguished (Fig. 114). The
free denticles are entirely surrounded by pulp tissue; attached denticles
are partly fused with the dentin; embedded denticles are entirely sur-
rounded by dentin. They are formed free in the pulp, and some become
attached or embedded as formation of the dentinal wall progresses.
 
Pulp stones are frequently found close to nerve bundles, as shown in
Fig. 115. Occasionally, this may bring about a disturbance if the pulp
stones come close enough to the nerves to exert pressure. This may entail
pain in the jaw in which the affected tooth is located, rendering a satisfac-
tory diagnosis difficult. The close proximity of pulp stones to blood vessels
may cause atrophy of the pulp if the growing pulp stones exert pressure
upon the vessels. It is improbable that the pulsation of the blood in
the arteries, close to pulp stones, causes suflicient movement of the stone
to irritate nerves and cause pain. Pulp calcifications are more common in
older teeth. Diffuse calcium deposits may be found in and around the
pulpal vessels especially in the roots of older teeth. Well-outlined cal-
cified bodies are more frequently found in the coronal portion of the pulp.
In twenty-nine teeth from individuals between ten and thirty years of age,
Hill" found pulp calcifications in 66 per cent; in sixty-two teeth from
individuals between thirty and fifty years of age, 80 to 82.5 per cent
showed calcification in the pulp, and in thirty-one teeth from individuals
over fifty years of age, 90 per cent had pulp calcification.
 
With advancing age the pulp chamber and the root canals become
narrower due to secondary dentin formation. In secondary dentin the
dentinal tubuli are sparse and irregular. This is due to the fact that
odontoblasts degenerate with advancing age, or are destroyed by some
 
irritation, whereas the matrix formation persists or even increases (see
chapter on Dentin).
 
It has been pointed out that, with advancing age, the cellular elements
decrease 111 number whereas the fibrous components increase in the pulp.
PULP 151
 
In older individuals this shift in tissue elements can be considerable and
fibrosis may thus develop in the pulp. Thereby, the vitality of the pulp
may be lowered without any consequence to the function of the teeth.
 
VI. CLINICAL CONSIDERATIONS
 
For all operative procedures it is important to bear in mind the shape
of the pulp chamber, and its extensions into the cusps, the pulpal horns.
The wide pulp chamber, in the tooth of a young person, will make a deep
cavity preparation hazardous to the pulp, and it should be avoided if
possible. In some rare instances the pulpal horns remain projected high
into the cusps and this may, in some cases, explain the exposure of a pulp
when it is least anticipated” (Fig. 116). Sometimes, a roentgenogram will
help to determine the size of a pulp chamber and the extensions of the
pulpal horns. Roentgenograms of anterior maxillary teeth often lack
detail concerning the exact location of pulp horns and the presence of
denticles. Information on this subject can be obtained by allowing the
rays to strike the crown at almost right angles and double the exposure.
Such a film will not only show greater detail concerning pulp horns and
pulp calcification, but also orient the position of the pulp chamber more
reliably.
 
If it becomes necessary to open a pulp chamber for treatment, its size
and variation in shape must be taken into consideration. With advanc-
ing age the pulp chamber becomes smaller and, due to excessive dentin
formation at the roof and floor of the chamber, it is sometimes difficult to
locate the root canals. In such cases, it is advisable, when opening the
pulp chamber, to advance toward the distal root in a lower molar and
toward the lingual in the upper molar; in this region, one is most likely
to find the opening of the pulp canal without risk of perforating the
floor of the pulp chamber. In the anterior teeth the extreme coronal
part of the pulp chamber may be filled with secondary dentin, making it
difficult to locate the root canal. Pulp stones lying at the opening of
the root canal may cause considerable difficulty when an attempt is made
to locate the canals (Fig. 97, B).
 
The shape of the apical foramen, and its location, may play an impor-
tant part in the treatment of root canals, especially as regards the root
canal filling. When the apical foramen is narrowed by cementum forma-
tion it is more readily located, because further progress of the broach
will be stopped at the foramen. If the apical opening is at the side of
the apex, as shown in Fig. 101, A, not even the roentgenograms will reveal
the true length of the root canal, and this may lead to misjudging the
length of the canal and the root canal filling.
 
The problem of accessory canals, in root canal work, plays an important
part in making the outcome of the root canal treatment questionable. Side
branches of the pulp are rarely seen in the roentgenograms and are usu-
152 oruu. HISTOLOGY AND EMBRYOLOGY
 
ally overlooked in the treatment and filling of the root canal. If these
accessory canals are infected they may cause a recurrence of inflammation.
 
There "is another condition in which accessory canals may play an im-
portant part, especially if they are located in the bifurcation, or high up
toward the crown (Fig. 100, B). In periodontal diseases, e.g., where pocket
formation progresses, accessory canals may be exposed and infection of
the pulp may follow. This may account for some causes of pulp necrosis
in periodontal diseases, not only in molars but also in single-rooted teeth.
 
 
 
Enamel (lost
in decals]-
flcatlon)
 
Fig. 116.-—Pulp horn reaching far into the cusp of a molar. (0rba,n.")
 
For a long time it was believed that an exposed pulp meant a lost pulp.
The fact that “defense cells’ ’ have been recognized in the pulp has changed
this contention.” Extensive experimental work has shown that exposed
pulps can be preserved if proper pulp capping or pulp amputation pro-
cedures are applied.“ 2° This is especially so in noninfected, accidentally
exposed pulps in young individuals. In many instances new dentin was
formed at the site of the exposure, forming a dentin barrier or bridge.
Thus, the pulp may remain in a healthy and vital condition. Pulp cap-
ping of deciduous teeth has been shown to be remarkably successful.
PULP 153
 
References
 
1. Aprile, E. C. de and Aprile, H.: Topografia de los conductos radiculares, Rev.
Odontologia 35: 686, 1947.
la. Becks, Hermann: Dangerous Eifects of Vitamin D Overdosage on Dental and
Paradental Structures, J. A. D. A. 29: 1947, 1942.
Bodecker, C. F.: The Soft Fiber of Tomes, J. Nat. Dent. A. 9: 281, 1922.
. Bodeglsrerbgg. 117‘S.),3and Applebaum, E.: Metabolism of the Dentin, Dental Cosmos
: 1.
Bodecker, C: F., and Lefkowitz, W.: Concerning the “Vitality” of the Cal-
cified Dental Tissues, J. Dent. Research 16: 463, 1937.
Boling, L. R.: Blood Sup ly of Dental Pulp, J. Dent. Research 20: 247, 1941.
Brunn, A. v.: Die Aus ehnung des Schmelzorganes und seine Bedeutung fiir
die Zahnbildung (The Extension of the Enamel Organ and Its Significance
in the Formation of Teeth), Anat. Anz. 1: 259, 1886.
Formation of Teeth, Anat. Anz. 1: 259, 1886.
7. Cooligge,‘  1151 Anatomy of Root Apex in Relation to Treatment Problems,
. . . . 6: 1456 1929.
8. Ebner, V. v.: Ueber die Entwicklung der leimgebenden Fibrillen im Zahnbein
lglgtse Development of Collagenous Fibrlls in Dentin), Anat. Anz. 29: 137,
9. Ebner, V: v.: Histologie der Ziihne (Histology of the Teeth, Schefi’s Handbook
of Dentistry), ed.' 4, Vienna, 1922, A. Hoelder.
10. Fish, E. W.: An Experimental Investigation of Enamel, Dentin and the Dental
Pulp, London, 1932, John Bale Sons & Danielsson, Ltd.
11. Hess, W., and Zurcher, E.: The Anatomy of the Root Canals, London, 1925,
John Bale Sons & Danielsson, Ltd.
12. Hill, T. J.: Pathology of the Dental Pulp, J. A. D. A. 21: 820, 1934.
13. Johnston, H. B., and Orban, B.: Interradicular Pathology as Related to Ac-
cessory Root Canals, J. Endodontia 3: 21, 1948.
14. Kronfggif  Igefitgl Histology and Comparative Dental Anatomy, Philadelphia,
1 ea e iger.
15. Lehner J., and Plenk H.: Die Ziihne (The Teeth) M6llendorfi’s Handb. der
Mikrosk. Anat. vol. 5, pt. 3, p. 449, 1936.
16. Magnus, G.: Ueber den Nachweis der Lymphgefiisse in der Zahn Pulpa
§D;n]11on:tr4:(1)t1o1:5 of Lymph Vessels in the Dental Pulp), Deutsche Monatschr.
. an. :611922.
17. Maximow, A. A.: Morphology of the Mesenchymal Reactions, Arch. Path. &:
Lab. Med. 4: 557, 1927.
18. Maximow, A. A., and Bloom, W.: Textbook of Histology, Philadelphia, W. B.
Saunders Co. ed. 4 1942.
19. Meyer, W.: Ist’ das ’Foramen Apicale stationiirl (Is the Apical Foramen
Stationary?) Deutsche Monatschr. f. Zahnh. 45: 1016, 1927.
20. Noyes, F. B., and Dewey, K.: Lymphatics of the Dental Region, J. A. M. A. 71:
1179 1918.
21. Noyes, F.’ B.: Review of the Work of Lymphatics of Dental Origin, J. A. D. A.
14: 714 1927.
22. Noyes, F. Bi, and Ladd, R. L.: The Lymphatics of the Dental Region, Dental
Cosmos 71: 1041 1929.
22a. Okumura, '11: Anat’om_v of the Root Canals, .T. A. D. A. 14: 632,1927.
23. Orban B.: Contribution to the Histolo of the Dental Pulp J. A. D. A. 16:
9%" 1929 gy ’
o, .
24. Orban, B.: Epithelial Rests in the Teeth, Proc. Am. Assn. of Dental Schools,
5th Annual Meeting Washington, D. C. 1929, p. 121.
25. Orban, B.: Biologic Cohsiderations in Restorative Dentistry, J. A. D. A. 28:
1069 194].
26. Restarski: J. S.: Preserving Vitality of Pulps Exposed by Caries in Young
Children Illinois Dent. J. 9: 2, 1940.
27. Schweizer, Gt: Die Lymphgefiisse des Zahnfleisches und der Ziihne (Lymph
Vessels of the Gingiva and Teeth), Arch f. mikr. Anat. 69: 807, 1907; 74:
927 1909.
28. Wasserniann, F.: The Innervation of Teeth, J. A. D. A. 26: 1097, 1939.
29. Zander, H. A.: Reaction of the Pulp to Calcium Hydroxide, J. Dent. Research
 
13: 373, 1939.
 
?’S"£“°°.N’
CHAPTER V1
CEMENTUM
 
1. DEFINITION
 
2. PHYSICAL CHARACTERISTICS
 
3. CHEMICAL COMPOSITION
 
4. CI‘-MIE‘-NTOGENESIS
 
5 MORPHOLOGY
 
6. CEMENTO-ENAMEL JUNCTION
7. CEMI'.NTO~DENTINAL JUNCTION
8. FUNCTION
 
9. EYPERCEMENTOSIS
 
10. CLINICAL CONSIDERATIONS
 
1. DEFINITION
 
Cementum is the hard dental tissue covering the anatomical roots of
the human teeth. It was first microscopically demonstrated in 1835 by
two pupils of Purkinje.5 It begins at the cervical portion of the tooth
at the cemento-enamel junction, and continues to the apex. Cementum
furnishes a medium for the attachment of the fibers that bind the tooth
 
to the surrounding structures. It can be defined as a specialized, calcified
tissue of mesodermal origin, a modified type of bone covering the anatomic
 
root of the teeth.
 
2. PHYSICAL CHARACTERISTICS
 
The hardness of adult or fully formed cementum is less than that of
dentin.“ 2‘ It is light yellowish and is easily distinguished from the
enamel by its darker hue; it is somewhat lighter in color than dentin.
By means of vital staining and other chemical-physical experiments the
cell containing cementum has been proved to be permeable.”
 
3. CHEMICAL COMPOSITION
 
Adult cementum consists of about 45 to 50 per cent inorganic sub-
stances and 50 to 55 per cent organic material and water (see table in chap-
ter on Enamel). The inorganic substances consist mainly of calcium
salts. The molecular structure is hydroxyl apatite which, basically, is the
same as that of enamel, dentin and bone. The chief constituent of the or-
ganic material is collagen.
 
4. CEMENTOGENESIS
 
The development of cementum is known as cementogenesis. During
enamel formation the crown of the tooth is covered by the enamel epi-
thelium. The basal part of the epithelium (inner and outer layers) is the
 
First draft submitted by Emmerich Kotanyi.
154
CEMENTUM 155
 
He1'twig‘s epithelial root sheath which is of particular importance in root
development; it forms the mold into which the root dentin is deposited.
Therefore, the newly formed dentin, in this region, is covered at first by
the epithelium, and is separated by it from the surrounding connective
tissue (Fig. 117). Cementum is formed by this connective tissue but it
 
I‘.
x
 
 
   
 
 
Epithelial sheath "
broken, sepa-
rated from root
 
\‘ 5
Epithelial sheath-,-.—‘ .
in contact with . .'- ‘-
dentin
 
- Epithelial
diaphragm
 
Fig. 117.—-Hertwig’s epithelial root sheath at end of forming root. At the side of the root
the sheath is broken up and cementum formation begins. (Gottliel).“)
 
cannot be deposited on the outer surface of the root dentin as long as
the epithelial sheath separates it from the dentin. A contact between
connective tissue and tooth is accomplished by invasion of connective
tissue through the epithelial layers. By this process the epithelial sheath
loses its continuity but persists as a network of epithelial strands which
Gementobluts
 
156 om. HISTOLOGY AND nnnaronocr
 
lie fairly close to the root surface. The remnants of the epithelial
sheath are known as “epithelial rests” of Malassez.“ (See chapter
on Periodontal Membrane.) When the separation of the epithelium from
the surface of the root dentin has been accomplished, the periodontal
connective tissue comes into contact with the root surface and cementum
is laid down.
 
‘x
 
Enamel epithelium; , it
 
 
 
 
- Enamel
 
— Cemento-enamel
junction
 
Remnants at epithelial
sheath
 
 
 
L’.
 
Fig. 118.—Epithelia.I sheath is broken and separated from root surface by connective
US$116.
 
In the first stage of cementum formation two tissue elements can be
observed; First, cells of the connective tissue (undiflferentiated meson-
chymal cells) are arranged along the outer surface of the dentin (Fig. 118).
These change into flat," cuboidal cells and are the cementoblasts. At the
same time the second tissue element, pre-collagenous (argyrophil) fibers,
 
can be seen at right angles to the root surface, and attached to the outer
surface of the dentin (Fig. 119). These fibers soon assume a collagenous
CEMENTUM 157
 
 
 
1% nu-
ma“
.9» ’
Argyrophil  H.‘
nbera  _ ,
59.; —— Dentin
"V
4’ ”" " Attach an
‘e . 111
.'$w$ :~_ of fibers
 
 
fibers
 
w‘
 
Fig. 119.—Argy1-ophil fibers of the periodontal membrane. attached to the dentin (silver
impregnation).
 
Couagenous _ __M__  ___,_..,,~:, , WW , _ '- Dentin
fibers
 
* Cementum
 
 
 
M _ _
 
Fir. 120.—-Cementum ground substance develops from fibers of the periodontal membrane
- (silver impregnation).
158 ORAL HISTOLOGY AND EMBRYOLOGY
 
character and become a. part of the ground substance of the cementum
(Fig. 120). This mechanism is similar to that observed in dentinogonesis
(see chapter on Dentin).
 
Definite knowledge of the function of the cementoblasts is incomplete,
but it is presumed that they play the same role in cementum formation
 
Dentln
'1.
Cementoblastsfr ' >-' ' :7 - ‘—:~=~-= ’ " " "*-
ex
——-V-n--—-~ W cementum
Periodontal ” ’ '—,-
membrane
,.__—_—————~— -r—— Cementold
' tissue
Cementoblast ' ‘  ’” "'-‘"“:““‘ ' "f"
 
Fig. 121.—Cementoid tissue on the surfaceflgf calcified cementum. Cementoblasts between
ers.
 
as the osteoblasts play in bone formation. In the first phase of develop-
ment the cementoblasts, apparently by enzymatic action, elaborate a
homogenous material, the cementoid tissue. In the second phase, calci-
fication takes place by the deposit of calcium salts in the cementing sub-
stance of the intercellular substance. Simultaneously the organic com-
ponent changes radically, becoming soluble by proteolytic enzymes.“
GEMENTUM 159
 
During the continuous apposition of cementum a thin layer of non- °¢m°“"°i°-
 
calcified matrix, termed cementoid tissue, which is analogous to osteoid
tissue and predentin, is seen on the surface of the cementum (Fig. 121).
This cementoid tissue is lined by cementoblasts. Connective tissue fibers
from the periodontal membrane pass between the cementoblasts into the
cementum. These fibers are embedded in the cementum and serve as an
attachment for the tooth to the surrounding bone. Their embedded por-
tions are known as Sharpey’s fibers. These were accurately described
in 18872 as an essential part of the suspensory apparatus.
 
-—» —— -1
 
 
 
 
3:355 25' 7
-f, if In '
.4‘  J»
gag‘!
 
at .
' ‘r 7 i
 
Periodontal
membrane
 
 
 
T-»"'"‘, .A.ceuu1a.r
3:?“ cementum
ax» .
 
 
Alveolar bone
 
Fig. 122.——Increment2.l lines in the accellular cementum.
 
5. MORPHOLOGY
 
From a morphologic standpoint two kinds of cementum can be differ-
entiated: (a) acellular, and (b) cellular cementum. Functionally, how-
ever there is no difference between the two.
Acellular
cementum
 
160 om. HISTOLOGY AND EMBRYOLOGY
 
Acellular cementum may cover the root dentin from the cemento-enamel
junction to the apex, but is often missing on the apical third of the root.
Here the cementum may be entirely of the cellular type. The aeellular
cementum is thinnest at the cemento-enamel junction (20 to 50 microns),
and thickest toward the apex (150 to 200 microns). The apical foramen
is surrounded by cementum. Sometimes the cementum extends to the
inner wall of the dentin for a short distance, forming a lining of the root
canal.
 
Both acellular and cellular cementum are separated by incremental
lines‘ into layers that indicate periodic formation (Fig. 122). Acellular
 
"  "— " ‘“. ‘
.3‘: ' j
 
_. Principal fibers of
periodontal
membrane
 
Dentin .
 
Cementum _
 
F1E- 123.——'1‘he principal fibers ot the periodontal membrane continue into the surface
layer of the cementum.
 
cementum consists of the calcified matrix and the embedded Sharpey’s
fibers. The matrix is composed of two elements: the collagenous fibrils
and the calcified cementing substance. The fibrils in the matrix are
perpendicular to the embedded Sharpey’s fibers and parallel to the
cementum surface. The fibrils are less numerous than in lamellated
bone and about as numerous as those of bundle bone. Due to identical
 
‘The term incremental lines was introduced by Salter in 1874 as including the stripes
 
of Remus In the enamel, the contour lines at Owen in the dentin and the stratification
In the cementum.
U1‘JJ.V.l.EJN'l'UL1 .10.].
 
optical qualities, i.e., the same refractive index, the fibrils and inter-
fibrillar cementing substance can be made visible only by special stain-
ing methods. Fibrils and Sharpey’s fibers are easily distinguished by
means of silver impregnation. In dried ground sections Sha.rpey’s fibers
are disintegrated and the spaces and channels which they formerly oc-
cupied are filled with air; the areas thereby become discernible as dark
lines.
 
   
 
  ‘ 'r.-,z Dentin
. ‘
 
Periodontal ‘
 
“L I Acellular
membrane —
 
cementum
 
Cementoid
 
tissue ’——«g Cellular
 
1 cementum
 
 
F--“fl Acellular
cementum
.e
 
Alveolar bone A
 
Fig. 124.——Cellula.r cementum on the surface or acellular cementum, and again cov-
 
ercd by acellular cementum (incremental lines). The _la.cunae _of the cellular cementum
are empty, indicating that this part of the cementum is necrotic.
 
While the cementum remains relatively thin, Sharpey’s fibers can be
observed crossing the entire thickness of the cementum. With further
apposition of cementum a larger part of the fibers is incorporated in the
cementum. At the same time, the portion of the fibers lying in the deeper
layers of the cementum becomes obscure. The attachment proper is
probably confined to the most superficial or recently formed layers of
162 ORAL HISTOLOGY AND EMBRYOLOGY
 
Periodontal Dentin
membrane ‘ ‘
Cementoid __ __ _____
 
tissue _— —  cellular
 
cementum
 
 
Fig. 125.—Cel1u1'ar cementum forming the entire thickness of cementum. (Orban.W)
 
F_?  - -—-—-——-v---—-———-—J..-g‘
:
 
     
 
Dentin
 
 
Apex formed » ~.—_.—— I-~~———~————
by cemen-.
tum
 
2‘-T ‘
 
373- 136-——Cementum tyiickest at apex contributing to the length or the root,
cnmrmrun 163
 
cementum (Fig. 123). This would seem to indicate that the thickness
of the cementum does not enhance functional efficiency by increasing the
strength of attachment of the individual fibers. Continuous apposition
of cementum is essential for the continuous eruptive movements of the
functioning tooth and the continuous reorganization of the periodontal
membrane which is necessitated by these movements. The surface of the
cementum is vital Whereas the inner layers become necrotic as recognized
by empty lacuni in the cellular cementum (Fig. 124) .
 
The location of acellular and cellular cementum is not definite. Layers
of acellular and cellular cementum may alternate in almost any arrange-
ment. The acellular cementum, which is normally laid down on the sur-
face of the dentin, may occasionally be found on the surface of cellular
cementum (Fig. 124). Cellular cementum is usually formed on the sur-
 
 
Fig. 127.—Cementum lacuna and canaliculi filled with air (ground section).
 
face of acellular cementum (Fig. 124), but it may comprise the entire
thickness of the apical cementum (Fig. 125). It is always thickest around
the apex and, in this manner, contributes to the lengthening of the root
(Fig. 126).
 
The cells in cellular cementum (cementocytes) are similar to osteocytes.
They lie in spaces designated as lacunae. Frequently, the cell body has
the shape of a plum stone, with numerous long processes radiating from the
cell body. These processes may branch, and frequently anastomose
with those of a neighboring cell. Most of the processes are directed
toward the periodontal suflface of the cementum, differing in this respect
from the evenly distributed processes of the bone cells.
 
Cellular
cementum
164 ORAL HISTOLOGY AND EMBRYOLOGY
 
Some canaliculi, containing processes of the cementocytes, have been
said to anastomose with peripheral branches of the dentinal tubulifi» 9"
The cells are irregularly distributed throughout the thickness of the
cellular cementum. The cavities can be best observed, however, in
ground sections of dried teeth, where they appear as dark spider-like
figures (Fig. 127). The dark appearance is due to the fact that the
spaces are filled with air; these spaces also can easily be filled with dyes.
 
Enamel I Enamel
 
 
 
 
Enamel ,_,___._-_.__, , ‘ Enamel
epithelium  epithelium
. ff‘ ‘EC:
, Z t .,l u
"’ I  - ‘- ‘ ‘="'::—:-—- cementum over-
_ . _ lapping enamel
Cemento-enamel «— . ' 7 ~ ‘ .i
junction ‘
Cementum—— --
 
 
A. B.
 
Fig. 128.-—Cemento—enamel junction.
A. cementum and enamel meet in a. sharp line.
B. cementum overlaps enamel.
 
6. CEMENTO-ENAMEL JUNCTION
 
The relation between cementum and enamel at the cervical region of
the teeth is variable.“ In about 30 per cent of the examined teeth the ce-
mentum meets the cervical end of the enamel in a sharp line (Fig. 128, A).
Here, the cementum, as Well as the enamel, tapers into a knife-edge. In
other teeth, about 60 per cent, the cementum overlaps the cervical end
of the enamel for a short distance (Fig. 128, B). Developmentally, this
CEMENTUM 165
 
may occur only when the enamel epithelium, which normally covers the
entire enamel, degenerates in its cervical end, permitting the connective
tissue, which is responsible for the deposition of cementum, to come in con-
tact With the enamel surface.
 
Enamel
 
 
     
 
i . Enamel
 
epithelium
End of —
enamel
Enamel
epithelium
Q7‘ Cemente-
enamel
- junction
‘ ‘;
Cementum
epithelium
Cementum
 
Fig. 129.—Variations at the cemento-enamel junction.
4. Enamel epithelium attached to dentin surface preventing cementum formation.
 
1 BhEnamel epithelium breaking continuity of cementum near the cemento-enamel
unc on.
 
In about 10 per cent of all teeth various aberrations of the cemente-
enamel junction may be observed. Occasionally, the enamel epithelium
which covers the cervical part of the root does not separate from the
dentin surface at the proper time.‘ In other words, it remains attached
to the dentin of the root for variable distances (Fig. 129, A), and prevents
the formation of cementum. In such cases there is no cemento-enamel
junction, but a zone of root dentin is devoid of cementum and covered by
166 ORAL HISTOLOGY AND EMBRYOLOGY
 
enamel epithelium. In other instances cementum is formed at the ce-
mento-enamel junction for a short distance only and, following it apically,
Her-twig’s epithelial root sheath remains in contact with the dentin in a
limited area (Fig. 129, B). Enamel spurs, pearls or drops 1nay be formed
 
by such epithelium.“
 
7. CEMEN TO—DENTIN AL J UN GTION
 
The surface of the dentin upon which the cementum is deposited is
normally smooth in permanent teeth. The eemento-dentinal junction,
 
- Dentin
 
Periodontal membrane ,_ 7
 
Intermediate cementum
layer
 
-I--—» -- - Acellular
cementum
 
Fig. 130.—Intermediate layer of cementum.
 
in deciduous teeth, however, is sometimes scalloped. The attachment of
 
the cementum to the dentin, in either case, is quite firm although the
nature of this attachment has not been fully investigated.
 
Sometimes the dentin is separated from the cementum by an inter-
mediate layer, known as the intermediate cementum layer, which does
not exhibit the characteristic features of either dentin or cementum (Fig.
130). This layer contains large and irregular cells which can be regarded
CEMENTUM 167
 
as embedded connective tissue cells. The development of this layer may
be due to localized, premature disintegration of 1'-lertwig ’s epithelial sheath
after its cells have induced the diflerentiation of odontoblasts, but before
the production of dentinal intercellular substance. It is found mostly
in the apical two-thirds of the root. Sometimes it is a continuous layer;
sometimes it is found only in isolated areas.“
 
8. FUNCTION
 
The functions of cementum are, first, to anchor the tooth to the bony
socket by attachment of fibers; second, to compensate by its growth for
loss of tooth substance due to occlusal wear; third, to enable, by its con-
tinuous growth, the continuous vertical eruption and mesial drift of the
teeth; and fourth, to make possible the continuous rearrangement of the
principal fibers of the periodontal membrane.
 
The attachment of the fibers of the periodontal connective tissue to the
surface of the tooth is the medium by which functional connection be-
tween tooth and surrounding tissues is established. Due to physiological
movements of the functioning tooth, fibers have to be replaced con-
tinually. I11 order to maintain a functional relationship new cementum
has to be deposited continuously on the surface of the old cementum.‘
By this continued formation of cementum new fibers of the periodontal
membrane are attached to the surface of the root, and loosened or degen-
erated Sharpey’s fibers are thus continuously replaced. By this mecha-
nism an adequate attachment of the tooth to the supporting tissues is
maintained. The morphologic evidence of the continuous formation of
cementum is shown by the presence of cementoblasts and a layer of cemen-
toid tissue on the surface of the cementum. Cementoid tissue may be found
on acellular (Figs. 121, 122, 124), as well as on cellular (Fig. 125) ce-
mentum.
 
The continuous deposition of cementum is of great biologic impor-
tance.“ 3' 13 In contrast to the ever alternating resorption and new for-
mation of bone, cementum is not resorbed under normal conditions. If a
layer ages or, functionally speaking, loses its vitality, the periodontal
connective tissue and cementoblasts must produce a new layer of cemen-
tum on the surface to keep the attachment apparatus intact. In bone the
loss of vitality can be recognized by the fact that the bone cells degen-
erate and the bone lacunae are empty. Lowered vitality in acellular
cementum cannot be so readily ascertained but, in cellular cementum, the
cells in the deepest layers may degenerate and the lacunae may be
empty (Fig. 124). This indicates necrosis of the cells. On the surface,
the lacunae contain normal cementocytes. The nuclei of degenerating
cells in the deeper layers are pyknotic and the cells are shrunken: near
the surface the cells fill the entire space of the cementum lacunae (Fig.
125) and the nuclei stain dark.“ 3
168 ORAL HISTOLOGY AND EMBRYOLOGY
 
9. HYPERGEIVLENTOSIS
 
Hypercementosis designates an abnormal thickening of the cementum.
It may be difiuse or circumscribed, i.e., it may affect all teeth of the
dentition, or it may be confined to a single tooth. It may even affect
only certain parts of one tooth. If the overgrowth improves the func-
tional qualities of the cementum, it is termed a cementum hypertrophy;
if overgrowth occurs in nonfunctional teeth or if it is not correlated with
increased function, it is termed hyperplasia.
 
 
 
 
Hypertrophic
cementum
‘i
 
5 ‘C
Alveolar ‘bone .
 
Periodontal. _ _.. -.. N 73- i 1"
membrane
 
Dentin
 
3»-:,
1,,
‘S1,.
 
:1
 
_,,‘ I-Iypertrophic
cementum
 
Fig. 131.——Pronglike excementoses.
 
In localized hypertrophy a spur or pronglike extension of cementum
may be observed (Fig. 131). This condition is frequently found in teeth
which are exposed to great stress. The pronglike extensions of ce-
mentum provide a larger surface area for the attaching fibers, thus se-
curing a firmer anchorage of the tooth to the surrounding alveolar bone.’
 
Localized hyperplasia of cementum may sometimes be observed in areas
where enamel drops have developed on the dentin. The hyperplastic ce-
mentum, covering the enamel drops (Fig. 132), is occasionally irregular
CEMENTUM 169
 
and sometimes contains round bodies which may be calcified epithelial
rests. The same type of embedded calcified round bodies are frequently
found in localized areas of hyperplastic cementum (Fig. 133). Such
knoblike projections are designated as excementosis. They, too, develop
around disintegrated, degenerated epithelial rests.‘
 
‘V 5%.;
in '9.
3% 1-3,
 
--1;
 
Hyper-plastic cementum _: ~ Denun
 
—-—-- '- Enamel drop
 
Hyperplastic cementum
 
as
 
Fig. 132.—Irreg'ula.r hyperplasia or cementum on the surface or an enamel drop.
 
Extensive hyperplasia of the cementum of a tooth is found, occasion-
ally, in connection with chronic periapical inflammation. Here the hyper-
plasia is circumscribed and surrounds the root like a cuff.
 
A thickening of the cementum is often observed on teeth which are not
in function. The hyperplasia may extend around the entire root of the
nonfunctioning teeth or may be localized in small areas (see chapter
on Periodontal Membrane). Hyperplasia of cementum in nonfunctioning
teeth is characterized by the absence of Sharpey’s fibers.
170 ORAL HISTOLOGY AND EMBRYOLOGY
 
Excementosis '
 
cementum
 
Excementosis
 
Alveolar bone
 
‘ ~«__... . . __.
 
Fig. 133.~—Excementoses in bifurcation of a. molar. (Gottliebfl)
I71
 
CEMENT Ul\I
 
Remnants of
fractured cementum
Hype!-plastic cementum
 
._ Hyperplastic cementum
 
 
 
X
e
n.
A
 
Fig. 134..—E:xtens1ve spikelike hyperplasia of cementum-
172 omu. HISTOLOGY AND EMBRYOLOGY
 
The cementum is thicker around the apex of all teeth and in the
bifurcation of multirooted teeth than on other areas of the root. This
thickening can be observed in embedded, as well as newly erupted,
teeth.”
 
In some cases an irregular overgrowth of cementum can be found with
spikelike extensions and calcification of Sharpey’s fibers, accompanied by
numerous cementicles. This type of cementum hyperplasia can, occa-
sionally, be observed on many teeth of the same dentition and is, at least
in some cases, the sequelae of injuries to the cementum (Fig. 134).
 
10. CLINICAL CONSIDERATIONS
 
The fact that cementum appears to be more resistant to resorption than
bone renders orthodontic treatment possible. When a tooth is moved by
means of an orthodontic appliance, bone is resorbed on the side of pres-
sure new bone is formed on the side of tension. On the side toward which
the tooth is moved pressure is equal on the surfaces of bone and cementum.
Resorption of bone, as well as of cementum, may be anticipated. How-
ever, in careful orthodontic treatment cementum resorption, if it occurs, is
usually localized and shallow. Moreover, it is readily repaired if the
intensity of pressure is reduced and the surrounding connective tissue
remains intact. If resorption is extensive it may indicate a. systemic
disorder, possibly of the endocrine system.‘
 
Excessive lateral stress may compress the periodontal connective tissue
between bone and cementum and cause bleeding, thrombosis and necrosis.
After resorption of the damaged tissues, accompanied by bone resorption,
repair may take place.‘~ 9~ “’~ 23
 
It has been the aim of some investigators to determine why resorption
takes place in some cases and not in others when external conditions
seem to be identical. The reasons are as yet unknown. The potentiality
to form new cementum does not seem to be equal in all individuals; in
some, cementum forms readily; in others it does not. The latter are those
cases which react unfavorably to trauma or any kind of irritation. These
are the cases that develop periodontal diseases easily. The dilference in
cementum formation may be explained by constitutional factors. Cemen-
tum resorption without obvious cause is called idiopathic.
 
Severe resorption of cementum may be followed by resorption of the
dentin. After resorption has ceased the damage is usually repaired,
either by formation of acellular (Fig. 135, A) or cellular (Fig. 135, B)
cementum, or by alternate formation of both (Fig. 135, 0). In most cases
of repair there is a tendency to re-establish the former outline of the
root surface. However, if only a thin layer of cementum is deposited on
the surface of a deep resorption, the root outline is not reconstructed and a
baylike recess remains. In such areas sometimes the periodontal space is
GEMENTUM 173
 
restored to its normal width by formation of new bone, so that a
proper functional relationship will result. The outline of the alveolar
bone, in these cases, follows that of the root surface (Fig. 136). In con-
trast to anatomical repair, this change is called functional repair.“
 
 
 
 
 
 
 
I
T  4»:
 
 
 
JCT '
X‘
;‘f5.."-‘4K:»:('si
 
 
Fig. 135.—Repair of resorbed cementum.
 
4. Repair by acellular cementum (a:).
 
B. Repair by cellular cementum (2).
 
0. Repair flrst by cellular (ac) and later by acellular (wz) cementum.
D = Dentin; I1’. = line or resorption; P = periodontal membrane.
 
If teeth are subjected to acute trauma, such as a blow, smaller or
larger fragments of cementum may be severed from the dentin. The
tear occurs frequently at the cemento-dentinal junction, but may also be
in the cementum or dentin. Transverse fractures of the root may heal
by formation of new cementum uniting the fragments.
 
Frequently, hyperplasia of cementum is secondary to periapical inflam-
mation or extensive occlusal stress. The fact is’ of practical significance
174 ORAL HISTOLOGY AND EMBRYOLOGY
 
in so far as the extraction of such teeth necessitates the removal of bone.
This also applies to extensive excementoses, as shown in Fig. 133.
These can anchor the tooth so tightly to the socket that the jaw or parts
of it may be fractured in an attempt to extract the tooth. These facts
indicate the necessity of taking roentgenograms before an extraction.
Small fragments of roots, left in the jaw after extraction of vital teeth,
may be surrounded by cementum, and remain in the jaw without causing
 
any disturbance.
 
   
 
" 5,
:,.--' Repaired
 
     
 
       
 
 
 
'_;é,'_‘.:__i_uW' 1%“, resorption
----.-I-:a..;.sa£g
. A .- New perio-
- dontal
membrane
 
Perio(11:)nta.1._:. \ ‘
mem a. . ‘ ~' "
r ne_rh\g,"",3_.'
 
Fi8- 136.—-Functional repair of cementum resorption by bone apposition. Normal width
of periodontal membrane re-established.
 
If the cementum does not cover the cervical part of the root, recession
of the gingiva will expose the highly sensitive dentin in the cervical area.
When calculus is removed it is frequently impossible to avoid the re-
moval of the thin cementum covering the cervical region of the exposed
root. As the individual gets older, more cementum is gradually exposed
and subject to the abrasive action of some dentifrices. Since the ce-
CEMENTUM 175
 
inentuin is the softest of the hard dental tissues, a considerable amount
of cementum may be removed by these mechanical means.” The de-
nuded dentin is then highly sensitive to thermal, chemical or mechani-
 
cal stimuli. The hypersensitivity can often be relieved with astringent
chemicals which coagulate the protoplasmic odontoblastic processes.
 
References
 
. Becks, H.: Systemic Background of Paradentitis, J. A. D. A. 28: 1447, 1941.
 
. Black, G. V.: A Study of Histological Characters of the Periosteum and Peri-
dental Membrane, Dental Review 1886-1887; and W. T. Keener 00., Chicago,
1887.
 
Box, H. K.: The Dentinal Cemental Junction (Bull. No. 3), Canad. Dent. Res.
Found., May, 1922.
 
Coolidge, E. D.: Traumatic and Functional Injuries Occurring in the Support-
ing Tissues of Human Teeth, J. A. D. A. 25: 343, 1938.
 
Denton, G. H.: The Discovery of Cementum, J. Dent. Research 18: 239, 1939.
 
Gottlieb, B.: Zementexostosen, Schnielztropfen und Epithelnester (Cementexos-
tosis, Enamel Drops and Epithelial Rests), Oesterr. Ztschr. f. Stomatol. 19:
515 1921.
 
. Gott1ieb’,B.: Tissue Changes in Pyorrhea, J. A. D. A. 14: 2173,1927.
 
. Gottlieb, B.: Biology of the Cementum, J. Periodont. 13: 13, 1942.
 
Gottlieb, B., and Orban, B.: Die Veriinderungen der Gewbe bei iibermiissiger
Beanspruchung der Ziihne (Experimental Traumatic Occlusion), Leipzig,
1931.
 
10. Gottlieb, B., and Orban, B.: Biology and Pathology of the Tooth (Translated
 
by M. Diamond), New York, 1938, The Macmillan Co.
11. Kitchin, P. G.: ’l‘he Prevalence of Tooth Root Exposure, J. Dent. Research 20:
565 1941.
 
12. Kitchin,,P. 0., and Robinson, H. B. G.: The Abrasiveness of Dentifrices as
Measured on the Cervical Areas of Extracted Teeth, J. Dent. Research 27:
195 19-18.
 
13. Kronfeld, R.: Die Zementhyperplasien an nicht funktionierenden Ziihnen (Ce-
mentum Hyperplasia on Nonfunctioning Teeth), Ztschr. f. Stomatol. 25:
1218 1927.
14. Kronfeld: R.: The Biology of Cementum, J. A. D. A. 25: 1451, 1938.
15. Malassez, M. L.: Sur le r6le des débris epitheliaux paradentaires (The Epithe-
lial Rests Around the Root of the Teeth), Arch. de Physiol. 5: 379, 1885.
Oppenheim, A.: Human Tissue Response to Orthodontic Intervention, Am. J.
Orthodont. & Oral Surg. 28: 263, 1942.
17. Orban, B.: Resorption and Repair on the Surface of the Root, J. A. D. A. 15:
1768 1928.
 
18. Orban, B.,: Dental Histology and Embryology, Philadelphia, 1929, P. Blakiston’s
Son & Co.
 
19. Sicher, H., and Weinmann, J. P.: Bone Growth and Physiologic Tooth Move-
ment, Am. J. Orthodo_n_t.. Kr Oral _Surg. 30: 109, 1944.
 
20. Skillen, W. G.: Permeability: A Tissue_ Characteristic, _J. A. D. A. 9: 187, 1922.
 
21. Sorrin, S., and Miller, S. G.: The Practice of Pedodontia, New York, 1928, The
Macmillan Co. _
 
22. Stones, H. H.: The Permeability of Cementum, Brit. D. J. 56: 273, 1934.
 
23. Stuteville, O. H.: Injuries Caused by Orthodontic Forces, Am. J. Oi-thpdont.
85 Oral Surg. 24: 103, 1938. _ _
 
24. Tainter, M. L., and Epstein, S.: A Standard Procedure for Determining Abra-
sion, J. Am. Coll. Dentists 9: 353, 1942.
 
25. Thomas, N. G., and Skillen, W. G.: Staining the Granular Layer, Dental Cosmos
 
26
 
[Old
 
?°°~1 9”?‘ 2"‘ 9°
 
I-
P’
 
62: 725, 1920.
. Weinmann, J. P., and Sicher, H.: Bone and Bones. Fundamentals of Bone
 
Biology, St. Louis, 1947, The C. V. Mosby Co.
CHAPTER VII
 
PERIODONTAL MEMBRANE
 
D1‘-I'INITION
 
FUNCTION
 
DEVELOPMENT
STRUCTURAL ELELIENTS
PHYSIOLOG-I0 CHANGES
CLINICAL CONSIDERATIONS
 
9’S"'.“9°!°!"
 
1. DEFINITION
 
The periodontal membrane is the connective tissue which surrounds
the root of the tooth and attaches it to the bony alveolus; it is continuous
with the connective tissue of the gingivae. Various terms have been
given to this tissue: peridental membrane; pericementum; dental perios-
teum; and alveolodental membrane. The variety of terms may be ex-
plained by the difficulty of classifying this tissue under any anatomic
group. The term periodontal is derived from the Greek pert meaning
around, and odous meaning tooth, thus signifying the relationship of the
tissue to the tooth. This tissue is called a membrane though it does not
resemble other fibrous membranes, like fasciae, capsules of organs, peri-
chondrium, and periosteum. It has some structural and functional
similarities to these tissues, but is different in that it not only serves as a
pericementum for the tooth, a periosteum for the alveolar bone, but
mainly as the suspensory ligament for the tooth. Therefore, the term
periodontal ligament would be most appropriate.
 
2. FUNCTION
 
The functions of the periodontal membrane are formative, supportive,
sensory and nutritive. The formative function is fulfilled by the cemento-
blasts and osteoblasts which are essential in building cementum and bone,
and by the fibroblasts forming the fibers of the membrane. The suppor-
tive function is that of maintaining the relation of the tooth to the sur-
rounding hard and soft tissues. This is achieved by connective tissue
fibers which comprise the bulk of the membrane. Functions which are
sensory and nutritive to the cementum and alveolar bone are carried out
by the nerves and blood vessels.
 
3. DEVELOPMENT
 
The periodontal membrane is derived from the follicle, or sac which
envelops the developing tooth germ. Around the tooth germ three zones
can be seen: an outer zone containing fibers related to the bone; an inner
zone of fibers adjacent to the tooth; and an intermediate zone of un-
 
First dratt submitted by Helmuth A. Zander.
176
rmuonommn MEMBRANE 177
 
orientated fibers between the other two (Fig. 137). During the formation
of cementum, fibers of the inner zone are attached to the surface of the
root. As the tooth moves toward the oral cavity, gradually a functional
orientation of the fibers takes place.“ Instead of loose and irregularly
arranged fibers, fiber bundles extend fi'om the bone to the tooth. When
the tooth has reached the plane of occlusion, and the root is fully formed,
 
- - Dentin
 
   
 
- —— cementum
 
Bone fibers
 
Cemental fibers
 
Bone
 
 
Fig. 137.—Three zones in the periodontal membrane of a developing tooth.
 
this functional orientation is complete. However, due to changes in func-
tional stresses, some changes in the structural arrangement of the perio-
dontal membrane occur throughout life.
 
4. STRUCTURAL ELEMENTS
 
The main tissue elements in the periodontal membrane are the principal
fibers, all of which are attached to the cementum?’ 3 The fiber bundles
extend from the cementum to the alveolar wall, or over the alveolar wall
to the cementum of the adjacent tooth, or into the gingival tissue. The
principal fibers of the periodontal membrane are white collagenous connec-
tive tissue fibers and cannot be lengthened. There are no elastic fibers in
the periodontal membrane. The apparent elasticity of the periodontal mem-
brane is due to the arrangement of the principal fiber bundles. They follow
a wavy course from bone to cementum, thereby allowing slight movement
178 ORAL msvronomz AND EMBRYOLOGY
 
of the tooth upon stress. Near the bone the fibers seem to form larger
bundles before their insertion into it. Although the bundles run directly
from bone to cementum, it is most probable that the single fibers do not all
span the entire distance. The bundles are “spliced" together from shorter
fibers and held together by a cementing substance. The principal fibers
are so arranged that they can be divided into the following groups:
 
Gingiva.
 
 
 
Cemente-
enamel
junction '_
 
155
 
«j.
 
E  ‘L
y‘, ‘\
 
 
 
Alveolar
crest
 
Fig. 138.——Gingival fibers of the periodontal membrane pass from the cementum into
' the gingiva.
 
The fibers of the gingival group (Fig. 138) attach the gingiva to the ce-
mentum. The fiber bundles pass outward from the cementum into the
free and attached gingiva. Usually they break up into a meshwork of
smaller bundles and individual fibers, interlacing terminally with the
fibrous tissue of the gingiva.
 
The fibers of the transseptal group (Fig. 139) connect adjacent teeth.
The fiber bundles run mesially and distally from the cementum of one
tooth, over the crest of the alveolus, to the cementum of the neighboring
 
tooth.
The fibers of the alveolar group (Fig. 140) attach the tooth to the bone
of the alveolus; they are divided into five groups: (1) Alveolar crest
PERIODONTAL MEMBRANE 179
 
group: the fiber bundles of this group radiate from the crest of the alveo-
lar process, and attach themselves to the cervical part of the cementum.
(2) Horizontal group: these fibers run at right angles to the long axis of
the tooth, directly to the bone. (3) Oblique group: the fibers run
obliquely; arising from the bone, they are attached in the cementum some-
what apically from their attachment to the bone. These fibers are ‘most nu-
merous and constitute the main support of the tooth against occlusal stress.
(4) Apical group: the fibers are irregularly arranged and radiate from
the apical region of the root to the surrounding bone (Fig. 1-11). (5)
I ntermdicular group: From the crest of the interradicular septum fibers
extend to the bifurcation of multiradicular teeth.
 
 
 
 
 
Enamel cuticle
 
Enamel cuticle Gingival papilla
 
Enamel
 
Enamel
Gingival fibers
 
Cemento-enamel
 
Dentin junction
 
Cemento-enamel
junction
 
cementum _
 
Fig 139.——Transseptal fibers of the periodontal membrane connect adjacent teeth.
 
The arrangement of the fibers in the different groups is Well adapted to
fulfill the functions of the periodontal membrane. No matter from which
direction a force is applied to the tooth, it is counteracted by some or all
of the fiber groups. The principal fibers, as a whole, may be regarded as
a ligament, alveolodental ligament, by which the tooth is attached to
the alveolar bone. Its function is, primarily, to transform pressure
exerted upon the tooth into traction on cementum and bone." The fibers
180 omu. I-IISTOLOGY AND EMBRYOLOGY
 
 
   
 
 
Enamel - Gingiva
 
Cemento-enamel
junction
 
Alveolar crest fibers
 
‘ Alveolar crest
 
Horizontal fibers?--: , T"
 
 
‘ Bundle bone
 
Lamellated bone
 
Oblique fibers
 
IP12. 140.——AJveo1a.r fibers or the periodontal membrane.
PERIODONTAL MEMBRANE 181
 
are arranged in response to functional stimuli. The structure of the
periodontal membrane changes continuously to meet the requirements of
the continuously moving tooth.°» 2°
 
Most cells of the periodontal membrane are typical fibroblasts. They
are long, slender, stellate connective tissue cells whose nuclei are large
and oval in shape. They lie at the surface of the fiber bundles and are,
probably, active in the formation and maintenance of the principal fibers.
 
 
 
 
 
V.‘ 'r.‘~ ~“I
“_—§‘ . ' Periodontal
membrane
 
 
 
Fig. 141.—Apica1 fibers of the periodontal membrane.
 
( Orban.“ )
 
Bone is in a constant state of transition. As elsewhere in the body, the
bone of the alveolus is constantly locally resorbed and rebuilt. Resorption
of bone is brought about by the osteoclasts; formation of new bone is
initiated by the activity of the osteoblasts.
 
Where bone formation is in progress osteoblasts are found along the
surface of the wall of the bony socket, the periodontal membrane fibers
passing between them. These cells are, usually, irregularly cuboid in
shape, with large single nuclei containing large nucleoli and fine chro-
matin particles. The fibers of the periodontal membrane are secured to the
 
Fibroblasts
 
Osteoblasts
and Osteo-
182 ORAL HISTOLOGY AND EMBRYOLOGY
 
bone by the formation of new bone around the ends of the fibers. There-
fore, osteoblasts seem to be necessary for the attachment and reattachment
 
of the fibers to the alveolar bone. Osteoclasts are mostly multinucleated,
and are believed to originate from undifferentiated mesenchymal cells in
the periodontal membrane; they are found only during the process of active
bone resorption. Presumably, the cytoplasm of the osteoclasts produces a
substance which dissolves the organic components of bone, while its mineral
 
Epithelial ——- ————
Test —~"-——~- —"'---*-" Principal
fibers
 
--‘-‘--2 '* Bundle bone
 
 
 
vessels
 
Cementum - I  V l  , ‘ ,‘ §
, . - ' “ I p . Blood
 
i i Interstitial
tissue
 
- —:~- - Principal
i fibers
 
I
 
-. — Bundle bone
 
.— -W
 
_. .r M .
 
Fig. 142.—Interstitia.l spaces in the periodontal membrane consist of loose connective
tissue and carry blood vessels and nerves. (0rban.=°)
 
contents are liberated and either removed in the tissue fluid or ingested
by macrophages. Wherever their cytoplasm lies in contact with bone,
hollows or grooves called “Howship’s lacunae,” or resorption lacunae,
are formed. When bone resorption ceases the osteoclasts disappear.
These cells are also active when resorption of the roots of teeth occurs
(see chapters on Bone and Shedding).
PERIODONTAL Il1EMBR.-\NE 183
 
Cementoblasts are connective tissue cells found on the surface of °°me’1*°b135t9
cementum betvveen the fibers. They are large cuboidal cells with spheroid
or ovoid nuclei, which are active in the formation of cementum (see chap-
ter on Cementum). The cells have irregular, fingerlike projections which
fit around the fibers as they extend from the cementum.
 
The blood vessels, lymphatics, and nerves of the periodontal membrane Interstitial
are contained in spaces between the principal fiber bundles (Fig. 142). mm‘
They are surrounded by loose connective tissue (interstitial tissue) in
which fibroblasts and some histiocytes, undifferentiated niesenchymal
cells and lymphocytes are found.
 
Blood vessels
 
- Dentin
 
 
 
 
- -~ —— Blood vessels
 
‘ — ~~ Cementum
 
Periodontal
membrane
 
7 —— Alveolar bone
 
Blood vessels
 
Fig. 143.—Blood vessels enter the periodontal membrane through openings in the alveolar
bone. (Orban.=‘)
 
The blood supply of the periodontal membrane is derived from three Blood Vessels
sources: (1) blood vessels enter the periapical area together with the
blood vessels for the pulp; (2) vessels branching from the inter-alveolar
arteries pass into the membrane through openings in the wall of the alveo-
lus (Fig. 143); they are the main source of supply; and (3) near the
Lymphatic:
 
NEWS!
 
184 om. msronoey AND nmmzvonoor
 
gingivae, the vessels of the periodontal membrane anastomose with ves-
sels passing over the alveolar crest from the gingival tissue. The capil-
laries form a rich network in the periodontal membrane, intertwining
between the fibers.”
 
A network of lymphatic vessels, following the path of the blood vessels,
provides the lymph drainage of the periodontal membrane. The flow is
from the membrane toward and into the adjacent alveolar bone, continuing
to the lymph nodes.“ 23
 
Epithelial rests- -— -»
 
" "\-s-rt
 
 
 
cementum I: , _.. Alveolar bone
 
-.
at
l
o
r
 
Periodontal mem- '
 
.. __ J1  .
brane “ Q‘, ‘.17 ‘l ‘-7 ' '
 
Epithelial rests _
 
Asa:
 
Fig. 144.—-—Epithe!ta1 rests in the periodontal membrane.
 
Generally, the nerves of the periodontal membrane follow the path of the
blood vessels, both from the periapical area and from the interdental
and interradicular arteries through the alveolar wall. A rich plexus is
formed in the periodontal membrane. Three types of nerve endings are
found: one terminating in a knob-like swelling; another, forming loops or
PERIODONTAL MEMBRANE 185
 
rings around bundles of the principal fibers; lastly, free endings of fibers
branching from the main axon. These terminal branches are free of myelin
sheaths. Most of the nerve endings are receptors for proprioceptive stimuli
(deep sensibility). The slightest touch at the surface of the tooth is trans-
mitted to the nerve endings through the medium of the periodontal mem-
brane. All sense of localization is through the periodontal membrane. The
sense of touch is not impaired by removal of the apical parts of the mem-
brane, as in root resection, nor by removal of its gingival portion (gingi-
vectomy). As elsewhere in the body, fibers from the sympathetic system
supply the blood vessels of the periodontal membrane." 13
 
Cementnm
(tangential ‘
section) ‘ '
 
Network of 9""
epithelial '.
rests
 
Network of ‘
epithelial }
rests -f‘
 
. .—N tw k t ithelial rests in the periodontal membrane. (Tangential section
Fig 145 e or 0 ep almost parallel to root surface.)
 
In the periodontal membrane epithelial cells are found which, usually, Elgtglictfll-llm
lie close to the cementum but not in contact with it (Fig. 144). They
were first described by Malassez in 1885.“ Since then much research has
been done as to their origin, structural arrangement and function. They
186 omu. I-IISTOLOGY AND EMBRYOLOGY
 
are, undoubtedly, remnants of the epithelium which forms Hertwig’s
epithelial root sheath“ (see chapter on Tooth Development). At the time of
formation of cementum the continuous layer of epithelium, bordering the
dentin surface, breaks into strands which persist as a network parallel‘ to
the surface of the root (Fig. 145). Only in a surface View, as in sections
almost parallel to the root, can the true arrangement of these epithelial
 
Alveolar bone
 
Epithelial
rest
 
’ -’ Periodontal
 
Cementurn  membrane
Dentin _.
Blood vessel
 
Fig. 146.-—Long strand or epithelium in the periodontal membrane.
 
strands be seen.“ Cross or central sections through the tooth cut through
the strands of the network and, thus, only isolated nests of epithelial cells
appear in the sections. It is not clear whether the epithelial sheath
breaks up because of degeneration of the epithelial cells, or due to active
proliferation of the mesenchyme, or both. This disintegration of the
epithelium enables the connective tissue to approach the outer surface
of the dentin and to deposit cementum on its surface. The frequent
appearane of the epithelial rests, in long strands (Fig. 146) or in tu-
187
 
PI*ZRIOD0i\'TAL MEMBRANE
 
bules (_Fig. 147 l, has given rise to the assumption that they may have
endocrine function. Under pathologic conditions they may proliferate
 
and give rise to epithelial masses, associated with grannlomas, cysts, or
tumors of dental origin.
 
Epithelial. rest ', . —.~
 
   
 
— Cemenmblast
 
Principal nbers
 
Fig. 1-l7.—Pseuclo-tubular structure of epithelial rest in the periodontal membrane.
 
Calcified bodies, cementicles, are sometimes found in the tissues of the
periodontal membrane, especially in older persons. These bodies may
remain free in the connective tissue; they may fuse into large calcified
masses, or they may be joined with the cementum (Fig. 148). As the
cementum thickens with advancing age, it may envelop these bodies in
which event the cemcnticles become interstitial in location. When they
are adherent to the cementum they form excementoses. The origin of
 
these calcified bodies is not established; it IS presumed that degenerated
cells, usually epithelial, form the nidus for their calcification.
 
5. PEYSIOLOGIG CHANGES
 
Several studies of the width of the periodontal membrane, in“human
specimens, have been reportecl.“ 3- “r 12 All reports agree that the thick-
ness of the periodontal membrane varies in different individuals, in dif-
 
cementicles
 
Measurements
and changes
in Dimen-
sions During
188 ORAL HISTOLOGY AND EMBRYOLOGY
 
ferent teeth in the same person, and in different locations on the same
tooth as is illustrated in Tables III to V1.5
 
TABLE III
THICKNESS or PERIODONTAL MEMBRANE or 172 TEETH FROM 15 HUMAN JAWS
 
 
AVERAGE AT AVERAGE AT AVERAGE AT AVERAGE OF‘
 
ALV. CREST MIDROOT APEX TOOTH
 
14:); MM MM MM
A es 11-10
83 teeth from 4 jaws 0 23 0 17 0 24 0 21
Ages 32-50
36 teeth from 5 jaws 0.20 0.14 0.19 0.18
Ages 51457 [ _
35 teeth from 5 jaws 0.17 0.12 0.16 0.1::
 
 
Table III shows that the width of the periodontal membrane decreases with age, and
that it is wider at the crest and apex than at the midroot. (Coo1idge.8)
 
TABLE IV
 
THICKNESS or PE1uoBoNTAL Trssuns IN VARYING CoNmTxoNs or FUNcTIoN
 
 
ALV. CREST MIDROOT APEX AVERAGE
 
MM. MM. MM. MM.
Teeth in heavy function
44 teeth from 8 jaws 0.20 0.14 0.19 0.18
Teeth not in function
20 teeth from 12 jaws 0.1-1 0.11 0.15 0.13
Embedded teeth
5 teeth 0.09 0.07 0.08 0.08
 
_Table IV shows that the width of the periodontal membrane is greater around teeth
which are subjected to heavy stress and decreases with loss of function. (Coolidgefi)
 
TABLE V
 
COMPARISON or THICKNESS or PERIODONTAL MEMBRANE or Foua INGISORS AND FOUR
MoLABs (SUBJECT AGED 11 YEARS)
 
 
ALv. CREST MIDROOT APEX AVERAGE
MM. MM. MM. MM.
4 incisors 0.33 0.25 0.28 0.29
4 molars 0.22 0.15 0.26 0.21
 
 
Table V demonstrates that there is a difierenee in the width of the membrane in
different teeth in the same individual. (Coolidge!)
 
TABLE VI
 
COMPARISON or PERIODONTAL MEMBRANE IN DIFFERENT LocAT1oNs AROUND THE SAME
'1‘ooTH (SUBJECT AGED 11 YEARS)
 
 
MESIAL DISTAL LABIAL LINGUAL
MM. MM. MM. MM.
Upper ri ht central incisor, mesial
and bial drift 0.12 0.24 0.12 _ 0.22
Upper left central incisor, no
drift 0.21 0.19 0.24 0.24
Upper right lateral incisor, distal
and labial drift 0.27 0.17 0.11 0.15
 
 
Table VI shows the variation in width of the mesial, distal, labial, and lingual sides
of the same tooth. (Coolidge!)
PERIODONTAL MEMBRANE 189
 
The measurements shown in the tables indicate that it is not feasible
 
to refer to an average figure of normal width of the periodontal mem-
brane. Measurements of large number of cases range from 0.15 to 0.38
 
mm. The ‘fact that the periodontal membrane is the thilmest in the
m1ddle region of the root shows that the fulcrum of physiologic move-
ment Is in this reglon. The thickness of the periodontal membrane seems
 
‘ Free cementicle
 
Alveolar bone
 
W’ i '_ Attached cementicle
 
' Periodontal membrane
 
Embedded cementicle
 
Fig. 148.—Cementicles in the periodontal membrane.
 
to be maintained by the ftmctional movements of the tooth. It is thinner
in flmctionless and embedded teeth. The fact that cementum and bone
do not fuse even in functionless teeth might be due to the fact that both
lose their growth potential if function is lost.
 
Physiologic movement of human teeth is characterized by their tendency
to migrate mesially in compensation for the wear at their contact points.”
In mesial migration a difference can be observed in the periodontal mem-
 
Physiologic
Changes
Marrow
space
 
190 om. nrsronoor mo nmsmzonoer
 
brane in the distal and mesial areas (Fig. 149, A and B). On the distal
side of the tooth, the interstitial spaces with their blood vessels, lymph
spaces and nerves, appear in sections elliptic in contrast to those on the
mesial side that appear round.” Bone resorption on the mesial side of the
tooth sometimes opens marrow spaces which become continuous with the
periodontal membrane (Fig. 149, A). Frequently, however, the drift is so
gradual that bone formation in the marrow spaces keeps pace with the re-
sorption on the periodontal membrane side, and the thickness of the al-
veolar bone is maintained. Due to the shift of the tooth, epithelial rests
may become incorporated in the bone on the side from which the tooth is
shifting.“
 
 
Alveolar - ' "
 
bone
 
Interstitial
space
 
Principal
fibers
 
 
 
Fig. 149.—Interstitie.1 spaces between the principal fiber bundles are round on the
pressure side (A) and elliptic on the tension side (3). Marrow spaces open up on the
pressure side and become interstitial spaces.
 
C : Cementum. D : Dentin.
 
6. CLINICAL CONSIDERATIONS
 
The complex functional relationship between the teeth and their sup-
porting tissues brings about continuous structural changes during life.
Between the two extremes of occlusal trauma and loss of function there
 
“ i‘ Lamellated
 
bone
 
Bundle bone
l’l<}RIODON'l‘AL MEMBRANE 191
 
are many intermediate stages. In loss of function the periodontal mem-
brane becomes narrower, due to decreased use of that particular tooth.‘ 1°’ 1‘
The regular arrangement of the principal fibers is lost and the periodontal
membrane appears as an irregularly arranged connective tissue. The
cementum becomes thicker but finally aplastic; it contains no Sharpey’s
fibers. Also, the alveolar bone is in an aplastic (inactive) state and lacks
Sharpey’s fibers (Fig. 150, B).
 
 
 
 
Bundle —
bone
~ lAlveola.r bone
_ ] (lamellated)
1;.  } - K
Periodontal  I‘ . .
membrane .1 g , -
.:l§
Bundle —--—---— . _
bone E P H do tal
‘ e o 11
membrane
Lamellated —— '5 .
Haversian “,
bone 1
 
   
 
 
59'
we
 
Fig‘. 150.—~Periodontal membrane or a. functioning (A) and nontunctioning (B) tooth.
In the functioning tooth the periodontal membrane is wide, principal fibers are present.
cementum (C) is thin; bundle bone with Sharpey's fibers. In the nonfunctioning tooth
the periodontal membrane is narrow, no principal fiber bundles are present. Cementu_m
is thick (0 and 0') ; alveolar bone is lamellated with no Shar-pey's fibers. D = Dentin.
 
For restorative dentistry the importance of these changes in structure is
obvious.” The supporting tissues of a tooth long out of function are
unable to carry the load suddenly placed upon the tooth by restoration.
This applies to bridge abutments, teeth opposing bridges or dentures, and
teeth used as anchorage for removable bridges. This may account for the
192 ORAL HISTOLOGY AND EMBRYOLOGY
 
inability of a patient to use a restoration immediately following its place-
ment. Some time must elapse before the supporting tissues are again re-
arranged in response to the new functional demands. This may be termed
an adjustment period which, likewise, must be permitted to follow ortho-
dontic treatment.
 
The stress, especially of a lateral type, often placed upon the support-
ing apparatus may be more than the tissue can tolerate. Sudden trauma
of the periodontal membrane, such as in accidental blows, condensing of
foil, rapid mechanical separation, may produce pathologic changes: frac-
tures or resorption of the cementum, tears of the fibers, hemorrhage and
necrosis. The adjacent alveolar bone is resorbed and the periodontal
membrane thickened; the tooth becomes loose. When trauma is eliminated
repair may take place. For practical purposes it is important that, in the
construction of fillings and bridges, the occlusion be carefully considered,
and interference in lateral movements (cusp interference) avoided or elimi-
nated. It is also important that missing teeth be immediately replaced to
avoid tipping and migration of remaining teeth; failure to do so may result
in loss of function and traumatism.
 
Orthodontic tooth movement depends upon bone resorption and bone
formation stimulated by properly regulated pressure and tension." These
stimuli are transmitted through the medium of the periodontal membrane.
If the movement of teeth is within physiologic limits (Which may vary
with the individual) the initial thinning of the periodontal membrane
on the pressure side, is compensated for by bone resorption, whereas
the thickening of the periodontal membrane, on the tension side, is bal-
anced by bone apposition. If new bone formation is impaired by faulty
manipulation or disease, the periodontal membrane may become wider
and the tooth may loosen, or even be completely lost. Under the stimulus
of inflammation such as occurs in a dental granuloma the epithelial rests
of the periodontal membrane may proliferate to form a periodontal cyst
around the root end of the tooth. The dental granulomas are found fre-
quently, and very careful studies“: 9“ have shown that 100 per cent
of dental granulomas have either proliferating or resting epithelium.
Since all dental granulomas contain this material, they must" all be con-
sidered as potential periodontal cysts.
 
References
 
1. Berkelbach van der Sprenkel, H.: Zur Neurologie des Zahnes (Neurology of
the Tooth), Ztschr. f. mikr.- anat. Forsch. 38: 1, 1935.
 
2. Black, G. V.: A Study of the Histological Characters of the Periosteum and
Peridental Membrane, Chicago, 1887, W. T. Keener Co.
 
3. Black, G. V.: The Fibers and Glands of the Peridental Membrane, Dental Cos-
mos 41: 101, 1899.
 
4. Box, K. F.: Evidence of Lymphatics in the Periodontium, J. Canad. D. A. 15:
8, 194.9.
 
5. Brunn, A. v.: Ueber die Ausdehnung des Schmelzorganes und seine Bedentung
fur die Zahnbildung (The Extension of the Enamel Organ and Its Sig-
nificance in Tooth Development), Arch. f. mikr. Anat. 29: 367, 1887.
PERIODONTAL MEMBRANE 193
 
6. Bruszt, P.: Ueber die netzartige Anordnung des paradentalen Epithels (The
Network Arrangement of the Epithelium in the Periodontal Membrane),
Ztschr. f. Stomatol. 30: 679, 1932.
 
7. Coolidge, E. D.: Clinical Pathology and Treatment of the Dental Pulp and
_Periodontal Tissues, Philadelphia, 1939, Les. & Febiger.
 
8. Cool1g§e,11;3éi93'17‘he Thickness of the Human Periodontal Membrane, J. A. D. A.
 
. , .
 
9. Gottlieb, B.: Paradental Pyorrhoe und Alveolar atrophie (Paradental Pyorrhea
and Alveolar Atrophy), Fortschr. d. Zahnheilk. 2: 363, 1926.
 
9a. Hilli J.: The Epithelium in Dental Granulomata, J. Dent. Research 10: 323,
 
10. Kellner,  Histologische Befunde an antagonistenlosen Ziihnen (Histologic
Findings on Teeth Without Antagonists), Ztschr. f. Stomatol. 26: 271, 1928.
 
11. Klein, A.: Systematische Untersuchungen iiber die Periodontalbreite (Sys-
tematic Investigations on the Width of the Periodontal Membrane), Ztschr.
f. Stomatol. 26: 417, 1928.
 
12. Kronfeld, R.: A Case of Tooth Fracture, With Special Emphasis on Tissue Re-
pair and Adaptation Following Traumatic Injury, J. Dent. Research 15:
429, 1935/6.
 
13. Lehner, J., and Plenk, H.: Die Ziihne (The Teeth), Moellendorfs Handbuch. d.
mikrosk. Anat. vol. 3, Berlin, 1936, J. Springer, p. 449.
 
14. Malassez, M. L.: Sur l’existence de masses epithéliales dans le ligament al-
veolodentaire (On the Existence of Epithelial Masses in the Periodontal
Membrane), Compt. rend. Soc. de biol. 36: 241, 1884.
 
15. McCrea, M. W.: Histologic Studies on the Occurrence of Epithelium in Dental
Granulomata, J. A. D. A. 24: 1133, 1937.
 
16. Noyes, F. B.: A Review of Work on the Lyniphatics of Dental Origin, J. A. D. A.
14: 714, 1927.
 
17. Oppenheim, A.: Human Tissue Response to Orthodontic Intervention of Short
and Long Duration, Am. J. Orthodont. & Oral Surg. 28: 263, 1942.
 
18. Orban, B.: Entwicklungsgeschichte und Histogenese (Embryology and Histo-
genesis), Fortschr. d. Zahnheilk. 3: 749, 1927.
 
19. Orban, B.: Biologic Considerations in Restorative Dentistry, J. A. D. A. 28:
1069 1941.
 
20. Orban, B’: A Contribution to the Knowledge of the Physiologic Changes in the
Periodontal Membrane, J. A. D. A. 16: 405, 1929.
 
21. Orban, B.: Dental Histology and Embryology, Philadelphia, 1929, P. Blakiston’s
Son & Co.
 
22. Robinson, H. B. G.: Some Clinical Aspects of Intra-Oral Age Changes, Geriatrics
2: 9 1947.
 
23. Schweitzer, G.: Die Lymphgeflisse des Zahnfieisches und der Ziihne (Lymph Vessels
of the Gingivae and Teeth), Arch. 1:‘. mikr. Anat. 69: 807, 1907; '74: 927,
1909.
 
24. Sicher, H.: Ban und Funktion des Fixationsapparates der Meerschweinchen-
molaren ( tructure and Function of the Supporting Apparatus in the Teeth
of Guinea Pigs), Ztschr. f. Z. Stomatol. 21: 580,.1923. .
 
25. Weinmann, J. P.: Progress of Gingival Inflammation into the Supporting Struc-
tures of the Teeth, J. Periodont. 12: 71. 1941. _
 
26. Weinmann, J. P.: Bone Changes Related to Eruption of the Teeth, Angle
 
Orthodontist 11: 83, 1941.
CHAPTER VIII
 
MAXILLA AND MANDIBLE
(ALVEOLAR PROCESS)
 
1. DEVELOPIMEENT OI‘ MAXJILA AND MANDIBLE
 
2. DEVELOPMENT 01' ALVEOLAB PROCESS
 
3. STRUCTURE OI’ AINEOLAR PROCESS
 
4. PHYSIOLOGIC CHANGES DI '1‘H.'.l':‘. ALVEOLAR PROCESS
5. I'N'TE.'R.N.A.L RECONSTRUCTION OF BONE
 
6. CLINICAL CONSIDERATIONS
 
1. DEVELOPMENT OF MAXILLA AND MANDIBLE
 
In the beginning of the second month of fetal life the skull consists
of three parts: The chondrocranium, which is cartilaginous, comprises
the base of the skull with the otic and nasal capsules; the desmocranium,
which is ‘membranous, forms the lateral walls and roof of the brain case;
the appendicular or visceral part of the skull consists of the cartilaginous
skeletal rods of the branehial arches.
 
The bones of the skull develop either by endochondral ossification, re-
placing the cartilage, or by intramembranous ossification in the mesen-
chyme. Intramembranous bone may develop in close proximity to car-
tilaginous parts of the skull, or directly in the desmocranium, the mem-
branous capsule of the brain (Fig. 151).
 
The endochondral bones are the bones of the base of the skull: eth-
moidal bone; inferior concha (turbinate bone); body, lesser wings, basal
part of greater wings, and lateral lamella of pterygoid process of the
sphenoid bone; petrosal part of temporal bone; basilar, lateral, and lower
part of squamous portion of occipital bone. The following bones develop
in the desmocranium: frontal bones; parietal bones; squamous and tym-
panic parts of temporal bone; parts of the greater wings, and medial
lamina of pterygoid process of sphenoid bone; upper part of squamous
portion of occipital bone. All the bones of the upper face develop by intra-
membranous ossification; most of them close to the cartilage of the nasal
capsule. The mandible develops as intramembranous bone, lateral to the
cartilage of the mandibular arch. This cartilage, Mecke1’s cartilage, is
in its proximal parts the primordium for two of the auditory ossicles:
incus (anvil) and malleus (hammer). The third auditory ossicle, the
stapes (stirrup), develops from the proximal part of the skeleton in the
second branchial arch which then gives rise to the styloid process, stylo-
hyoid ligament and part of the hyoid bone which is completed by the
derivatives of the third arch. The fourth and fifth arches form the
skeleton of the larynx.
 
 
First draft submitted by Harry Sicher and Joseph P. Welnmanu.
194
— — ~ - — — — — Greater win of
F '  sphenoid bgone
Medial plate of
pterygoid
A _ process
' 1 Frontal bone
I
Parietal bone 1"‘
 
i
 
5
 
3 xi ‘,2
 
i  v _/— Nasal capsule
 
3 1 _— Nasal bone
 
1 _ 4' .7 _ —_ Lacrlmal bone
l ‘ \ -ll ' es .
 
~ ‘ “rs .\ «<-
T'« . = ~; Maxilla
* . _ A.» ‘ was... —
E j (4 LT zygomatic bone
Occipitai —————.—- _
suuama I 0 k ‘ l - 7 ‘.__ Mandible
\ ‘Ir
Lateral part of ;’ \ \
occipital bone . \ Tympanic bone
Petrosal bone '——-é-—-?———’ \ Sm ‘d
0: process
Squama of ' '
temporal bone .
Medial plate or‘ _ Water Wins 0‘
pm-ygoid - sphenoid bone
process
Frontal bone
Parietal bone
4
I ‘ '
Nasal bone L... ‘
/
Nasal capsule —  'A
Lacrimal bone — _ 
‘ ' W‘ .
Maxilla ‘——— _.__;__ ",. j' .
,  ‘H
Palatine bone  _
l -  ' Occipltul
Mandible  squama
" ‘Ui-
. I
Meckel's ‘ I
cartilage . ‘ / v p , ‘ ,'
Hammer. , [ " . Pel;osa.l bone
‘ » Min 1
Styloid process ' ~ -— -—— --—--—‘--*-‘
 
Fig. 151.—Reconstruction of the sl_£u1l ot a. human embryo 80 mm. long. gtarfilagez
green. Intramembranous bones: punk. Endochondral bones: white. (Sxeher and
 
Tandlerfl)
 
A. Right lateral view.
B. Left lateral view after removal of left int:-amernbranous bones.
 
MAXILLA. AND MANDIBLE 195
 
The human maxillary bone is formed, on either side, from the union
of two bones, premaxilla and maxilla, which remain separate in most
other mammals. In man the two bones begin to fuse at the end of the
second month of fetal life. The line of fusion is indicated in young in-
dividuals by the intermaxillary (incisive) suture on the hard palate.
 
Developing
tooth
 
Inferior Bone
alveolar (mandible)
nerve
 
Meckel’s
cartilage
man 1 e g
I(Bone d_bI )
 
Fig. 152.——Deve1opment of the mandible as intramembranous hone lateral to Meckers
cartilage (human embryo 45 mm. long).
 
The maxilla proper develops from ‘one center of ossification which
 
appears in the sixth week. The bone is then‘ situated on the lateral side
of the cartilaginous nasal capsule and forms the wall of the nasal cavity
when the cartilage has disappeared. The prernaxilla, or os incisivum,
has two independent centers of ossification. Ultimately, it forms that
part of the maxilla which icarriesthe two incisors, the anterior part of
the palatine process, the rim of the piriform aperture, and part of the
frontal processfi“
 
Maxilla.
196 ORAL HISTOLOGY AND EMBRYOLOGY
 
   
 
' Connective
tissue
 
‘ Cartilage
 
Fig. 153.—Deve1opment of mandibular symphysis.
 
A. Newborn infant: symphysis wide open: mental ossicle (roentgenogram).
 
B. Child 9 months: symphysis partly closed; mental ossicies fused to mandible
(roentgenogram).
 
0. Frontal section through mandibular symphysis of newborn infant. Connective
tissue in midline is transformed into cartilage on either side which is later replaced
 
by bone.
MAXJLLA AND MANDBLE 197
 
The mandible makes its appearance as a bilateral structure in the sixth
week of fetal life and is a thin plate of bone lateral to, and at some dis-
tance from, Meckel’s cartilage (Fig. 152). The latter is a cylindrical rod
of cartilage; its proximal end (close to the base of the skull) is continu-
ous with the hammer, and is in contact with the anvil. Its distal end
(at the midline) is bent upwards and is in contact with the cartilage of the
other side (Fig. 151). The greater part of Meckel’s cartilage disappears
without contributing to the formation of the bone of the mandible. Only
a small part of the cartilage, some distance from the midline, is the site
of endochondral ossification. Here, it calcifies and is invaded and de-
stroyed by connective tissue and replaced by bone. Throughout fetal
life the mandible is a paired bone the two halves of which are joined in
the midline by fibrocartilage. This synchondrosis is called mandibular
symphysis. The cartilage at the symphysis is not derived from Meckel’s
cartilage but differentiates from the connective tissue in the midline. In
it small irregular bones, known as the mental ossicles, develop and, at
the end of the first year, fuse with the mandibular body. At the same
time the two halves of the mandible unite by ossification of the symphysial
fibrocartilage (Fig. 153).
 
2. DEVELOPMENT OF THE ALVEOLAB. PROCESS
 
Near the end of the second month of fetal life, the bones of maxilla and
mandible form a groove which is open towards the surface of the oral
cavity (Fig. 152). In a later stage the tooth germs are contained in this
groove which also includes the dental nerves and vessels. Gradually,
bony septa develop between the adjacent tooth germs, and much later the
primitive mandibular canal is separated from the dental crypts by a hori-
zontal plate of bone.
 
An alveolar process in the strict sense of the word develops only during
the eruption of the teeth. It is important to realize that during growth
part of the alveolar process is gradually incorporated into the maxillary
or mandibular body while it grows at a fairly rapid rate at its free
borders. During the period of rapid growth, a special tissue may de-
velop at the alveolar crest. Since this tissue combines characteristics of
cartilage and bone, it is called ch/(android bone (Fig. 154).
 
3. STRUCTURE OF THE ALVEOLAB. PROCESS
 
The alveolar process may be defined as that part of the maxilla and
mandible which forms and supports the sockets of the teeth (Fig. 155).
Anatomically, no distinct boundary exists between the body of the
maxilla or mandible and their respective alveolar processes. In some
places the alveolar process is fused with and partly masked by bone
which is not functionally related to the teeth. In the anterior part of the
maxilla the palatine process fuses with the alveolar process. In the pos-
 
Mandible
198 ORAL HISTOLOGY AND EMBRYOLOGY
 
terior part of the mandible the oblique line is superimposed upon the
bone of the alveolar process (Figs. 155, D and E’ ) .
As a result of its adaptation to function, two parts of the alveolar process
 
can be distinguished. The first consists of a thin lamella of bone which
surrounds the root of the tooth and gives attachment to principal fibers
 
of the periodontal membrane. This is the alveolar bone proper. The
 
:v'.>--—'‘ “-4
 
Proliferation
zone at
alveolar
crest
 
 
   
 
 
 
Chondroid  —
bone in
 
 
 
*-vie,
 
 
Chondroid  *--—'
bone - .
 
Uhwl 11    so 1;‘? V
 
‘ Resorptlon
 
ii
 
Fig‘. 154.—Vex-tical growth of mandible at alveolar crest. Formation of chontlrold bone
which is replaced by typical bone.
 
second part is the bone which surrounds the alveolar bone and gives sup-
port to the socket. This has been called supporting bone.” The latter, in
turn, consists of two parts: the compact bone (cortical plate) forming
the vestibular and oral plates of the alveolar processes, and the spongy
bone between these plates and the alveolar bone proper (Fig. 155).
The cortical plates, continuous with the compact layers of maxillary
and mandibular body, are generally much thinner in the maxilla than in
the mandible. They are thickest in the bicuspid and molar region of the
MAXILLA AND MANDIBLE 199
 
Fig. 155.—Gross relations of alveolar processes:
 
A. Horizontal section through upper alveolar process. _,.
 
B. Labiollngual section through upper lateral incisor.
 
0. Labiolingual section through lower cuspid.
 
D. Labiolingual section through lower second molar.
 
E. Labiolingual section through lower third molar. (Sicher and Tandlerfl)
 
 
Fig. 156.—Dia.gra.mma.tic illustration of the relation between the cemento-enamel
junction of adjacent teeth and the shape of the crests of the alveolar septa. (Ritchey,
B., and Orban, B.“".)
200 ORAL HISTOLOGY AND EMBRYOLOGY
 
lower jaw, especially on the buccal side. In the maxilla the outer cor-
tical plate is perforated by many small openings through which blood and
lymph vessels pass. In the lower jaw the cortical bone of the alveolar
process is dense and, occasionally, shows small foramina. In the region
of the anterior teeth of both jaws the supporting bone is, usually, very
thin. No spongy bone is found here and the cortical plate is fused with
the alveolar bone proper (Figs. 155, B and C).
 
Circumferen-
tial lamel lae
 
Reversal line
 
Haversian
sytem
 
Interstitial -—
lamellae
 
g Resting line
 
Fig. 157A.-—Appositiona.1 growth of mandible by formation of circumferential lamellae.
 
Ehetshe are replaced by Haversian bone; remnants of circumferential lamellae in the
ep .
 
The outline of the crest of the intraalveolar septa, as they appear in
the roentgenogram, are dependent upon the position of the adjacent
teeth. In a healthy mouth the distance between the cemento-enamel
junction and the free border of the alveolar bone proper is fairly con-
stant. In consequence the alveolar crest is often oblique if the neigh-
boring teeth are inclined. In the majority of individuals the inclination
is most pronounced in the premolar and molar region, the teeth being
MAXILLA AND MANDIBLE 201
 
tipped mesially. Then, the ceniento-enamel junction of the mesial tooth
is situated in a more occlusal plane than that of the distal tooth and the
alveolar crest, therefore, slopes distally (Fig. 156).
 
The interdental and interradicular septa contain the perforating canals
of Zuckerkandl and Hiischfeld, which house the interdental and inter-
radicular arteries, veins, lymph vessels and nerves.
 
 
 
 
PrinclpaJ
flgyers
o
perio- -I Lgmellated
' one
\.
BK
' "" Haversian
system
 
Fig. 157B.—Bundle bone and I-Iaversian bone on the distal alveolar wall (silver im-
pregnation).
 
Histologically, the cortical plates consist of longitudinal lamellae and
Haversian systems (Fig. 157A) . In the lower jaw circumferential or basic
lamellae reach from the body of the mandible into the cortical plates.
The trabeculae of the spongy bone of the alveolar process are placed
in the direction of the stresses to which it is subjected as a result
 
of mastication (Fig. 158). The functional adaptation of this spongy
bone is particularly evident between the alveoli of molars where the
202 ORAL HISTOLOGY AND EMBRYOLOGY
 
trabeculae show a parallel horizontal arrangement. From the apical part
of the socket of lower molars trabeculae are, sometimes, seen radiating in
a slightly distal direction. These trabeculae are less prominent in the
upper jaw, because of the proximity of the nasal cavity and maxillary
 
Fig. 158.—Suppox-ting trabeculae between alveoli.
A. Roentgenogram or a. mandible.
 
B. Meslodistal section through mandibular molars showing alveolar bone proper and
supporting bone.
 
sinus. The marrow spaces in the alveolar process may contain hemo-
poietic, but, usually, contain fatty marrow. In the condyloid process,
 
angle of mandible, maxillary tuberosity, and other foci cellular marrow
is frequently found, even in adults." 1‘
MAXILLA AND MANDIBLE 203
 
The alveolar bone proper which forms the inner wall of the socket
(Fig. 158) is perforated by many openings which carry branches of the
interalveolar nerves and blood vessels into the periodontal membrane
(see chapter on Periodontal Membrane). It is called cribriform plate or
lamina dura ; the latter term refers to the dense appearance of the alveo-
lar bone proper in roentgenograms. The alveolar bone proper consists
partly of lamellated, partly of bundle bone. The lamellae of the lamel-
lated bone are arranged roughly parallel to the surface of the adjacent
marrow spaces, others form Haversian systems. Bundle bone is that
bone to which the principal fibers of the periodontal membrane are an-
chored. The term bundle bone was chosen because the bundles of the
principal fibers continue into the bone as Sharpey’s fibers. The bundle
bone is characterized by the scarcity of the fibrils in the intercellular
substance. These fibrils, moreover, are all arranged at right angles to the
Sharpey’s fibers. The bundle bone appears much lighter in preparations
stained with silver than lamellated bone because of the reduced number
of fibrils (Fig. 157B). Because all the fibrils run in the same direction,
the bundle bone is not lamellated.
 
4. PHYSIOLOGIG CHANGES IN THE ALVEOLAR PROCESS
 
The internal structure of bone is adapted to mechanical stresses. It
changes continuously during growth and alteration of functional stresses.
In the jaws this change takes place according to the growth, eruption,
wear and loss of teeth. With advancing age parts of the bone and the
osteocytes lose their vitality, and regeneration has to follow. All these
processes are made possible only by a coordination of destructive and
formative activities. Specialized cells, the osteoclasts, have the function
of eliminating overaged bony tissue or bone which is no longer adapted
to mechanical stresses.
 
Osteoclasts are multinucleated giant cells (Fig. 159, A). The number of
nuclei in one cell may rise to a dozen or more. However, it is to be noted
that, occasionally, uninuclear osteoclasts are found. The nuclei are
vesicular, showing a prominent nucleolus and little chromatin. The cell
body is irregularly oval or club-shaped and may show many branching
processes. In general, osteoclasts are found in bay-like grooves in the bone
which are called Howship’s lacunae; they are hollowed out by the ac-
tivity of the osteoclasts. The cytoplasm which is in contact with the
bone is distinctly striated. These striations have been explained as the
expression of resorptive activity of these cells. The osteoclasts seem to
produce a proteolytic enzyme which destroys or dissolves the organic con-
stituents of the bone matrix. The mineral salts thus liberated are re-
moved in the tissue fluid or ingested by macrophages. A decaleification
of bone during life has often been claimed but has never been demonstrated.
 
Osteoclasts differentiate from young fibroblasts or undifferentiated mes-
cnchymal cells probably by division of nuclei without the usual division of
204 ORAL msronoev AND EMBRYOLOGY
 
the cytoplasm. Some investigators believe that the osteoclasts may arise by
fusion of osteoblasts, others believe that they difierentiate from endothelial
cells of capillaries. The stimulus which leads to the diiferentiation of mes-
enchymal cells into osteoblasts or osteoclasts is not known. Osteoclastic
resorption of bone is partly genetically patterned, partly functionally
determined. Also overaged bone seems to stimulate the differentiation
of osteoclasts‘ possibly by chemical changes that are the consequence of
degeneration and final necrosis of the osteocytes.
 
New bone is produced by the activity of osteoblasts (Fig. 159, B). These
cells also difierentiate from fibroblasts or the undifferentiated mesenchymal
 
   
 
.i.«r~$
 
 
 
-u.0m
 
 
 
E
 
as
 
an’
 
Fig. 159.—Resorption and apposition of bone.
A. Osteoclasts in Howship’s lacunae
 
B. Osteoblasts al 11 a ho tr b la. La. 1 1
fomafion (high magngflmflolxbe. a ecu yer o osteo 1! tissue as a sign of bone
 
- cells of the connective tissue. Functioning osteoblasts are arranged along
 
the surface of the growing bone in a continuous layer, similar in appear-
ance to a cuboidal epithelium.
 
The osteoblasts are said to produce the bone matrix by secretion. The
matrix is at first devoid of mineral salts. At this stage, it is termed
 
—--———-up-‘ I. ‘ , ‘ Osteoblas
MAXJLLA AND MANDIBLE 205
 
osteoid tissue. It is still undecided Whether the fibrils of the matrix are con-
nective tissue fibrils which become embedded in the substance of the matrix,
or whether the fibrils difierentiate in the primarily amorphous matrix. If a
certain amount of matrix is produced some of the osteoblasts become em-
bedded in the matrix, and are known as osteocytes. Normally, the organic
matrix calcifies immediately after formation?’ 1‘ The ratio of organic and
inorganic substance in dry bone is approximately 1 :2. (See Table in
chapter on Enamel for complete data.)
 
5. INTERNAL RECONSTRUCTION OF BONE
 
The bone in the alveolar process is identical to bone elsewhere in the body
and is in a constant state of flux. During the growth of jaw bones, bone
is deposited on the outer surfaces of the cortical plates.. The changes
are most readily observed in the mandible, with its thick cortical
layer of compact bone. Here bone is deposited in the shape of basic
or circumferential lamellae (Fig. 157A). When the lamellae reach a cer-
tain thickness they are replaced from the inside by Haversian bone. This
is a reconstruction in accordance with the functional and nutritional de-
mands of the bone. In the Haversian canals, closest to the surface, osteo-
clasts differentiate and resorb the Haversian lamellae, and part of the cir-
cumferential lamellae. After a time the resorption ceases and new bone is
apposed onto the old. The scalloped outline of Howsh:1p’s lacunae which
turn their convexity toward the old bone remains visible as a darkly stained
cementing line, sometimes called the “reversal” line. This is in con-
trast to those cementing lines which seem to correspond to a rest period
in an otherwise continuous process of bone apposition; they are called rest-
ing lines (Fig. 157A). Resting and reversal lines are found between
layers of bone of varying age.
 
Another type of internal reconstruction is the replacement of compact
bone by spongy bone. This can be observed following the growth of the
bone when the compact outer layer has expanded to a certain extent.
The process of destruction can be observed from a section through bone,
by noting the remnants of partially destroyed Haversian systems, or
partially destroyed basic lamellae which form the interstitial lamellae of
the compact bone.
 
Wherever a muscle, tendon, ligament, or periodontal membrane is at-
tached to the surface of bone, Sharpey’s fibers can be seen penetrating
the basic lamellae. During replacement of the latter by Haversian sys-
tems fragments of bone containing Sharpey’s fibers remain in the deeper
layers. Thus, the presence of interstitial lamellae containing Sharpey’s
fibers indicates the former level of the surface.“
 
Alterations in the structure of the alveolar bone are of great impor-
tance in connection with the physiologic movements of the teeth. Thee
movements are directed mesio-occlusally. At the alveolar fundus the con-
206 ow. HISTOLOGY AND nnmzvonoer
 
tinual apposition of bone can be recognized by resting lines separating
parallel lavers of bundle bone; when the bundle bone has reached a cer-
 
tain thickness it is partly resorbed from the marrow spaces and then re-
placed by Haversian bone or trabeculae. The presence of bundle bone in-
dicates the level at which the alveolar fundus was previously situated. Dur-
ing the mesial drift of a tooth, bone is apposed on the distal, and resorbed
 
 
 
:4; .
. - ii‘ , ' "i L ‘I
‘ I
.1‘-pl:  __ ‘
‘L’ ’,  Cementum
‘3 V _ 1 fr
;-«-3.  '* ‘
‘  *‘ R ‘ "  ‘.
i. ‘ _ t l ‘
‘ v —- ._.- ———1>-'--—-L Resorptlon
R‘-' L .,z' a
' ; ‘ :-
t:-‘; v  ,1?-
?  ~-  Lamellated
  ‘ ‘F bone
, is _
lg i_ -‘_ - _- —— -~—-—. Periodontal
3". membrane
:3. «
sat:
lg)!’ ‘/
‘ _ 9 Resorptlon
__‘__-_ _ _ _ _ *9
A B.
 
Fig. 160.-—-Meslel drift.
.4. Appositlon of bundle bone on the distal alveolar wall.
3. Resorption of bone on the mesial alveolar wall. (Weinmann.”)
 
on the mesial, alveolar wall (Fig. 160). The distal Wall is made up almost
entirely of bundle bone. However, the osteoclasts in the adjacent marrow
 
spaces remove part of the bundle bone when it reaches a certain thickness.
In its place lamellated bone is laid down (Fig. 157B).
 
On the mesial alveolar wall of a drifting tooth signs of active resorption
are observed by the presence of Ho\vship’s lacunae containing osteo-
clasts (Fig. 160). Bundle bone on this side is present in relatively few
areas. When found, it usually forms merely a thin layer (Fig. 161). This
is due to the fact that the mesial drift of a tooth occurs in a rocking mo-
MAXILLA AND MANDIBLE 207
 
tion. Thus, resorption does not involve the entire mesial surface of the
alveolus at one and the same time. Moreover, periods of resorption
alternate with periods of rest and repair. It is during these rest
periods that bundle bone is formed, and detached periodontal mem-
brane fibers are again secured. It is this alternating action that stabil-
izes the periodontal membrane attachment on that side of the tooth.
Islands of bundle bone are separated from the lamellated bone by reversal
lines which turn their convexities toward the lamellated bone (Fig. 161).
 
Bundle bone
 
Dentin  1 ' ~  ‘ —~——- Reversal line
 
Lamellated bone
 
Periodontal mem-
brane
 
' " *" Reversal line
 
Bundle bone
 
’,1
 
__ - wan istin fly or simple lamellated bone; islands of
Fig‘ 161 bfiilhslglbghgecfigghoringcggisnd giuoé-s of the periodontal membrane.
 
6. CLINICAL CONSIDERATIONS
 
Bone is one of the hardest tissues of the human body. Nevertheless,
bone is, biologically, a highly plastic tissue. Where bone is covered by a
vascularized connective tissue, it is exceedingly sensitive to pressure
whereas tension acts, generally, as a stimulus to the production of new
bone. It is this biologic plasticity which enables the orthodontist to move
208 ORAL HISTOLOGY AND EMBRYOLOGY
 
teeth Without disrupting their relations to the alveolar bone. Bone is re-
sorbed on the side of pressure, and apposed on the side of 1361131011; thus
allowing the entire alveolus to shift with the tooth.
 
The adaptation of bone structure to functional stresses is quantitative
as Well as qualitative, namely, decreased function leads to a decrease in
the bulk of the bone substance. This can be observed in the supporting
bone of teeth which have lost their antagonists.’ Here, the spongy bone
around the alveolus shows marked rarefication: the bone trabeculae are
 
> ;_=; '- _ :75-;_"'  '_“."t’:  .
A. ' B.
Fig. 162.-—Osteoporosis of alveolar process caused by inactivity or the tooth _which has
no antagonist Labiolingual sections through upper molars of the same individual:
 
4. Disappearance of bony trabeculae after loss of function; plane or mesiobuccal
root; alveolar bone proper remains intact.
 
3. Normal spongy bone in the plane of mesiobuccal root or functioning tooth.
 
less numerous and very thin (Fig. 162). The alveolar bone proper, how-
ever, is generally well preserved because it continues to receive some
stimuli by the tension exerted upon it via principal fibers of the perio-
dontal membrane. A similar distinction in the behavior of alveolar and
supporting bone can be seen in certain endocrine disturbances and vita-
min deficienciesli 2 (Fig. 163).
 
The independence of the growth mechanisms of the upper and lower
jaws accounts for their frequent variations in relative size. Trauma or
inflammatory processes can destroy the condylar growth center of the
MAXILLA AND MANDIBLE 209
 
mandible on one or both sides. I-Iyperfunction of the hypophysis, leading
to acromegaly, causes a characteristic overgrowth of the mandible, even
at a time when sutural growth has ceased.“ The maxillary growth in
such cases is confined to bone apposition on the surfaces, because a gen-
eral enlargement of the upper face is impossible.
 
During healing of fractures or extraction wounds, an embryonic type
of bone is formed which only later is replaced by mature bone. The
embryonic bone, immature or coarse fibrillar bone, is characterized by
 
Fig. 163.—Dlflerence in reaction of alveolar bone and supporting bone:
4. Normal bone structure in bifurcation of dog's tooth.
 
B. Osteoporosis of supporting bone in bifurcation ot dog’s tooth. Dog fed on diet
deficient in nicotinic acid. Alveolar bone proper intact. (Similar conditions could be
produced by other dietary deficiencies.) (Courtesy H. Becks,’ University of California.)
 
the great number, great size, and irregular arrangement of the osteocytes
and the irregular course of its fibrils. The greater number of cells and
the reduced volume of calcified intercellular substance renders this im-
mature bone more radiolucent than mature bone. This explains why
bony callus cannot be seen in roentgenograms at a time when histologic
examination of a fracture reveals a well-developed union between the
210 omu. HISTOLOGY AND EMBRYOLOGY
 
fragments and why a socket after an extraction wound appears to be empty
at a time when it is almost filled with immature bone. The visibility in
radiograms lags two to three weeks behind actual formation of new bone.
 
References
 
1. Becks, H.: Dangerous Consequences of Vitamin D Overdoage on Dental and
Paradental Structures, J . A. D. A. 29: 1947, 1942. _ _
2. Becks, H.: The Efiect of Deficiencies of the Filtrate Fraction of the Vitamin
B C0mp1eX42 and Nicotinic Acid on Teeth and Oral Structures, J . Periodont.
13: 18 19 .
3. Bloom, W.: and Bloom, M. A.: Calcification and Ossification. Calcification of
Developing Bones in Embryonic and Newborn Rats, Anat. Rec. 78: 497,
1940.
4. Box, H. K.: Red Bone Marrow in Human Jaws, Toronto, 1933, University of
Toronto Press.
5. Breitner, C.: Bone Changes Resulting From Experimental Orthodontic Treat-
ment, Am. J. Orthodont. & Oral Surg. 26: 521, 1940.
6. Brodie, A. G.: Some Recent Observations on the Growth of the Mandible, Angle
Orthodontist 10: 63, 1940.
7. Brodie, A. G.: On the Growth Pattern of the Human Head From the Third
Month to the Eighth Year of Life, Am. J. Anat. 68: 209, 194].
8. Gottlieb, B.: Zur Aetiologie und Therapie der Alveolarpyorrhoe (Etiology and
Therapy of Alveolar Pyorrhea), Oesterr. Ztschr. f. Stomatol. 18: 59, 1920.
9. Kellner, E.: Histologische Befunde an antagonistenlosen Zfihnen (Histological
Findings on Teeth Without Antagonists), Ztschr. f. Stomatol. 26: 271, 1928.
10. Lehner, J., and Plenk, H.: Die Ziihne (The Teeth), Moellendorfis Handbueh d.
mikrosk. Anat., vol. 3, Berlin, 1936, Julius Springer.
11. McLean, F. 0., and Bloom, W.: Calcification and Ossification. Calcification in
, Normal Growing Bone, Anat. Rec. 78: 333, 1940.
12. Orban, B.: Dental Histology and Embryology, ed. 1, Chicago, 1928, Rogers
Printing Co.
13. Orban, B.: A Contribution to the Knowledge of the Physiologic Changes in the
Periodontal Membrane, J. A. D. A. 16: 405, 1929.
139.. Ritchey, B., and Orban, B.: The Crests of the Interdental Alveolar Septa,
J. Period. 1953 (in print).
14. Sclmfier, J .: Die Verkniicherimg des Unterkiefers (0ssification of the Mandible),
Arch. f. mikr. Anat. 32: 266, 1888.
15. Schoenbaner, F.: Histologische Befunde bei Kieferosteomyelitis (Histologic
Findings in Osteomyehtis of the Jaw), Ztschr. f. Stomatol. 35: 820, 1937.
16. Schour, I., and Massler, M.: Endocrines and Dentistry, J. A. D. A. 30: 595, 763,
943, 194.3.
17. Sicher, EL, and Tandler, J.: Anatomie fiir Zahniirzte (Anatomy for Dentists),
Vienna, 1928, Julius Springer.
18. Weinmann, J. P.: Das Knochenbild bei Stiirungen der physiologischen Wander-
ung der Z§.hne (Bone in Disturbances of the Physiologic Mesial Drift),
Ztschr. f. Stomatol. 24: 397, 1926.
19. Weinmann, J. P.: Bone Changes Related to Eruption of the Teeth, Angle Ortho-
dentist 11: 83, 1941.
19a. Woo, Fu-Kang: Ossification on Growth of the Human Maxilla, Premaxilla
and Palate Bone, Anat. Rec. 105: 737, 1949.
20. Zawisch-Ossenitz, C. v.: Die basophilen Inseln und andere basophile Elemente
im menschlichen Knochen (Basophilic Islands and Other Basophilic Elements
in Human Bone), Ztschr. f. mikr.-Anat. Forsch. 18: 393, 1929.
CHAPTER IX
 
THE ORAL MUCOUS MEMBRANE
 
1. GENERAL CHARACTERISTICS
 
2. TRANSITION BETWEEN SKIN AND MUCOUS MEMBRANE
 
3. SUBDIVISIONS 01‘ THE ORAL MUCOSA
 
A. Mastlcatory Mucosa
a. Gingiva
b. Epithelial Attachment and Gingival Sulcus
c. Hard Palate
 
B. Lining mucosa.
a. Lip and Cheek
b. Vestibular Fornix and Alveolar Mucosa
 
c. Sublingual Mucosa and Mucous Membrane of the Interior Surface
of the Tongue
(1. Soft Palate
 
C. Specialized Mucosa or Dorsal Lingual Mucosa
4. CLINICAL CONSIDERATIONS
 
1. GENERAL CHARACTERISTICS
 
The oral cavity, as the first part of the digestive tract, serves a variety
of functions. It is both the portal of entry and the place of mastication
of food. It contains the taste organs. Entering it is the fluid saliva
which not only lubricates the food to facilitate swallowing, but also con-
tains enzymes which initiate digestion. The oral cavity is lined through-
out by a mucous membrane. This term designates the lining of any
body cavity which communicates with the outside.
 
The morphologic structure of the mucous membrane varies in the
different areas of the oral cavity in accordance with the functions of
specific zones and the mechanical influences which bear upon them.
Around the teeth and on the hard palate, for example, the mucous mem-
brane is exposed to mechanical influences in the mastication of rough
and hard food, whereas, on the floor of the mouth, it is largely protected
by the tongue. This is the reason why the mucous membrane around
the teeth and on the hard palate varies in structure from that of the
floor of the mouth, cheeks, and lips.
 
The mucous membrane is attached to the underlying structures by a
layer of connective tissue, the submucosa, which varies in character in
different areas. The oral mucous membrane is composed of two layers;
the surface epithelium and the lamina propria (Fig. 164). A basement
membrane separates the lamina propria from the stratified squamous
 
First dratt submitted by Balint Orban and Harry slcher.
211
212 om rusronoer AND EMBRYOLOGY
 
epithelium. The epithelium consists of several layers of cells which flat-
ten out as they approach the surface. All these cells are connected with
each ‘other by intercellular bridges. The innermost is the basal layer,
consisting of cuboid cells which effect the attachment of the epithelium
to the basement membrane of the connective tissue by numerous short
basal processes that fit into grooves of the lamina propria. The more
superficial cells form the so-called “prickle-cell” layer which consists
of several layers of polyhedral cells. The term is derived from the fact
 
Keratlnous layer
 
Granular layer Opening 0! duct
 
Prickle cell layer
 
Basal layer
Basement
membrane ‘
— Subepithelial
Capillaries M’-We Plexus
Lamina propria.
Nerve
 
Submucous layer
 
Artery
Vein
 
Periosteum
 
Bone
 
Fig. 164.-—Diagra.mmatic drawing of oral mucous membrane (epithelium and lamina
propria. and submucosa).
 
that the intercellular spaces are wide and the intercellular bridges prom-
inent, thus giving the isolated cell a spinous appearance. Basal and
prickle-cell layers are sometimes referred to as germinative layers. Re-
generation of epithelial cells, lost at the surface, occurs by mitotic di-
vision of cells in the deepest layers.
 
The cells of the prickle-cell layer flatten and pass into first the granu-
lar layer and then the keratinous layer as they move toward the surface.
The cells of the granular layer contain fine kerato-hyalin granules which
are basophil and stain blue in hematoxylin-eosin preparation. The nuclei
ORAL MUGOUS MEMBRANE 213
 
of the flattened cells are pyknotic. The keratinous layer is characterized
by its acidophil nature; here the nuclei have mostly disappeared. The
structure of the granular and keratinous layers varies in the diiferent
regions of the oral cavity. A stratum lucidum, such as is seen in regions
of the skin where hornification is abundant, is, as a rule, missing in the
oral mucosa.
 
The lamina propria is a dense connective tissue layer of variable thick-
ness. Its papillae, which indent the epithelium, carry both blood
vessels and nerves. Some of the latter actually pass into the epithelium.
The papillae of the lamina propria vary considerably in length and width
in different areas. The inward epithelial projections between the papillae
are described as epithelial pegs, because of their appearance in sections.
They are in reality, however, a continuous network of epithelial ridges.
The arrangement of the papillae increases the area of contact between
lamina propria and epithelium, and facilitates the exchange of material
between blood vessels and epithelium. The presence of papillae permits
the subdivision of the lamina propria into the outer papillary, and the
deeper reticular layer.
 
The submucosa consists of connective tissue of varying thickness and
density. It attaches the mucous membrane to the underlying structures.
Whether this attachment is loose or firm depends upon the character
of the submucosa. Glands, blood vessels, nerves, and also adipose tissue
are present in this layer. It is in the submucosa that the larger arteries di-
vide into smaller branches which enter the lamina propria. Here they
again divide, to form a subepithelial capillary network in the papillae. The
veins originating from the capillary network follow the course of the
arteries. The blood vessels are accompanied by a rich network of lymph
vessels which play an important part in the drainage of the mucous mem-
branes. The sensory nerves of the mucous membrane traverse the sub-
mucosa. These nerve fibers are myelinated but lose their myelin sheath
in the mucous membrane before splitting into their end arborizations.
Sensory nerve endings of various types are found in the papillae; some
of the fibers enter the epithelium where they terminate in contact with
the epithelial cells as free nerve endings. The blood vessels are accom-
panied by nonmyelinated visceral nerve fibers which supply their smooth
muscles; other visceral fibers supply the glands.
 
The oral cavity can be divided into two parts: the vestibulum oris*
(vestibule) and the cavum oris proprium (oral cavity proper). The ves-
tibule is that part of the oral cavity proper which is bounded by the lips
and cheeks on the outer side, and by the teeth and alveolar ridges on the
inner. The oral cavity lies within the dental arches and bones of the
 
jaw, being limited posteriorly toward the pharynx by the anterior pillars
of the fauces.
 
‘The use of the terms vestibular instead of labial and buccal, and oral instead of
lingual or palatal, is suggested.
214 ORAL HISTOLOGY AND EMBRYOLOGY
 
2. TRANSITION BETWEEN SKIN AND MUCOUS MEMBRANE
 
The transitional zone between the skin covering the outer surface of
the lip and the true mucous membrane lining the inner surface, is the
red area or Vermilion border of the lip. It is present in man only (Fig.
165). The skin of the lip is covered by a hornified epithelium of mod-
erate thickness; the papillae of the connective tissue are few and short.
Many sebaceous glands are‘ found in connection with the hairs; sweat
glands occur between them. The epithelium is typically stratified and
squamous with a rather thick hornified layer. The transitional region
 
 
 
.
4
t.‘» ,  ‘T’ Red zone of
 
3*‘ _ lip
Mucous mem- —— »
brane of lip
: Skin of lip
 
Labial glands
 
‘  orbiculafis
~ "  ' oris muscle
 
Fig. 165.—Section through lip.
 
is characterized by numerous densely arranged long papillae of the
lamina propria, reaching deep into the epithelium and carrying large
capillary loops close to the surface. Eleidin in the epithelialcells renders
them translucent. Thus, blood is visible through the thin parts of the
transparent epithelium covering the papillae; hence the red color of the
lips. Because this transitional zone contains only occasional single
sebaceous glands, it is particularly subject to drying if not moistened
by the tongue.
ORAL MUCOUS MEMBRANE 215
 
The boundary between the red zone of the lip and the mucous mem-
brane is found where hornification of the transitional zone ends. The
epithelium of the mucous membrane of the lip is not hornified.
 
3. SUBDIVISIONS OF THE ORAL MUGOSA
 
In studying any mucous membrane the following features should be
considered: (1) type of covering epithelium; (2) structure of lamina
propria, especially as to its density, thickness, and presence or lack of
elasticity; and (3) its fixation to the underlying structures, in other
words, the submucous layer. A submucosa may be present or absent
as a separate and well-defined layer. Looseness or density of its texture
determines whether the mucous membrane is movably or immovably at-
tached to the deeper layers. Presence or absence and location of adipose
tissue or glands should also be noted.
 
The oral mucosa may be divided primarily into three different types.
During mastication some parts are subjected to strong forces of pres-
sure and friction. These parts, gingiva and covering of the hard palate,
may be termed masticatory mucosa. The second type of oral mucosa is
that which is merely the protective lining of the oral cavity. These areas
may be termed lining mucosa. They comprise the mucosa of lips and
checks; the mucosa of the vestibular fornix and that of the upper and
lower alveolar process peripheral to the gingiva proper; the mucosa of
the floor of the mouth extending to the inner surface of the lower
alveolar process; the mucosa of the inferior surface of the tongue; and
finally, the mucous membrane of the soft palate. The third type of
mucosa is represented by the covering of the dorsal surface of the tongue
and is highly specialized; hence, the term specialized mucosa.
 
A. Masticatory Mucosa
 
Gingiva and covering of the hard palate have in common the thick-
ness and hornification of the epithelium, the thickness, density, and firm-
ness of the lamina propria, and, finally, their immovable attachment to
the deep structures. Hornification is absent or replaced by para-
keratinization in some individuals whose gingiva otherwise has to be re-
garded as normal. As to the structure of the submucosa, these two areas
differ markedly. In the gingiva, a well-differentiated submucous layer
cannot be recognized; instead, the dense and inelastic connective tissue
of the lamina propria continues into the depth to fuse with the periosteum
of the alveolar process or to be attached to the cervical region of the
tooth.
 
In contrast to this, the covering of the hard palate has, with the excep-
tion of narrow areas, a distinct submucous layer. It is absent only
in the peripheral zone where the tissue is identical with the gingiva, and
in a narrow zone along the midline, starting in front with the palatine
or incisal papilla and continuing as the palatine raphe over the entire
length of the hard palate. In spite of the presence of a well-defined
216 ORAL HISTOLOGY AND EMBRYOLOGY
 
submucous layer in the wide lateral fields of the hard palate between
palatine raphe and palatine gingiva, the mucous membrane is immovably
attached to the periosteum of maxillary and palatine bones. This at-
tachment is accomplished by dense bands and trabeculae of fibrous con-
nective tissue Which join the lamina propria of the mucous membrane to
the periosteum. The submucous space is thus subdivided into irregular
intercommunicating compartments of various sizes. These are filled
with adipose tissue in the anterior part and with glands in the posterior
part of the hard palate. The presence of fat or glands in the submucous
layer acts as a hydraulic cushion comparable to that which We find in the
subcutaneous tissue of the palm of the hand and the sole of the foot.
 
The presence or absence of a distinct submucous layer permits the sub-
division of the masticatory oral mucosa into the non—cushioned and the
cushioned zones. The non-cushioned zone consists of the gingiva and
the palatine raphe, the cushioned zone consists of the remainder of the
mucosa covering the hard palate.
 
A. GINGIVA
 
The mucous membrane surrounding the teeth, the gingiva, is sub-
jected to forces of friction and pressure in the process of mastication.
The character of this tissue shows that it is adapted to meet these
 
.7. 7 .. . T.‘
Alveolar R
 
 
 
 
mucosa.
-- “T Mucoginglval
Junction
Att hed —— —— ' ‘
{if in « -.,A r, F”? Interdental
g g  .— ,_“,~-~, papilla.
P
Free g'ing'lva.1 Attifilcéligi
g’°°"° Migicogingival
1 * _ junction
Alveo ar 1-vi" ..
mag.
mucosa 9. A \
_ * __ — _
 
Fig. 166.—Sur1‘a.ce of the gingivu of a young adult.
 
stresses. The gingiva is sharply limited on the outer surface of both jaws
by a scalloped line (mucogingival junction) which separates it from the
alveolar mucosa (Fig. 166). The gingiva is normally pink, sometimes With
a grayish tinge, a variation which is partly caused by differences in the
thickness of the stratum corneum. The alveolar mucosa is red, showing
numerous small vessels close to the surface. A similar line of demarcation
-‘M. ‘.g;-.;, 7,
 
Keratinous layer:jg__*,.:£, M  '
 
 
 
cells
 
Flattened surface  P v w ' , V
 
 
 
Parakeratotic ">
layer
3
 
g > .
 
3, ’ ._ ‘ ’f‘i
 
' in ‘ '
Prickle ce11s_" '*‘ 4%
 
3...
 
4
 
' 1’ ""4" *‘ ’ " ' ' ‘——, ’=' Basal layer
 
Fig. 167.——Varia.tions of glnglval epithelium.
A. Hornmcatlon.
 
B. No hornmcation.
 
0'. Paxakeratonia.
218 ORAL HISTOLOGY AND EMBRYOLOGY
 
is found on the inner surface of the lower jaw between gingiva and the
mucosa on the floor of the mouth. In the palate, there is no sharp dividing
line because of the dense structure and firm attachment of the entire
palatal mucosa.
 
Normally, the epithelium of the gingiva is hornified on its surface
(Fig. 167, A) and contains a granular layer. In the absence of hornifica-
tion (Fig. 167, B) there is no granular layer and the flat surface cells con-
tain nuclei which are, frequently, pyknotic. Other cases show a partial
or incomplete hornification (Fig. 167, 0) characterized by a well-defined
 
 
   
 
 
 
Epithelium? —  . f X ' ' H
{Q t,"  -Pngarggrlxted
 
I layer
‘ V i.
If " ‘ . "~
 
I Connective
tissue
 
Fig. 168A..—Pig'ment in basal cells of gingiva. of a. Negro.
 
surface layer containing flat cells which have lost their boundaries. Nuclei
are present but are extremely flat and pylmotic; this condition is termed
parakeratosis. All transitions from nonhornified to parakeratotic and
hornified epithelium of the gingiva should be considered as Within the
range of normal.
 
The epithelium covers the margin of the gingiva and continues into the
epithelial lining of the gingival sulcus to terminate on the surface of the
 
tooth as the epithelial attachment (see section on Epithelial Attach-
ment).
ORAL MUCOUS MEMBRANE 219
 
The cells of the basal layer may contain pigment granules (melanin)
 
(Fig. 168:1). While pigmentation is a normal occurrence in Negroes, it is
often found, too, in the white race, especially in people with dark com-
plexion. When found, it is most abundant in the bases of the inter-
dental papillae. It may increase considerably in cases of Addison’s
 
u— -*‘—"—*“‘ a
 
Fig. 168B.——Dendritic melanoblasts in the basal layer of the epithelium. Biopsy of
normal gingiva. (x1000.) (Courtesy Esther Carames de Aprile, Buenos Aires.)
 
1..
 
'5'-i:..
 
Fig. 1680.—Macropha.ges in the normal gingiva.._ Rio I-Iortega. stain. ()(1000.)
(Courtesy Esther Carames de Aprile, Buenos Aires.)
 
disease (destruction of the adrenal cortex). The melanin pigment is
stored by the basal cells of the epithelium, but these cells do not produce
the pigment. The melanin is elaborated by specific cells, melanoblasts,
situated in the basal layer of the epithelium (Fig. 168, B). These cells
have long processes and are also termed “dendritic” cells. In the usual
hematoxylin-eosin specimen, these cells appear with a clear cytoplasm and
are also known as “clear cells.”
220 ORAL I-1I§'l‘0LOGY AND EMBRYOLOGY
 
The lamina propria of the gingiva consists of dense connective tissue
Which is not highly vascular. Macrophages are present in the normal
ging-iva (Fig. 168, C). These cells play an important function in the de-
fense mechanism of the body. The papillae are characteristically long,
slender, and numerous. The presence of these high papillae permits the
sharp demarcation of the gingiva and alveolar mucosa in which the papillae
are quite low (Fig. 169). The tissue of the lamina propria contains only
few elastic fibers which are, for the most part, confined to the walls of the
 
 
 
 
Hard palate
 
   
 
—h—- Alveolar
mucosa.
 
 
, .- .’
‘ w.a,~;L.i' 1 Emu .
 
Fig. 169.—Structura1 dlflferences between glngiva. and alveolar mucosa. Region of
- upper bicuspid.
 
blood vessels. The gingival fibers of the Pariodontal membrane enter into
the lamina propria, attaching the gingiva firmly to the teeth (see chapter
on Periodontal Membrane). The gingiva is also immovably and firmly at-
tached to the periosteum of the alveolar bone; here, a very dense connective
tissue, consisting of coarse collagenous bundles (Fig. 170, A) extends from
the lamina propria to the bone. In contrast, the submucosa underlying the
alveolar mucous membrane is loosely textured (Fig. 170, B). The fiber
bundles of the lamina propria are here thin and regularly interwoven.
The alveolar mucosa and the submucosa contain numerous elastic fibers
which are thin in the lamina propria and thick in the submucosa.
omu. MUCOUS MEMBRANE 221
 
The gingiva. is well innervated.“ Difierent types of nerve endings can
be observed, such as the Meissner 01- Krause eorpuscles, end bulbs, loops or
fine fibers. Fine fibers enter the epithelium as “ultra-terminal” fibers.
(Figs. 171A and B.)
 
 
 
, S. ,
Lamlna propria L "
 
Submucosa
 
Epithelium
 
Lamina proprla.
 
Submucosa.
 
Fig. 170.—Differences between ging-Iva. (A) and alveolar mucosa (8). Silver im-
pregnation ot collagenous fibers. Note the coarse bundles of fibers in glngiva. and finer
fibers in alveolar mucosa.
 
The gingiva can be divided into the free gingiva and attached
gingiva (Figs. 172A and 172B).” The dividing line between these two
parts of the gingiva is the free gingival groove which runs parallel
to the margin of the gingiva at a. distance of 0.5 to 1.5 mm. The free
222 omu. HISTOLOGY AND EMBRYOLOGY
 
0».
 
 
:
 
Fig. 171A.—Meissner tactile corpuscle in the human gingiva. S_i1veg- impregnation
after Bielschowsky-Gros. (Courtesy F. VV. Gan-ns and J. AltchlS0n.3“)
 
 
. 1:
 
Fig. 171B.——-Intraepithelial “uli:raterminal" extensions and nerve endings in the human
 
gingiva. Silver impregnation after Bielschowsky-Gros. (Courtesy F. W. Gaitns and J.
A.itchiaon.'-)
ORAL MUCOUS MEMBRANE 223
 
   
 
Marginal
 
   
 
Inter-
 
—'—‘ glngiva
dental Fr”
pagirlla. / gingiva
 
. 93 Margin of
gigrgoggé the gingiva.
 
Inter- ‘' ° ° ° ' ° ‘’ Fr.“
dental o , ° I ,, ° 6 0 II‘ o 0 _ ‘’ H 0 ° ° gmgival
‘°‘‘‘s -» ., ~ ‘’ ., ,° ° ,, ° . " .. ,° . "—_.._._° A‘?'t2‘3’.§a
., ° ' 0 glngive.
 
3 6
_Muco- ° ” G (stippled)
 
gmgwal
junction
Alveolar
mucosa
 
Fig. 172A.—Diag'ram illustrating the surface characteristics of the gingiva.
 
Margin of the
glngiva.
 
Free ginglva.
 
Free gingival
groove
 
Attached gingiva
( stlppl ed )
 
Mucogingival
Junction
 
Alveolar mucosa.
 
   
 
-¢_—.r‘.—"‘..
 
 
 
—
.4-
.1‘
 
 
 
Fig. 172B.—Diag-ram illustrating the diflerence between the tree ginglva. attached
glnglva, and alveolar mucosa.
224 ORAL HISTOLOGY AND EMBRYOLOGY
 
gingival groove is, on histologic section (Fig. 173), a shallow V-shaped
groove corresponding to the heavy epithelial ridge which divides the free
and the attached gingiva. The free gingival groove develops at the
level of, or somewhat apical to, the bottom of the gingival sulcus. In
 
' 9  ’../,2",-I 'j}r""‘_ 
 
1 .
 
   
 
——.-- Free ginglval
groove
 
 
 
 
- »»»» ——»-—— . —— . A .-«r‘x".‘.&=;
 
Fi§- 173-—Bi0Dsy specimen of gingiva. showing_ tree gingival groove and stippled at.
tached ging-Ava.
 
501119 03868, the free gingival groove is not as Well defined as in others,
and then the division between the free and attached gingiva is not clear.
The tree gingival groove and the epithelial ridge are brought about by
functional impacts upon the free gingiva, folding the movable free part
back upon the attached and immovable zone.
ORAL MUCOUS MEMBRANE 225
 
The attached gingiva is characterized by high connective tissue papillae
elevating the epithelium, the surface of which appears stippled (Fig. 173).
Between the elevations there are small depressions which correspond to
the center of heavier epithelial ridges and show signs of degeneration
and hornification at their depth. The stippling is most probably an ex-
pression of functional adaptation to mechanical impacts. The degree of
 
.,-.,.,3,..,
  ' ‘Oral epithelium
 
«- K .
~ /, : ‘ Reduced enamel
“ g _ ' " ‘ epithelium
 
 
 
 
 
Enamel
 
Reduced enamel
epithelium
 
Pulp
 
 
.1 ‘ -’
Cemento-enamel
 
.  junction
 
   
 
iii;
l » ,
-.I----=- :9: _Periodonta.l mem-
 
., ‘; ‘E brane
 
sea
 
3,
' ,‘»".
T’ *1
 
1 .
 
 
 
 
Undeveloped apical
 
   
 
Fig. 174.—I-Iuman permanent incisor. The entire surface of the enamel is covered
léybrediiced enamel epithelium. Mature enamel is lost by decalciflcation. (Gottlieb and
1- an. )
 
stippling varies with different individuals. The disappearance of stip-
pling is an indication of edema, an expression of an involvement of the
attached gingiva in a progressing gingivitis.
 
The attached gingiva appears slightly depressed between adjacent teeth,
corresponding to the depression on the alveolar bone process between
eminences of the sockets. In these depresssions, the attached gingiva
often forms slight vertical folds.
226 ORAL I-IISTOLOGY AND EMBRYOLOGY
The interdental papilla is that part of the gingiva that fills the space
 
between two adjoining teeth and is limited at its base by a line connect-
ing the margin of the gingiva at the center of one tooth and the center
 
Ora.l——— -—-—  2. .'
epithelium , Q "K;
 
Fusion oi’ oral
 
and enamel "3 .,g
epithelium , , f V.‘
._ .
 
I ‘~ _ ""”'—“—'.‘1{e(luced enamel
 
~ ._ ' __ epithelium
( ,, an
Reduced enamel :15,’ <-‘J
epithelium § 93;‘? -
. .5‘.
 
 
Fusion of oral and enamel
epithelium X
 
Oral epithelium
 
Cemento-enamel junction
 
cementum
 
 
Fig. 175.—Rednce_d enamel epithelium fuses with oral epithelium. X in the diagram
indicates area from which the photomlcrograph was taken.
 
of the next. The interdental papilla is composed of free gingiva and at-
tached gingiva in various relations, depending largely upon the relation-
ship of the neighboring teeth.
ORAL MUCOUS MEMBRANE 227
 
B. EPITHELIAL ATTACHMENT AND GI.\‘GIVAL SULcus*
 
At the conclusion of enamel matrix formation the ameloblasts pro- De"91°Pm°nt
 
duce a thin membrane on the surface of the enamel: the primary enamel
cutwle. It is a. limiting membrane, connected with the intei-prismatic
 
L
our ll - -- “ oral
epithelium ' " - epithelium
.' F.
4-Gr * .
. in
 
Enamel ’ "‘-—“  J‘ ".73"
cuticle ‘r.
.-9.
 
- "3' Y‘
 
5* -it
 
” Epithelial
Enamel , attachment
 
 
.1: ,
Epithelial
‘I
 
attachment _.
 
 
 
Reduced enamel epithelium
(now epithelial
attachment)
 
Dentin
 
Pulp
 
Cemento-enamel junction
 
Cementum
 
Fig. 176.—'I‘ooth emerges through a perforation in the fused epithelial. X in the diagram
indicates area from which the photomicrograph was taken.
 
enamel substance. The ameloblasts shorte11 after the enamel cuticle
is formed, and the epithelial cells comprising the enamel organ are re-
duced to a few layers of cuboidal cells which are then called reduced
 
‘First draft of this section submitted by Bemliard Gottlieb.
228 ORAL HISTOLOGY AND EMBRYOLOGY
 
enamel epitheliunt. Under normal conditions it covers the entire enamel
surface extending to the cemento-enamel junction (Fig. 174) and re-
mains attached to the primary enamel cuticle. During eruption the tip
of the tooth approaches the oral mucosa and the reduced enamel epi-
thelium fuses with the oral epithelium (Fig. 175).
 
The epithelium which covers the tip of the crown degenerates in its
center, and the crown emerges through this perforation into the oral
cavity (Fig. 176). The reduced enamel epithelium remains organically
attached to that part of the enamel which has not yet erupted. Once
the tip of the crown has emerged, the reduced enamel epithelium is
termed the epithelial attachment.‘ At the marginal gingiva the epithelial
attachment continues into the oral epithelium (Fig. 177). As the tooth
 
Erupted enamel
Glngival sulcus
Free gingiva
 
Oral epithelium
 
Epithelial attachment
 
Enamel
 
Cemento-enamel
junction
 
Dentin
 
Pulp
 
Fig 177.—Diagramma.tic illustration of epithelial attachment and gingival sulcus at an
early stage of tooth eruption. Bottom of the sulcus at x.
 
erupts, the epithelial attachment is gradually separated from its surface.
The shallow groove which develops between the gingiva and the surface
of the tooth and extends around its circumference is the gingival sulcus
(Fig. 177). It is bounded by the surface of the tooth on one side, and
by the gingiva on the other. The bottom of the sulcus is found where
the epithelial attachment (formerly reduced enamel epithelium) separates
from the surface of the tooth. The part of the gingiva which is coronal
to the bottom of the sulcus is the marginal gingiva. While the epithelial
attachment is separated from the surface of the enamel, it produces often
the secondary enamel cuticle} This is a hornified layer, 2 to 10 microns
in thickness.
ORAL MUCOUS MEMBRANE
 
A. B. 0.
 
Fig. 178.-—Three sections oi.’ the same tooth showing different relations of tissues at cemento-enamel junction.
4. Epithelial attachment reaching to cemento-enamel Junction.
 
B. Epithelial attachment leaves the enamel free at cemento-enamel junction.
 
0. Epithelial attachment covers part or the cementum. cementum overlaps the end of the enamel.
 
EA = epithelial attachment; E = enamel (lost in decaiciflcetion); 0 = cementum: X = end of epithelial attach-
ment. (Or-ba.n.")
 
229
$5
 
230 omu. HISTOLOGY AND EMBRYOLOGY
 
In erupting teeth the epithelial attachment extends to the cemente-
enamel junction (Fig. 177). Occasionally, the epithelium degenerates in the
cervical areas of the enamel; then the surrounding connective tissue
frequently deposits cementum upon the enamel. This does not always
occur aI'Ol111(l the entire surface of a tooth. Different sections of the
same tooth may, and frequently do, show varying relationships in the
area Where enamel and cementum meet (Fig. 178).
 
Enamel
 
Cuboidal cells of
epithelial attach-
ment
 
Flattened cells in
epithelial attach-
ment
 
Dentin
 
: Basal cells of
epithelial attachment
 
 
 
Cemento-enamel
junction
 
Fig. 179.——Arra.ngement of cells in the epithelial attachment indicate functional in-
fluences. (Orban.“')
 
The epithelial attachment is the derivative of the reduced enamel
epithelium. In some cases, ameloblasts may still function at the apical
end of the attachment when the tip of the crown has already emerged
through the oral mucosa. The ameloblasts flatten out rapidly and then
the reduced enamel epithelium forms the epithelial attachment. This
is thin at first and consists of 3 to 4 layers of cells (Figs. 181, 182) but
thickens gradually with advancing age to about 10 to 20 rows of cells,
or more (Figs. 183, 184).
 
The epithelium which forms the attachment is stratified squamous
epithelium. As a rule, the junction between epithelial attachment an_d
connective tissue is smooth. It may be considered as a sign of irrita-
tion if the epithelial attachment sends fingerlike projections, epithelial
pegs, into the conective tissue. The cells within the epithelial attach-
ORAL MUCOUS MEMBRANE 231
 
ment are elongated, and are arranged more or less parallel to the surface
of the tooth (Fig. 179). There is a distinct pattern in the direction of
these flattened cells which may be the result of functional influences
upon the attachment.“ The cells at the surface of the epithelial attach-
ment are firmly fastened to the tooth and must follow all its movements.
The basal layer of the epithelial attachment, on the other hand, is
anchored to the surrounding connective tissue and must follow all the
movements to which the gingival margin is subjected. The cells within
the epithelial attachment are exposed to these different stresses. The
 
-. Epithelial bridge cross»
ing tear in attachment
 
Epithelial cells attached
to cementum
 
p Epithelial bridge cross-
ing tear in attach-
ment
 
‘ Epithelial attachment
torn from cementum
 
 
 
Epithelial cells attached
‘ ‘Q to cementum
¥
 
 
 
Fig. 180.—Artitlcia1 tear in epithelial attachment. Some cells are attached to the
‘ cementum, others bridge the tear. (Orban and Muellenl‘)
 
attachment of the surface cells to enamel or cementum seems to be more
firm than the connection of these cells to the deeper layers of the epi-
thelium. For this reason tears occur frequently between the cuboidal
cells attached to the tooth and the rest of the epithelial attachment.
Such tears are found as artifacts in microscopic specimens (Fig. 180) but
 
may also occur during life.“
shift of
Epithelial
Attachment
 
First Stage
 
232 omu. HISTOLOGY AND EMBRYOLOGY
 
The relation between epithelial attachments and the surface of the
tooth changes constantly. When the tip of the enamel first emerges
through the mucous membrane of the oral cavity, the attachment
covers almost the entire enamel (Fig. 181). Tooth eruption is relatively
fast (see chapter on Tooth Eruption) until the tooth reaches the plane
of occlusion. This causes the epithelial attachment to separate from
the enamel surface, gradually exposing the crown. When the tooth
reaches the plane of occlusion, one-third to one-fourth of the enamel is
still covered by the epithelial attachment (Fig. 182). The gradual ex-
 
 
 
I
I
I
I
/I ‘
I \
rll
II \
I \
I \
F ’ I \
ree(gnn§:;:i \\ Free gingiva
sulcus) \ -
- ' ’ ' ""‘ Gingival sulcus
Enamel
Dentin - —- - ‘ Enamel
Epithelial —-' E lth ll l tta -
attachment Bnelfta 8' ch
_ " *"»-"' Pulp
Cementmenamel —— .
junction  _
 
" '—'- Cemento-enamel
Junction
 
Fig. 181.—Epithelial attachment and glngival sulcus in an erupt‘ t th.
of enamel is indicated by dotted line. Enamel lost in decalcifllgagtloii? (K1:-J¢!:'ii.i!)etl%1.1°‘))ut
 
posure of the crown by separation of the epithelial attachment from the
enamel is known as passive eruption. The simultaneous elevation of
the teeth, toward the occlusal plane, is termed active eruption (see chap-
ter on Tooth Eruption).
 
The bottom of the gingival sulcus remains in the region of the enamel-
covered crown for some time, and the apical end of the epithelial attach-
ment stays at the cemento-enamel junction. This relationship of the
epithelial attachment to the tooth characterizes the first stage in passive
omu. MUCOUS MEMBRANE 233
 
eruption (Fig. 183). It persists in primary teeth almost up to one year
before shedding and, in permanent teeth, usually to the age of about twenty
or thirty; however, this is subject to great variations.
 
The epithelial attachment forms, at first, a wide band around the cervical
part of the crown which becomes gradually narrower as the separation
of epithelium from the enamel surface proceeds. Long before the bottom
of the sulcus reaches the cemento—enamel junction, the epithelium pro-
liferates along the surface of the cementum and the apical end of the
 
=‘ as
 
 
 
 
Enamel T
‘I
9
Dentin *'“" '*
-:
V \ Gingival sulcus
.. _, ,3,‘
-4 p ’_ Free gingiva.
.
g“‘“ '' " —. Epithelial attachment
Cemento-enamel '— ""
junction
 
' 4' 4 Alveolar crest
 
Fig. 182.—Tooth in occlusion. One-fourth of the enamel is still covered by the epithelial
attachment. (Kr-onfeld."')
 
epithelial attachment is then found in the cervical part of the root, on
the cementum. This is the second stage in the passive eruption of teeth.
In this phase the bottom of the gingival sulcus is still on the enamel; the
apical end of the epithelial attachment has shifted to the surface of the
cementum (Fig. 184).
 
The downgrowth of the epithelial attachment along the cementum is
impossible as long as the gingival and transseptal fibers are still intact.
It is not yet understood whether the degeneration of the fibers is
 
Second stage
Third Stage
 
234 omu. msronoev AND EMBRYOLOGY
 
primary or secondary to the proliferation of the epithelium.“ Recent
findings indicate that destruction of the fibers is secondary, the proliferat-
ing epithelial cells actively dissolving the principal fibers byenzymc action
(desmolysis). A primary destruction of the principal fibers had been ex-
plained by the action of bacterial toxins from the gingival sulcus. The
second stage of passive tooth eruption may persist to the age of forty or
 
Enamel cuticle
 
Bottom 01
glnglval
snlcus
 
Enamel
 
Epithelial
attachment
 
Cemento-enamel
junction
 
Cementum
 
Fig. 183.—-Epithelial attachment on the enamel. First stage in passive tooth eruption.
(Gotflieb and Orbanfi)
 
later. With advancing age the epithelial attachment further separates
from the enamel surface, and the apical end of the epithelium continues
to grow down along the cementum.
 
For a short time, the bottom of the gingival sulcus is just at the cemente-
enamel junction, the epithelial attachment is entirely on the cementum,
and the enamel-covered crown is exposed (Fig. 185). This is the third
stage in passive tooth eruption. Because of the continuous active and
235
 
ORAL MUCOUS MEMBRANE
 
 
 
Fre_e
gmgiva
 
gingival
sulcus
 
0-.
0
m
o
t
t
o
B
 
Epithelial
attachment
to enamel
 
Cemento-enamel
 
junction
 
cementum
 
Epithelial , . _
attachmentn -‘«‘
to cementum .
 
End of
epithelial
attachment
 
 
Second
 
Fig. 184.—EpitheIia.l attachment partly 01.1 the enamel, partly on the cementum.
stage in passive tooth eruption. (Gottiieb and Oz-ba.n.')
E‘ourth Stage
 
236 ORAL HISTOLOGY AND EMBRYOLOGY
 
passive eruption of the teeth, the epithelium shifts gradually along
the surface of the tooth and the attachment does not remain at the linear
cemento-enamel junction for any length of time. The third stage in
passive eruption marks only a moment in a more or less continuous proc-
ess. If a part of the cementum is already exposed by separation of the
 
Enamel
 
 
 
1 E
 
,’ . Bottom of Einglval
. I sulcus
 
I ‘ !
, .
 
Cemento-enamel -
junction
 
 
Oral epithelium
 
Epithelial
attachment ;
 
 
End of epithelial - j ' _ "L _ '
attachment , .
 
Fig. 185.—Epithelial attachment on the cementum; bottom of the gingival sulcus at the
cemento-enamel junction. Third stage in passive tooth eruption. (Gottlieb.')
 
epithelial attachment from the tooth surface, the fourth stage of passive
eruption is reached. The epithelium is entirely attached to the cementum
(Fig. 186).
 
It would appear that the epithelial attachment has to maintain a cer-
tain Width* to assure normal function of the tooth. Therefore, this
proliferation along the cementum should be considered a physiological
 
 
'The width of the epithelial attachment varies from 0.25 to 6 mm.“
ORAL MUCOUS MEMBRANE 237
 
process, if it is in correlation to active eruption and attrition. If it
progresses too rapidly or precociously and loses, therefore, correlation
to active eruption, it must be considered as a pathologic process.
 
An atrophy of the gingiva. is correlated with the apical shift of the
epithelial attachment, exposing more and more of the crown, and, later,
of the root, to the oral cavity. The recession of the gingiva is therefore
a physiologic process if it is correlated both to the occlusal wear and to
the compensatory active eruption.
 
.*"*r.--vj _"“'*'~""""" '
x 1-: - ‘ .» - ,, . a
 
 
 
Enamel
 
‘ .
 
Cemento~ena.mel
junction
 
Free gingiva.
 
 
Cementum
(exposed)
 
Bottom of gingival
sulcus
 
Free gingival groove  -,  V‘
 
cementum
 
 
Oral epithelium " —'
 
'7 End of epithelial
attachment
 
 
Fig. 186.—Epithelial attachment on the cementum; bottom of_the ginglva-1 sulcns also
on the cementum Fourth stage in passive tooth eruption. (Gott1ieb_6)
 
The rate of passive tooth eruption varies in difierent persons, and in
different teeth of the same individual, as well as on different surfaces
of the same tooth. In some cases, the fourth stage of passive tooth erup-
tion is observed in persons during their twenties; in others, even at the
age of fifty or later, the teeth are still in the first or second stage of erup-
tion. The rate varies also in diflerent teeth of the same jaw: the earlier
,-,.,,_ __ _ K
 
88%
 
l'.‘)O'l0.\lI9I-\I(E[ (INV ;\’9()’I0£|LSIl-I 'IV}IO
 
A. B. C.
 
Fig. 187.—-Three sections of the same tooth showing different relationship of soft to hard tissues.
A. Bottom of the sulcua on the enamel (second stage).
 
B. Bottom of the sulcus at cemento-enamel junction (third stage).
 
0. Bottom of the aulcua on cementum (fourth stage).
 
E = enamel lost in decalciflcation—outline indicated by dotted line; EA = epithelial attachment; 5: - bottom of
 
gingival sulcus: mm = and of epithelial attachment. ’
Mode of At-
tachment of
Epithelium
 
 
ORAL MUCOUS MEMBRANE 239
 
a tooth erupts, the more advanced can be its passive eruption. Even
around the same tooth there is a variation; one side may be in the first
stage, the other in the second or even the fourth stage (Fig. 187). At
no time are all parts of the bot_tom of the gingival sulcus in the same
relation to the tooth.
 
Gradual exposure of the tooth to the oral cavity makes it possible
to distinguish between the anatomical and clinical crowns of the tooth
(Fig. 188). That part of the tooth which is covered by enamel is the
anatomical crown; the clinical crown is that part of the tooth exposed
in the oral cavity.“ In the first and second stages, the clinical crown
 
II III IV
 
Fig. 188.—Diagrammatie illustration of the four stages in passive tooth eruption:
in Stages I and 11 the anatomic crown is larger than the clinical; in Stage III anatomic
and inical crowns are equal; in Stage IV the clinical crown is larger than the
anatomic. The arrow in the small diagram indicates the area from which the draw-
ings were made.
 
E = enamel; E4 = epithelial attachment; 0 = cemento-enamel junction; 5.‘ = bot-
tom of gingival sulcus.
 
is smaller than the anatomical. In the third stage, the enamel-covered
part of the tooth is exposed and the clinical crown is equal to the ana-
tomical. It should be emphasized that this condition is not actually
encountered, because the bottom of the gingival sulcus is never at the
same level all around the tooth. In the fourth stage the clinical crown
is larger than the anatomical because parts of the root have been ex-
posed.
 
The means by which the epithelium is attached to the enamel is not
as yet fully understood. Several explanations have been advanced.
Formerly it was claimed that the epithelium is not organically attached
to the tooth but is kept in place by tissue tone and elasticity of the con-
240 ORAL HISTOLOGY AND EMBRYOLOGY
 
nective tissue of the gingiva pressing the epithelium against the tooth
surface. This concept has been disproved by microscopic evidence,
which shows that there is an organic union between the epithelium and
the tooth surface. The strength of the attachment was demonstrated by
the following experiment: The teeth and surrounding tissues in young
dogs were frozen and ground into relatively thin sections. These were
placed under the dissecting microscope, and the free margin of the
giiigiva was pulled away from the tooth with a needle. By this method
it was possible to demonstrate that the attachment can be severed from
 
Epithelial
attachment
 
Epithelial
 
'3. attachment
 
to  189.—e-LG:-ound section of hard and soft tissues of teeth. Epithelial attachment
 
A. General view of inter-dental papilla.
3- Higher ma.g'nifl<‘£ti011 01 Elnsival sulcus and epithelial attachment
 
#4: ‘L fnaettnzfliafiaf a‘l€.?;‘l,‘;.§e.§iP($m‘;%‘:.Ef€.Ea?;:’éi“ji..f‘cu‘:‘n ,‘t°*‘€§3,d:£k§‘:z‘;,;Lb:‘:§g:;
the tooth only to a certain depth; from there on it tears instead of
separating from the tooth.” The firmness of the attachment may be
further shown by studying ground sections prepared by a. special method
of investing soft and hard tissues (Fig. 189). In such specimens the
enamel. is not lost as in decalcified sections, and the relations between
epithelium and enamel are undisturbed. Another confirmation of the
organic connection between tooth surface and epithelium is the fact that,
omar. MUCOUS MEMBRANE 241
 
after extraction of teeth, epithelium is often found adherent to the ex-
tracted tooth,’ The firm connection between epithelium and enamel is
a primary 11111011, the enamel being a cuticular product of the ameloblasts.
 
The layer of the epithelial attachment that is attached to the surface of the
enamel is the regressed ameloblast layer.
 
It has also been claimed that the secondary cuticle plays an important
role in cementing the epithelium to the surface of the tooth. This cuticle‘
is a hornified structure, homogenous and brittle. It lies outside the pri-
mary enamel cuticle (see chapter on Enamel) and stains bright yellowish-
red in hematoxylin-eosin preparations. It is resistant to acids and
 
Secondary '< ' l
enamel
cuticle
 
   
 
 
Epithelial  . .
 
attachment a l
 
‘ .
 
Cemento- —— --
enamel
junction
 
Cements.)
cuticle ;
(dental .’
 
cuticle)’  fl “j
s §:}is._.
 
31
 
Fig. 190.—Seconda.ry enamel cuticle follows epithelial attachment to the cementum
forming the “dental cuticle." Arrow in diagram indicates area. from which the photo-
micrograph was taken.
 
 
 
 
alkalies and may act as a protective layer on the tooth surface. Even
yet its method of formation is not quite clear: some investigators claim‘
that it develops by transformation of the cells which are adjacent to
the tooth surface in a manner similar to normal hornification. Others
contend that this cuticle is a secretory product of the epithelial cells.“
The secondary cuticle is not limited to the surface of the enamel, as
is the primary cuticle, but follows the epithelial attachment when it shifts
along the cementum; hence it is designated by the term cuticula. dentis
The Gtngival
suleus
 
242 ORAL msronocv AND EMBRYOLOGY
 
(dental cuticle) (Fig. 190). The formation of the dental cuticle by the
epithelial attachment is believed to be a reaction of the epithelium to
its contact with a hard structure. It is further assumed that formation
of the cuticle is the first phase of a process which, ultimately, leads to
separation of the epithelium from the tooth. However, some investi-
gators claim that this cuticle is a pathologic structure, induced by in-
flammation of the gingiva."
 
~7
Cuticle
:l'l‘
F."
cementum  '
xx’,
‘.1:
 
5'3:
'  Extension or cuticle Into
_ ' space in cementum
Dentin _ "
 
 
Fig. 191.—Horny substance of the dental cuticle extends into the spaces of the cementum.
(Gottlieb and Orbanfi)
 
The mechanism of attachment of the epithelium to the enamel is still
open to further investigation. The attachment of the epithelium to the
cementum is accomplished by fine processes of the epithelial cells, ex-
tending into minute spaces of the cementum where Sharpey’s fibers were
previously located. This mode of attachment can be likened to the at-
tachment of the basal cells of an epithelium to the underlying basement
membrane. When the dental cuticle is formed on the surface of the
cementum,-the horny substance extends into these spaces (Fig. 191).
 
The erupting crown is surrounded by a tissue formed by the fusion
of the oral and reduced enamel epithelium. The gingival suleus forms
when the tip of the crown emerges through the oral mucosa. It deepens
as a result of separation of the reduced enamel epithelium from the
actively erupting tooth. Shortly after the tip of the crown has appeared
in the oral cavity the tooth establishes occlusion with its antagonist.
otm. MUCOUS MEMBRANE 243
 
During this interval the epithelium separates rapidly from the surface
of the tooth. Later, when the tooth reaches its occlusion, separation
of the epithelial attachment from the surface of the tooth slows down.
 
Actual movement of the tooth (active eruption) and peeling off of
the epithelial attachment (passive eruption) are the two integral factors
of tooth eruption. The normal correlation between the two may be broken.
In accelerated active eruption (teeth Without antagonists), the rate of pas-
sive eruption does not necessarily increase. On the other hand, in the case
of a pathologic recession of gingiva, the peeling off of the epithelial at-
tachment may be accelerated without appreciable change in the rate of
active eruption.
 
E E E
 
EA EA
 
 
II III IV
 
_ Fig. 192.—Dia.grarnmatic illustration of diflerent views on the formation of the
gmgival sulcus as discussed in the text. Arrow in the small diagram indicates area.
from which the drawings were made.
 
The formation and relative depth of the gingival sulcus, at different
ages, has proved an extremely controversial subject. Until the epithelial
attachment was recognized, it was believed that the gingival sulcus ex-
tended to the cemento—enamel junction, immediately after the tip of the
crown pierced the oral mucosa (I in Fig. 192). It was assumed that
the attachment of the gingival epithelium to the tooth was linear
and existed only at the cemento—enamel junction. Since the epithelial at-
tachment has been first described, it has been recognized that no cleft exists
between epithelium and enamel, but that enamel and epithelium are in firm
organic connection. The gingival sulcus is merely a shallow groove, the
bottom of which is at the point of separation of the attachment from the
tooth (II in Fig. 192) . The separation of the epithelium from the tooth is
now considered a physiologic process.
244 ORAL HISTOLOGY AND EMBRYOLOGY
 
Some investigators contend that the deepening of the gingival sulcus is
due to a tear in the epithelial attachment itself (III in Fig. 192). Tears
may deepen the gingival sulcus when the free margin of the gingiva is ex-
posed to excessive mechanical trauma.
 
Others claim‘, 22 that the gingival sulcus forms at the line of fusion be-
tween the enamel epithelium attached to the surface of the enamel, and the
oral epithelium (IV in Fig. 192). Accordingly, the oral epithelium pro-
liferates at the connective tissue side of the epithelial attachment and re-
places the former enamel epithelium which degenerates progressively.
 
The depth of the normal gingival sulcus has been a frequent cause of
disagreement, investigations, and measurements.“ Under normal condi-
tions, the depth of the sulcus varies from zero to six millimeters; 45 per
cent of all measured sulci were below 0.5 mm., the average being about 1.8
mm. It can be stated that the more shallow the sulcus, the more favorable
are the conditions at the gingival margin. Every sulcus may be termed
“normal,” regardless of its depth, if there are no signs of a pathologic
condition in the investing tissues.
 
The presence of leucocytes and plasma cells in the connective tissue at
the bottom of the gingival sulcus should not, in itself, be considered a
pathologic condition. It is evidence, rather, of a defense reaction in
response to the constant presence of bacteria in the gingival sulcus.
These cells form a barrier against the invasion of bacteria and the pene-
tration of their toxins.“
 
The blood supply of the gingiva is derived chiefly from the branches of
the alveolar arteries which penetrate the alveolar septum,” and from
arteries lying on the outside of the alveolus and jawbones. The blood
vessels of the gingiva anastomose with those of the peridontal membrane.
There is a rich network of lymph vessels in the gingiva along the blood
vessels leading to the submental and submaxillary lymph nodes. There
is also a rich plexus of nerve fibers and numerous nerve endings in the
gingiva.
 
C. HARD PALATE
 
The mucous membrane of the hard palate is tightly fixed to the un-
derlying periosteum and, therefore, immovable. Its color is pink, like that
of the gingiva. The epithelium is uniform in character throughout the
hard palate, with a rather thick hornified layer and numerous long pegs.
The lamina propria, a layer of dense connective tissue, is thicker in the
anterior than in the posterior parts of the palate. Various regions in
the hard palate differ because of the varying structure of the submu-
cous layer. The following zones can be distinguished (Fig. 193): (1)
the gingival region, adjacent to the teeth; (2) the palatine raphe, also
known as the median area, extending from the incisive (palatine) papilla
 
posteriorly; (3) the anterolateral area, or fatty zone between raphe and.
 
gingiva, (4) -the posterolateral zone or glandular zone, between raphe
and gingiva.
om. MUCOUS MEMBRANE 245
 
 
   
 
 
E Palatine papilla
 
Gmgiva
 
Raphe
 
Soft palate
 
.... ..
 
._.., _
 
Alveolar crest _
 
Fig. 194.—Structura.l differences between gglngivs. and palatine mucosa. Region or first
m a.r.
246 ORAL rnsronocv AND EMBRYOLOGY
 
The marginal area shows the same structure as the other regions of
the gingiva. Therefore, in this zone, a submucous layer cannot be dif-
ferentiated from the lamina propria or periosteum (Fig. 194). Similarly,
the layers of the lamina propria, submucosa, and periosteum cannot be
distinguished in the palatine raphe, or median area (Fig. 195). If a
palatine torus is present, the mucous membrane is noticeably thin and
the otherwise narrow raphe spreads over the entire torus.
 
In the lateral areas of the hard palate (Fig. 196), in both fatty and
glandular zones, the lamina propria is fixed to the periosteum by strands of
dense fibrous connective tissue which are at right angles to the surface
and divide the submucous layer into irregularly shaped spaces. The dis-
tance between lamina propria and periosteum is smaller in the anterior
than in the posterior parts. In the anterior zone the connective tissue
 
 
 
‘. Nasal septum
 
Median palatine
suture
 
‘-'Connective tissue
' ‘i. strands
 
Fig. 195.—'1‘r-ansverse section through hard palate. Palatine raphe; fibrous strands con-
necting mucosa and periosteum; palatlne vessels. (E. C. Pendletonfi)
 
spaces contain fat (Fig. 195) while in the posterior part lobules of mu-
cous glands are packed into the spaces (Fig. 196). The glandular layer of
the hard palate extends posteriorly into the soft palate.
 
In the sulcus between alveolar process and hard palate, the anterior pala-
tine vessels and nerves are found surrounded by loose connective tissue.
This area being wedge-shaped in cross section (Fig. 197) is relatively large
in the posterior parts of the palate and gradually diminishes in size an-
teriorly.
 
The pear-shaped or oval incisive (palatine) papilla is formed of dense 1“°i‘iY°
connective tissue. It contains the oral parts of the vestigial nasopalatine mun‘
ducts. These are blind epithelial ducts of varying lengths. They are
lined by a simple or pseudostratified columnar epithelium, rich in goblet
cells; small mucous glands open into the lumen of the ducts. Frequently,
ORAL mucous MEMBRANE 247
 
the ducts are bordered by small irregular islands of hyalin cartilage, ves-
tigial extensions of the paraseptal cartilages. The nasopalatine ducts
are patent in most mammals a11d, together with Jacobson ’s organ, are
considered as auxiliary olfactory sense organs. The cartilage is some-
times found in the anterior parts of the papilla; it then shows no ap-
parent relation to nasopalatine ducts (Fig. 198).
 
The transverse palatine ridges (palatine rugae), irregular and often
asymmetric in man, are ridges of mucous membrane -extending later-
ally from the incisive papilla and the anterior part of the raphe. Their
core is a dense connective tissue layer with finely interwoven fibers.
 
In the midline, especially in the region of the palatine papilla, epithe-
lial pearls may be found in the lamina propria. They consist of concen-
trically arranged epithelial cells which are frequently hornified. They
are remnants of the epithelium in the line of fusion between the palatine
processes (see chapter on Development of the Face).
 
B. Lining Mucosa
 
All the zones of the lining mucosa are characterized by a relatively
thin, nonhornified epithelium and by the thinness of the lamina propria.
They differ from one another in the structure of their submucosa. Where
the lining mucosa reflects from the movable lips, cheeks and tongue to
the alveolar bone, the submucosa is loosely textured. In regions where
the lining mucosa covers muscles, as on the lips, cheeks, and underside
of the tongue, it is immovably fixed to the epimysium or fascia of the
respective muscle. In these regions the mucosa is also highly elastic.
These two characteristics safeguard the smoothness of the mucous lining
in any functional phase of the muscle and prevent a folding which
would interfere with the function; for instance, the teeth might injure
the lips or cheeks if such folds protruded between the teeth. The mucosa
of the soft palate is a transition between this type of lining mucosa and
that which is found in the fornix vestibuli and in the sublingual sulcus
at the floor of the oral cavity. In the latter zones, the submucosa is
loose and of considerable volume. The mucous membrane is loosely and
movably attached to the deep structures which allows for a free move-
ment of lips and checks and also tongue.
 
Thus, it is possible to subdivide the lining mucosa into the two main
types of tightly and loosely attached zones; the tightly fixed area, how-
ever, should be subdivided once more on the basis of the absence or
presence of a distinct submucous layer. This layer is lacking on the
underside of the tongue but is present in the lips, cheeks, and soft palate.
In the latter areas, the mucous membrane is fixed to the fascia of the
muscles, or to their epimysium, by bands of dense connective tissue be-
tween which either fat lobules or glands are situated.
 
A. Ln> AND CHEEK
 
The epithelium of the mucosa on the lips (Fig. 165) and the cheek
(Fig. 199) is typically stratified and squamous, Without hornification.
 
Palatine Eu-
gae (trans-
verse pala-
tine ridges)
 
Epithelial
Pearls
Soft palate
End of hard palate
Lamlna. propria.
 
 
 
Musculua inclslvus
 
Alveolar crest
 
Fig. 196.—Longltudlna.l section through hard and soft palate lateral to mldllne. Fatty and glandular zones of hard palate.
Palatine vessels
' . and nerves
 
 
 
 
Alveolar crest
 
Fig‘. 197.—'1‘z-ansverse section through posterior part of hard palate, region or second
molar. Loose connective tissue in the furrow between alveolar process and hard palate
around palatine vessels and nerves.
 
, Incisal canal
 
Cystic remnant of
nasopalatine duct
 
Central lncior—
 
Fig. 198.—Sa.gitta.l section through palagne pai1l>lll.la and anterior palatine canal. Cartilage
Dan
250 ORAL HISTOLOGY AND EMBRYOLOGY
 
The surface layer consists of very flat cells containing pyknotic nuclei.
These superficial cells are continuously shed and replaced.
 
The lamina propria of the labial and buccal mucosa consists of dense
connective tissue which sends irregular papillae of moderate length into
the epithelium.
 
"The submucous layer connects the lamina propria to the thin fascia of
the muscles and consists of strands of densely grouped collagenous fibers.
Between these strands loose connective tissue containing fat and small
mixed glands is found. The strands of dense connective tissue limit
the mobility of the mucous membrane against the musculature and pre-
vent its elevation into folds. Small Wrinkles appear in the mucosa during
the contraction of the muscles, thus preventing the mucous membrane
of the lips and cheeks from lodging between the biting surfaces of the
teeth during mastication. The mixed glands of the lips are situated in
the submucosa, While in the check the larger glands are usually found
between the bundles of the buccinator muscle, and sometimes on its outer
surface. A horizontal middle zone on the cheek, lateral to the corner
of the mouth, may contain isolated sebaceous glands (“Fordyce spots”).
These occur in the zone of embryonic fusion between the lateral parts of
the primary lips during the development of the cheek (see Chapter I).
 
The epithelium and lamina propria of the mucous membrane in the
vestibular fornix do not differ from those of the lips and cheeks. How-
ever, the submucosa here consists of loose connective tissue, which often
contains a considerable amount of fat. This layer of loose connective
tissue is thickest at the depth of the fornix. The labial and buccal frenula
are folds of the mucous membrane, containing loose connective tissue. No
muscle fibers are found in these folds.
 
B. VESTIBULAR FORNIX AND ALVEOLAR MUCOSA
 
The vestibular fornix is the area where the mucosa of lips and checks
reflects to become the mucosa covering the jaws. The mucous mem-
brane of the cheeks and lips is firmly attached to the buccinator
muscle in the cheeks and the orbicularis oris muscle in the lips. In the
fornix, the mucosa is loosely tonnected to the underlying structures
and thus permits the necessary movements of lips and cheeks. The mu-
cous membrane covering the outer surface of the alveolar process is
loosely attached to the periosteum in the area close to the fornix. It
continues into, but is sharply limited from, the gingiva, which is firmly
attached to the periosteum of the alveolar crest and to the teeth.
 
Gingival and alveolar mucosae are separated by a scalloped line,
muco-gingival junction. The altered appearance of tissues on either
side of this line is due to a difference in their structures. The at-
tached gingiva is stippled, firm, thick, lacks a separate submucous layer,
is immovably attached to the bone, and has no glands. The gingival
epithelium is thick and hornified; the epithelial ridges and the papillae
omu. MUGOUS MEMBRANE 251
 
of the lamina propria are high. The alveolar mucosa is thin and loosely
attached to the periosteum by a well-defined submucous layer of loose
connective tissue and may contain small mixed glands. The epithelium
is thin, not hornified, and the epithelial ridges and papillae are low
and: are often entirely missing. Structural differences also cause the
difference in color between the pale pink gingiva and the dark red lining
mucosa.
 
Epithelium
 
Dense con-
nectlve
tissue
strands
 
Submucosa
 
Buccinator  _ , . _ _.
muscle _ —; » . pi
 
 
Fig. 199.—Section through mucous membrane of check. Note the strands ot dense con-
nective tissue attaching the mucous membrane to the buccinator muscle.
 
0. Mucous IVIEMBRANE or TI-IE INFERIOR SURFACE on THE TONGUE
AND on THE FLOOR on‘ THE ORAL CAVITY
 
The mucous membrane on the floor of the oral cavity is thin and loosely
attached to the underlying structures to allow for the free mobility of
the tongue. The epithelium is not hornified and the papillae of the
252 ORAL msvronoev AND EMBRYOLOGY
 
 
   
   
 
Epithelium
 
Lamina propria
 
Submucosa
 
Submucosa
 
Lamina. propria :
 
Fig. 201.—Mucous membrane on interior surface of tongue.
can. MUCOUS MEMBRANE 253
 
lamina propria are short (Fig. 200). The submucosa contains adipose
tissue. The sublingual glands lie close to the covering mucosa in the sub-
lingual fold. The sublingual mucosa joins the lingual gingiva in a sharp
line that corresponds to the mucogingival line on the vestibular surface of
both jaws. At the inner border of the horseshoe-shaped sublingual sulcus,
the sublingual mucosa reflects onto the lower surface of the tongue and con-
tinues as the ventral lingual mucosa.
 
The mucous membrane of the inferior surface of the tongue is smooth
and relatively thin (Fig. 201). The epithelium is not hornified; the
papillae of the connective tissue are numerous but short. Here, the sub-
mucosa cannot be identified as a separate layer; it binds the mucous
membrane tightly to the connective tissue surrounding the bundles of
the striated muscles of the tongue.
 
D. SOFT PALATE
 
The mucous membrane on the oral surface of the soft palate is highly
vascularized and of reddish color, noticeably differing from the pale
color of the hard palate. The papillae of the connective tissue are few
and short. The stratified squamous epithelium is not hornified (Fig. 202).
 
Fig. 202.—Mucous membrane from oral surface of soft palate.
254 ORAL HISTOLOGY AND EMBRYOLOGY
 
The lamina propria shows a distinct layer of elastic fibers separating it
from the submucosa. The latter is relatively loose and contains an al-
most continuous Iayer of mucous glands. Typical oral mucosa continues
around the free border of the velum palatinum and is replaced, at a
variable distance, by nasal mucosa with a pseudostratified, ciliated, col-
 
umnar epithelium.
 
G. Specialized Mucosa or Dorsal Lingual Mucosa
 
The superior surface of the tongue is rough and irregular (Fig. 203).
A V-shaped line divides it into an anterior part, or body, and a posterior
part, or base of the tongue. The former comprises about two-thirds
of the length of the organ, the latter forming the posterior one-third.
The fact that these two parts develop from different areas of the
branchial region (see chapter on Development of the Face) accounts
for the different source of nerves of general sense: the anterior two-
thirds is supplied by the trigeminal nerve through its lingual branch; the
posterior one-third by the glossopharyngeal nerve. '
 
The body and base of the tongue differ widely in the structure of their
covering mucous membrane. On the anterior part are found numerous
fine-pointed, cone-shaped papillae which give it a velvet-like appearance.
These projections, the filiform papillae (thread-shaped) are built of a
core of connective tissue which carries secondary papillae (Fig. 204, A).
The covering epithelium is hornified, especially at the apex of the papillae.
This epithelium forms hairlike tufts over the secondary papillae of the
connective tissue.
 
Interspersed between the filiform papillae are the isolated mushroom-
shaped or fungiform papillae (Fig. 204, B) which are round, reddish
prominences. Their color is derived from a rich blood supply visible
through the relatively thinner epithelium. Some fungiform papillae con-
tain a few taste buds.
 
In front of the dividing V-shaped line, between the body and base of the
tongue, are found the vallate or circumvallate (walled—in) papillae (Fig.
205) ; they are 8 to 10 in number. They do not protrude above the sur-
face of the tongue, but are bounded rather by a deep and circular furrow
which seems to cut them out of the substance of the tongue. They are
slightly narrower at their base. Their free surface shows numerous sec-
ondary papillae which are covered by a thin and smooth epithelium. On
the lateral surface of the vallate papillae and occasionally on the walls sur-
rounding them, the epithelium contains numerous taste buds. Into the
trough open the ducts of small albuminous glands (von Ebner’s glands)
which serve to Wash out the furrows into which the soluble elements of
food penetrate to stimulate the taste buds.
 
At the angle of the V-shaped line on the tongue is found the foramen I
 
cecum which is a .remnant of the thyroglossal duct (see chapter on De-
velopment of the Face). Posterior to the vallate papillae, the surface of
ORAL MUCOUS MEMBR.-XNE 255
 
the tongue is irregularly studded with round or oval pron1inences known as
the lingual follicles. Each of the latter show one or more lymph nodules,
sometimes containing a germinal center (Fio-. 206). Most of these prom-
mences have a small pit at the center, the lingual crypt, which is lined with
stratified squamous epithelium. Innumerable lymphocytes migrate into the
crypts through the epithelium. The ducts of the medium—sized posterior
lingual mucous glands open into the crypts. Together the lingual fol-
licles form the lingual tonsil.
 
Filiform
papillae
 
         
 
 
Fungitorni - - - — — — — _
papilla
Foliate
papillae
Vallate
D9-Dilla.
z’ Foramen
cecum
335' 2)-r’ Lingual tonsil
hr» Entrance to
larynx
, , Pha.ryngo-
_ _ . 1 .' . , epiglottic
Eplglottis“ "‘ p, " _ * .  I -‘ : fold
" L‘ '  .‘,,—' Cuneiform
~ tubercle
. _ P’?
: §«:,...— Fold of supe-
‘ I, rlor laryn-
"" geal nerve
i‘_' " ‘ ' Corniculate
; ' tubercle
c. ,7 “~ Piriform
sinus
Interarytenoid - * — — - -* ‘
notch
 
Fig. 203.—Surtace view of human tongue. (Sicher and Tandler.)
 
On the lateral border of the posterior parts of the tongue sharp parallel
furrows of varying length can often be observed. They bound narrow
folds of the mucous membrane and are the vestiges of the large foliate
papillae found in many mammals. They may contain taste buds.
Taste Buds
 
256 ORAL ELISTOLOGY AND EMBRYOLOGY
 
The taste buds are small ovoid or barrel-shaped intra-epithelial organs
of about 80 microns in height and 40 microns thickness (Fig. 207). They
touch with their broader base the basement membrane while their nar-
rower tip almost reaches the surface of the epithelium. The tip is cov-
 
wefcfl 4 395
 
 
Fig. 204.——-Filiform (A) and fungiform (B) papillae.
 
ered by a. few flat epithelial cells, which surround a small opening, the
taste pore. It leads into a narrow space between the peripheral ends of
the sustentacular (supporting) cells of the taste bud. The outer support-
ing cells are arranged like the staves of a barrel, the inner and shorter ones
ow. MUOOUS mmmmm 257
 
   
 
 
 
,5-5 Taste bud
 
5  3%:
 
 
 
 
“ of v. Ebnel-'5
 
{——— _..._’  Opening of duct
' " ' gland
 
zland
 
Lymph nodule
with germinal _
center
 
Fig. 206.—L1ng'u8.l follicle.
258 ORAL HISTOLOGY AND EMBRYOLOGY
 
are spindle-shaped. Between the latter are arranged 10 to 12 neuroepi-
thelial cells, the receptors of taste stimuli. They are thin, dark-staining
cells that carry a stiff hairlike process at each superficial end. This hair
reaches into the space beneath the taste pore.
 
A rich plexus of nerves is found below the taste buds. Some fibers
enter the taste bud from the base and end in contact with the taste cells.
Others end in the epithelium between the taste buds.
 
Taste buds are numerous on the inner wall of the trough surrounding
the vallate papillae, in the folds of the foliate papillae, on the posterior
surface of the epiglottis and on some of the fungiform papillae at the
tip and the lateral borders of the tongue.
 
Stratified
squamous
epithelium
Taste pore
Taste cells
Supporting cells
 
Connective tissue
 
Supporting cells
 
Fig. 20'l'.—Taste buds from the slope of a. vallate papilla. (From .1’. Schafter.)
 
The primary taste sensations, namely, sweet, salty, bitter, and sour,
are not perceived in all regions of the tongue. Sweet is tasted at the
tip, salty at the lateral border of the body of the tongue. Bitter and
sour are recognized in the posterior part of the tongue, bitter in the
middle, sour in the lateral areas. The distribution of the receptors for
primary taste qualities can, diagrammatically, be correlated to the dif-
ferent types of papillae. They are mediated by different nerves. The
vallate papillae recognize bitter, the foliate papillae sour, taste. The
ORAL MUCOUS MEMBRANE 259
 
taste buds on the fungiform papillae at the tip of the tongue are re-
ceptors for sweet, those at the borders for salty, taste. Bitter and acid
(sour) taste are mediated by the glossopharyngeal, sweet and salty taste
by the intermediofacial nerve via chorda tympani.
 
4. CLINICAL CONSIDERATIONS
 
To understand the pathogenesis of periodontal diseases and the path-
ologic involvements of the difierent structures, it is essential to be thor-
oughly familiar with the structure of cementum, periodontal membrane,
alveolar bone, and the structure of the marginal gingiva, gingival sulcus,
and epithelial attachment, as Well as their biologic relation to each
other. Periodontal disturbances, frequently, have their origin in the
gingival sulcus and marginal gingiva, leading to the formation of a deep
gingival pocket.‘ Moreover, the safe and speedy reduction of the depth
of the gingival pocket is the primary objective of treatment. The su-
periority of any given method of treatment should be judged by its
ability to accomplish this end whether the method be surgical, chemical,
or electrical.
 
In restorative dentistry, the extent of the epithelial attachment plays
an important role. In young persons, this attachment of the epithelium
to the enamel is of considerable length and the clinical crown is smaller
than the anatomical. The enamel cannot be removed entirely without
destroying the epithelial attachment. It is, therefore, very difficult to
prepare a tooth properly for an abutment or crown in young individu-
als. On the other hand, the preparation may be mechanically inadequate
when it is extended only to the bottom of the gingival sulcus. It should
be understood, therefore, that, in young persons, a restoration may serve
merely as a temporary measure and require ultimate replacement.
 
When large areas of the root are exposed, and a restoration is to be
placed, the preparation need not cover the entire clinical crown. The
first requirement is that the restoration be adapted to mechanical needs.
 
In extending the gingival margin of any restoration in the direction
of the bottom of the gingival sulcus, the following rules should be ob-
served: If the epithelial attachment is still on the enamel, and the
gingival papilla fills the entire proximal space, the gingival margin of a
cavity should be placed below the marginal gingiva. Special care should
be taken to avoid injury to the gingiva and epithelial attachment, to
prevent premature recession of the gingiva. When the gingiva is patho-
logically affected, treatment should precede the placing of a filling. If
the gingiva has receded from the enamel, if the gingival papilla does
not fill the interproximal space and if the gingival sulcus is very shallow,
the margin of a cavity need not necessarily be carried below the free
margin of the gingiva. The gingival margin of a cavity should be placed
far enough from the contact poi11t to permit proper cleansing.
 
‘The term gingival pocket designates the pathologic condition of the gingival sulcus.
260 ORAL msrronocv AND EMBRYOLOGY
 
When the anatomical root is exposed, a predisposition to cemental
caries and abrasion exists. Improperly constructed clasps, overzealous
scaling, and too abrasive dentifrices may result in marked abrasion.
After loss of the cementum the dentin may be extremely sensitive to
thermal or chemical stimuli. Drugs, judiciously applied, may be used
to accelerate sclerosis of the tubules and secondary dentin formation.
 
It is desirable to keep the depth of the gingival sulcus at a minimum.
The more shallow the sulcus, the less opportunity for irritating material
to be deposited. This can be done in part by proper massage and brush-
ing.
 
The diflerence in the structure of the submucosa in various regions
of the oral cavity is of great practical importance. Wherever the sub-
mucosa consists of a layer of loose connective tissue, edema or hemor-
rhage causes much swelling and infections spread speedily and ex-
tensively. Generally, inflammatory infiltrations in such parts are not
very painful. If possible, injections should be made into loose sub-
mucous connective tissue. Such areas are the region of the fornix and
the neighboring parts of the vestibular mucosa. The only place in the
palate where larger amounts of fluid can be injected without damaging
the tissues is the furrow between the palate proper and alveolar process
(Fig. 197). Also, it will be found that in the areas where the mucosa
is loosely fixed to the underlying structures, it is easier to suture sur-
gical wounds than in those places where the mucous membrane is im-
movably attached.
 
The gingiva is exposed to heavy mechanical stresses during mastica-
tion. Moreover, the epithelial attachment to the tooth is relatively
weak, and injuries or infections can cause permanent damage here.
Strong hornification of the gingiva may afford relative protection.
Therefore, measures to increase hornification can be considered a pre-
vention against injuries. One of the methods of inducing hornification is
mechanical stimulation, such as massage or brushing.
 
Unfavorable mechanical irritations of the gingivae may ensue from
sharp edges of carious cavities, overhanging fillings or crowns, and ac-
cumulation of calculus. These may cause chronic inflammation of the
gingival tissue.
 
Many diseases show their symptoms, initial and otherwise, in the oral
mucosa. For instance, metal poisoning (lead, bismuth) causes charac-
teristic discoloration of the gingiva margin. Leukemia, pernicious ane-
mia, and other blood dyscrasias can be, and often have been, diagnosed by
characteristic infiltrations of the oral mucosa. In the first stages of
measles, small red spots with bluish-white centers can be seen in the
mucous membrane of the cheeks, even before the skin rash appears; these
spots are known as Koplik’s spots. Endocrine disturbances, including
those of the estrogenic and gonadotropic hormones and of the pancreas
may be reflected in the oral mucosa.
ORAL MUCOUS MEMBRANE 261
 
In denture construction it is important to observe the firmness or
looseness of attachment of the mucous membrane to the underlying bone.
Denture—bearing areas should be those where the attachment of the
mucosa is firm. The margin of dentures should not reach into areas
where the loose mucous membrane is moved by muscle action.“’v 2°
 
In old age, the mucous membrane of the mouth may atrophy in the
cheeks and lips; it is then thin and parchment-like. The atrophy of the
lingual papillae leaves the upper surface of the tongue smooth, shiny
and varnished in appearance. A senile atrophy of major and minor
salivary glands may lead to xerostomia and sometimes an accompanying
atrophy of the mucous membrane. In a large percentage of individuals,
the sebaceous glands of the cheek may appear as fairly large, yellowish
patches. Such a condition is known as Fordyce’s disease, but does not
represent a pathologic change.
 
References
 
1. Aprile, E. C. de: Contribucion al estudio de los elementos reticulo endoteliales
de la mucosa gingival, Arch. Hist. normal y Pat. 3: 473, 1947.
la. Becks, H.: Normal and Pathological Pocket Formation, J. A. D. A. 16: 2167,
1929.
2. Bodecker, C. F., and Applebaum, E.: The Clinical Importance of the Gingival
Crevice, Dental Cosmos 176: 1127, 1934.
3. Fish, E. W.: Bone Infection, J. A. D. A. 26: 691, 1939.
3a. Gairns, F. W., and Aitchison, J. A.: A Preliminary Study of the Multiplicity
of Nerve Endings in the Human Gum, The Dental Record 70: 180, 1950.
4. Gottlieb, B.: Der Epithelansatz am Zahne (The Epithelial Attachment),
Deutsche Monatschr. f. Zahnh. 39: 142, 1921.
5. Gottlieb, B.: Aetiologie und Prophylaxe der Zahnkaries (Etiology and Pro-
phylaxis of Caries), Ztschr. f. Stomatol. 19: 129, 1921.
6. Gottlieb, B.: Tissue Changes in Pyorrhea, J. A. D. A. 14: 2178, 1927.
7. Gottlieb, B., and Orban, B.: Biology of the Investing Structures of the Teeth,
Gordon ’s Dental Science and Dental Art, Philadelphia, 1938, Lea av Febiger.
8. Gottlieb, B., and Orban, B.: Biology and Pathology of the Tooth (Translated by
M’. Diamond), New York, 1938, The Macmillan Co.
9. Kronfeld, B.: The Epithelial Attachment and So-Called Nasmyth’s Membrane,
J. A. D. A. 17: 1889, 1930.
10. Kronfeld, 3.: Increase in Size of the Clinical Crown of Human Teeth With
Advancing Age, J . A. D. A. 18: 382, 1936.
11. Lehner, J.: Ein Beitrag zur Kenntniss vom Schmelzoberhiiutchen (Contribution
to the Knowledge of the Dental Cuticle), Ztschr. f. mikr.-anat. Forsch. 27:
613, 1931.
12. Meyer, W.: Ueber strittige Fragen in der Histologie des Schmelzoberhiiutchens
(Controversial Questions in the Histology of the Enamel Cuticle), Vrtljsschr.
f. Zahnh. 46: 42, 1930.
13. Orban, B., and Kohler, J.: Die physiologisiche Zahnfleischtasche, Epithelansatz
und Epitheltlefenwucherung (The Physiologic Gingival Sulcus), Ztschr.
f. Stomatol. 22: 353, 1924.
14. Orban, B., and Mueller, E.: The Gingival Crevice, J. A. D. A. 16: 1206, 1929.
15. Orban, B.: Hornification of the Gums, J . A. D. A. 17: 1977, 1930.
16. Orban, B.: Zahnfleischtasche und Epithelansatz (Gingival Snlcus and Epithelial
Attachment), Ztschr. f. Stomatol. 22: 353, 1924.
17. Orban, B.: Clinical and Histologic Study of the Surface Characteristics of the
Gingiva, J . Oral Surg., Oral Med., Oral Path. 1: 827, 1948.
18. Orban, B., and Sicher, 11.: The Oral Mucosa, J. Dent. Educ. 10: 94-103, 163-164,
1946.
19. I-‘endleton, E. 0.: The Minute Anatomy of the Denture Bearing Area, .1’. A. D. A.
21: 488, 1934. _ _
20. Pendleton, E. 0., and Glupker, 11.: Research on the Reaction of Tissues Sup-
porting Full Dentures, J. A. D. A. 222 76, 1935-
262 ORAL HISTOLOGY AND EMBRYOLOGY
 
21. Robinson, H. B. G., and Kitchin, P. 0.: The Effect of Massage With the Tooth
brush on Keratinization of the Gingivae, Oral Surg., Oral Med., Oral Path.
1: 1042, 1948.
 
22. Skillen, W. G.: The Morphology of the Gringivae of the Rat Molar, J. A. D. A.
17: 645, 1930.
 
23. Toller, J. R.: Studies of the Epithelial Attachment on Young Dogs, Northwestern
U. Bull. 11: 13, 1940.
 
24. Wassermann, F.: Personal communication.
 
25. Weinmann, J. P.: Progress of Gingival Inflammation Into the Supporting
Structures of the Teeth, J. Periodont. 12: 71, 1941.
 
26. Weinmann, J. P.: The Keratinization of the Human Oral Mucosa, J. Dent.
Research 19: 57, 1940.
 
27. Wermuth, J.: Beitrag zur Histologie der Gregend seitlich Von der Papilla pala-
tina (Histology of the Region Lateral to the Incisive Papilla), Deutsche
Monatschr. f. Zahnh. 45: 203, 1927.
CHAPTER X
GLANDS OF THE ORAL CAVITY
 
INTRODUCTION; SALIVA
 
EISTOGENESIS
 
CLASSIIPICATION OF SALIVARY G-LANDS
SEGRETORY CELLS OI‘ THE SALIVARY G-LANDS
MYOEPITHELIAL CELLS
 
DUCT ELEMENTS
 
INTERSTITIAL TISSUE
 
SAI.-IVARY G-LAITDS OI‘ MAJOR SECRETION
SALIVABY G-LANDS O1‘ MINOR SECRETION
 
. CLINICAL CONSIDERATIONS
 
H
°S°9°.“.°°9‘!*“."°!°!"
 
1. INTRODUCTION
 
The salivary glands of man are exocrine glands, the primary function
of which is to transform and secrete materials brought to them via the
circulating fluids of the body. This function represents active Work in
producing and discharging complex substances, such as mucin and
ptyalin, which are not found in the circulating blood and lymph. The
cells give morphologic evidence of their secretory function, and because
they remain intact throughout a cyclic process of formation and dis-
charge, these glands are classified as merocrine in type.
 
A secondary function of the salivary glands is to excrete certain sub-
stances. Evidence of this may be seen in comparing the constancy of
the ratio between salivary and blood urea, nitrogen and creatinine.”
 
Saliva is the term applied to the accumulated secretory and excretory
products discharged by the salivary glands into the oral cavity. The
saliva is the first of many digestive fluids to act upon the food elements
in the diet, its main actions being to assist in the mastication of food
and to act as a solvent for bringing components into solution, thus
facilitating the stimulation of the taste organs. Albuminous or serous
cells of the glands liberate the enzyme ptyalin or amylase which
causes a preliminary breakdown of carbohydrates. The mucous celLs liber-
ate mucin which counteracts tendencies to desiccation of the oral mem-
branes and dental hard structures, and aids in the lubrication of the
bolus of food for deglutition. The proteins and salts of saliva act as
bufiers which tend to counteract the acids and alkalies in the oral cavity.
Saliva is mechanically protective inasmuch as it serves to flush the sur-
 
Flrst draft submitted by Virgil D. Cheyne.
263
264 emu. HISTOLOGY AND ammevocoev
faces of the teeth and mucous membranes of food and debris. Its action of
removing bacteria from ducts and surfaces is a safeguard against infection.
 
There is some indication that saliva, normally, contains an antibacterial
factor which inhibits the growth and activity of aciduric bacteria in the
oral cavity, and may act to prevent dental caries.‘ 1° There is also evi-
dence, however, that the saliva of some individuals may supply the proper
culture medium needed for the bacteria found in the mouth. Because of
these contradictions the role of saliva in dental caries is as yet unsettled
and requires further investigation.
 
The total daily amount of saliva secreted by man is approximately
1,500 c.c. This quantity is subject to great variation, depending upon
age, exercise, and diet. It is materially influenced by physical and psycho-
logic stimulation and varies Widely in different individuals. Of the total
amount secreted, the large salivary glands (parotid, submaxillary, and
sublingual) contribute by far the greatest amount. The quality is directly
dependent upon the type of glands which participate in its formation.
 
The methods of collection and the type of stimulus have an important
influence upon the composition of saliva. In man, the mixed excretions
from the glands may be collected in the unstimulated or resting state by
simply cxpectorating into a receptacle or, in the stimulated or active state,
by chewing parafiin. Pure secretions from the individual glands may be
collected by the use of Lashley’s double metal cup instrument which can be
applied to the mucous membrane surrounding the papillae of the salivary
ducts,” or by direct canalization of the ducts of the parotid, submaxillary,
or sublingual glands. Saliva obtained in this manner is a clear, colorless
fluid. The function of certain glands or groups of glands in animals has
been clarified by selectively removing salivary tissue,‘ or by the experi-
mental production of a fistula, the duct being diverted to the outside of
the oral cavity.
 
Mixed saliva is a frothy, slightly opalescent fluid containing water,
proteins, mineral salts, ptyalin, mucin, food particles, desquamated epi-
thelial cells and salivary corpuscles. Its viscosity is dependent upon the
predominating type of saliva secreted. Serous saliva imparts the Watery
characteristics to the fluid; mucin in the saliva renders it thick and ropy.
 
The specific gravity of mixed saliva varies from 1.000 to 1.020, the freez-
ing point being lower than for the other secretions of the digestive glands.
Results of hydrogen-ion determinations (pH) of saliva vary greatly, owing
to individual variation, time of day, and difierence in methods used for
its determination. The mean or average pH of resting saliva is approxi-
mately 6.8, ranging from 5.6 to 7.6 and being highest just before meals.‘
Undoubtedly, oral hygiene and the nature of the oral flora are also influ-
encing factors.
 
Chemically, human, mixed saliva is a dilute solution containing about 0.2
per cent inorganic solutes and 0.5 per cent organic matter. The bulk of the
inorganic portion consists of potassium and phosphate ions. The following
 
Quantity
 
Methods of
Study
 
characteristics
GLANDS on THE ORAL CAVITY 265
 
elements, however, are found in appreciable amounts: Cl, P. Na, K, Mg,
Ca, and S. The amount of NaCl is approximately 90 mg. per 100 c.c.; the
amount of carbonate, as C0,, 13.0 mg. The C0._., Ca, and K present in the
saliva exceed the concentration in the blood, While the sodium chloride con-
centration is lower in saliva. Oxygen is present in the human parotid
saliva in amounts varying from 0.84 to 1.46 c.c. per 100 c.c.
 
Leucocytes
 
Epithelial
 
Leucocytes
 
 
Fig. 208.—Smear of human saliva (Wright's stain). (Orban and Weinmannfl)
 
A large portion (0.4 per cent) of the organic matter in mixed secretions
is mucin. With the exception of mucin, the principal organic constituents
of saliva are albumin, globulin, amylase, and cholesterol. Urea, uric acid,
creatinine, maltase, and ammonia are found in varying amounts. The
ammonia originates largely from the decomposition of urea. In normal
subjects values range from 1.28 to 13.66 mg. of ammonia nitrogen per
100 c.c. of saliva.” Total nonprotein nitrogen, urea plus ammonia, nitro-
gen, and uric acid average 37 per cent and 40 per cent, respectively, of
the corresponding constituents of blood.” Blood amino-acids and poly-
peptides are not found in appreciable amounts in the saliva.
Histology
 
266 can. msronocr AND snnsronoer
 
Sulfocyanate is generally present in the saliva to the extent of several
milligrams per cubic centimeter. It is greatest in habitual smokers. The
significance of sulfocyanate in the saliva is not known, but it probably
comes from ingested cyanides present in certain fruits, tobacco, and from
the disintegration of protein material. It is, apparently, not related to
tooth decay.”
 
The opacity of saliva is attributed mainly to the presence of desqua-
mated epithelial cells and salivary corpuscles (Fig. 208), the latter con-
sisting of polymorphonuclear leucocytes and lymphocytes. The epithelial
cells are large and flat with oval nuclei. They may be round or roughly
irregular, with a granular cytoplasm. The salivary corpuscles are de-
rived from the mucous membrane of the mouth, the tonsils and salivary
glands. The average number of salivary corpuscles is, usually, less than
25 cells per cubic mm. of saliva, but higher counts (500 to 1,000) have been
reported.” Lymphocytes constitute a relatively minor proportion of this
number. Corpuscle counts are high after a night’s rest, low after meals.
Their role is as yet imperfectly understood but it is the opinion of some
investigators that they are phagocytic, reducing the bacterial flora of
the mouth.
 
2. HISTOGENESIS
 
The salivary glands are formed during fetal life as solid buds of oral
epithelium with club-shaped ends pushing into the subjacent mesoderm.
As the bud or anlage grows it proliferates distally, forming a cord of
cells. The most distal portion forms the alveoli or fimctional elements of
the gland. Cords and buds are at first solid and are later hollowed out
to form ducts and alveoli.
 
The bud of the parotid salivary gland appears as a shelflike outgrowth
of epithelium during the fourth week of fetal life at the angle of the
maxillary process and the mandibular arch (sulcus buccalis) ; the bud of
the submaxillary appears in the sixth week, and that of the major sub-
lingual (Bartholinian) during the eighth to ninth week from similar out-
growths located at the medial angle of the hollow between the tongue
and mandibular arch (sulcus lingualis). The minor sublingual glands
(Rivinian) arise as independent proliferations in the alveolingual region
associated with the sulcus lingualis at the lateral margin of the plica sub-
lingualis. Accessory and secondary lobes of the parotid and submaxil-
lary glands become visible during the eighth to ninth weeks, as out-
growths arising from the cords of their respective glands. All the ele-
ments of the smaller sublingual, glossopalatine and palatine groups
develop from the primitive oral epithelium. The anterior lingual glands
are noticeable for the first time at ten weeks. They start as epithelial
proliferations located on the ventral surface near the tip of the tongue on
both sides of the median line. Development of the labial glands takes
place simultaneously with the anterior lingual glands. Lymphoid tissue
GLANDS on THE ORAL CAVITY 267
 
is, frequently, found in the fetal salivary glands; this is especially common
in the parotid. Occasionally, remnants of lymphatic tissue are found in
the adult.
 
3. CLASSIFICATION OF THE SALIVARY GLANDS
 
The human salivary glands are usually classified either according to
the type of cells or according to the location of the gland. Cells
which liberate mucin are named mucous cells, and those Which se-
crete some form of protein (enzyme) are called albuminous or serous
cells, but it is now quite evident that all mucous cells, as Well as
all albuminous cells, do not produce identical products. In many cases
the secretory granules of albuminous cells give a distinct reaction for
mucin with mucicarmine stain. This would indicate that it is possible
for these cells to secrete both mucin and protein substances. Although a
simple classification of the glands according to the chemical qualities of
their secretion remains unsatisfactory, the glands are best classified as
albuminous, mixed and mucous glands. The parotid gland of the adult
is a pure albuminous gland. Glands with very few or no mucous cells are
those of the vallate papillae. Glands in which both serous and mucous
cells are present (true mixed glands) are referred to as predominantly
serous or predominantly mucous, depending upon the ratio of the cell
types. Those with a few mucous cells include the submaxillary gland
(and the parotid gland of the newborn). Those predominantly of mucous
character include the labial glands, small buccal glands, anterior lingual
glands, and the sublingual gland. In man pure mucous glands are those
at the base and border of the tongue, the glossopalatine glands and the
palatine glands.
 
Classification of the Oral Glands According to Location?‘
 
A. Glands of the vestibule:
1. labial glands:
a. superior labial glands
b. inferior labial glands
 
2. buccal glands:
a. minor buccal glands
b. parotid gland
 
B. Glands of the oral cavity proper:
1. glands of the floor of the mouth (alveolingual complex)
 
a. submaxillary (submandibular) gland
 
b. major sublingual gland
 
c. minor sublingual glands
 
d. glossopalatine glands
The
Albuminous
Cell
 
means
 
268 ORAL msronoov AND nmnnvonoev
 
2. glands of the tongue:
 
a. anterior lingual glands
b. posterior lingual glands
 
(1) glands of the vallate papillae
(2) glands of the base of the tongue
 
3. palatine glands
 
4. SECRETORY CELLS OF THE SALIVARY GLANDS
 
Both albuminous and mucous cells vary in appearance with the flinc-
tional changes of the gland.
 
The albuminous or serous cells of the parotid gland and other glands
of the mouth probably do not perform an identical function; the cells,
however, resemble each other closely. Their secretion is a thin watery
fluid containing a high percentage of organic and inorganic substances.
 
Albuminous cells are roughly pyramidal or polyhedral in shape, and
form globular alveoli, the lumina of which are very narrow. The cells
drain, for the most part, by intercellular secretory capillaries or canalic-
uli. In resting cells of a fixed specimen the small highly refractive
secretory granules, embedded in a closely reticulated cytoplasm, obscure
the cell boundaries. These zymogen granules are the antecedents of the
enzyme ptyalin. They accumulate between the nucleus and the free end
of the cell. They are easily dissolved by chemical agents, but are more
stable than the granules in the mucous cell. Following stimulation they
diminish in number (Fig. 210).
 
In addition to the secretory granules the cytoplasm contains rod-shaped
mitochondria, a Golgi net, and a cytocentrum which can be demonstrated
only by special staining methods (Fig. 210). Intracellular fat droplets
are common. The nucleus of the albuminous cell is large, spheroidal,
and filled with abundant chromatin substance. Its size and location are
somewhat dependent upon the stage of activity of the cell.
 
The mucous cell of the salivary glands secretes mucin, a glycoprotcin
which, dissolved in water, becomes a lubricating solution called mucus.
It makes the saliva highly viscid. In man, mucous cells are studied best
in sublingual glands, the mucous glands of the tongue, the glossopalatine
and palatine glands. They are also found in small mixed glands where
they make up the greater number of alveoli; in the submaxillary gland
they are few in number.
 
The mucous cells are irregularly cuboidal in form and aligned against
a basement membrane (Fig. 211). Mucous alveoli vary from globular to
long branching masses, their lumina forming large ovals or elongated
tubules. In the fixed preparation the nucleus is often deformed, shrunken;
it is located at the base of the cell. The accumulation and removal of
‘,'.~
 
Buccal mt pad ".
. “K, ‘In...
 
Parofid gland -"""" 3’~‘“
I
 
Minor sublingual --.-/‘V g’ ':-4-_..,m».“‘
ducts »
 
Sublingual gland ———— —— Ii‘ '
 
V
Submaxillary duct — — — — ~ — — - J
 
Submaxillary _. L _' ______ .../
gland
 
Fig. 209.-Salivary glands of mad 1:1
muscle mug: ed.5°°?esi:11l1(-er a1;3&flT:‘f1dlt:1:P;nudib1e and mylohyold
 
5
_—:
.3.
 
‘a
 
Different functional stages at
(zknmermannfi)
 
Fig. 210.——A1buminoua gland.
cycle is indicated by the letters 9. to g.
 
   
 
0" - Mucous cell
Arrangement
o1'_ cells in
 
Glands
 
Intercellular secre-
 
270 ORAL HISTOLOGY AND EMBRYOLOGY
 
mucigen can be studied under favorable conditions. As the stimulated
cell liberates its contents, the nucleus rises from the base and assumes an
ovoid shape.
 
Mucigen granules cannot be observed because of their labile character
except in fresh condition or by special methods of fixing and staining,
whereby they can be stained specifically with mucicarmine and muci-
hematin. Mucous cells which have lost their granules have an empty ap-
pearance and the remaining cytoplasm takes a faintly blue stain with
hematoxylin. In properly prepared specimens a few irregular mito-
chondria, a Golgi net and a cytocentrum can be demonstrated; fat glob-
 
ules are a constant feature.
 
 
 
 
Albuminous
cell of
demllune
 
Lumen of
alveolus
 
— Mucous cell
tory capillary
 
Fig. 212.-7Semidiagr-ammatic drawing or a. section through a mixed alveolus in the sub-
maxillary gland. Serous cells forming a. demllune around the mucous cells.
 
In mixed glands mucous and serous cells are combined in such a Way
that either all the cells of some alveoli are serous, and all the cells of
others mucous; or that within the same alveolus both serous and mucous
cells are present. In a mixed alveolus the albuminous cells occupy a
position at the terminal or peripheral region. They are found as small
crescent-shaped clumps which cap the mucous cells: crescents or demi-
lunes of Gianuzzi (Figs. 212 and 215, a). Crescent cells are somewhat
smaller, more finely granular, and darker staining than mucous cells in
ordinary preparations.
Albuminous cell
 
Process of myo-
epithelial cell
 
GLANDS or run om. cmrr 271
 
The secretory surfaces of the mucous cells form the lumen of a mixed
alveolus. The cells of the crescents do not reach the lumen and discharge
 
their secretion through fine secretory capillaries which pass between the
mucous cells (Fig. 212).
 
5. MYOEPITHELIAI. CELLS
 
In all salivary glands a syncytium of branching stellate cells surrounds
the ducts and cells of the terminal secretory portions. They are in close
 
contact with the bases of the glandular cells and lie between them and the
basement membrane. They lie in a similar location in the ducts. Viewed
 
cell
Fibroblast
 
Fat
 
Fibroblast
 
 
 
 
 
s
 
2 .‘  Basement
Blood vessel
duct
 
Fig. 213.—A1buminous alveoli and striated duct or subma.xilla.ry gland with myoepithelial
cells. (Modified after Zimmennannfi)
 
from the periphery, they appear as spider—like structures embracing
the alveoli (Fig. 213). Although probably of epithelial origin, these
cells function as a part of the supporting structure of the glandular
elements and are called basal or basket cells, or myoepithelial cells.
The body of the myoepithelial cell is made up of a dark, angular nucleus
with a scanty amount of cytoplasm containing fine, straight fibrils
which continue into many tentacle-like processes that encircle the
basal portion of the alveolar cells. In cross section only their nuclei
are visible. The cells become especially prominent after treating fresh
glandular tissue in the state of active secretion with osmic acid or by
teasing fresh glandular substance in water.“
 
It is generally believed that myoepithelial cells are contractile cells
 
which facilitate the movement of the secretion into and through the ducts.
The phenomenon which is known as motor effect of the sympathetic
 
Myoepithelial
 
membrane
Lumen of striated
 
Location
 
Albumlnous cell
 
' ‘ Myoepithelial cell
.— Striated cell
_._ __. Excretory duct
 
4.
.1 _._ Striated duct
__ Intercalated duct
Secretory alveoll
__ Excretory duct
B.
 
———. — Striated duct
Intercalated duct
 
Secretory alveoll
 
.__ ;._ Excretory duct
 
__ __ Striated duct
 
0.
 
8] 214.——Dia.g-rams of the duct system and terminal‘ secretory portions or salivary
 
A. Parotid.
B. Subma.xil.Ia.ry.
G’. Sublzlngual. (Modified after Brauafi)
GLANDS on THE ORAL CAVITY 273
 
nerves on the large salivary glands is probably caused by contraction of
these cells under nervous stimulation.“ True muscular tissue is absent
in the salivary glands.
 
6. DUCT ELEMENTS
 
The duct system of the salivary glands is complex and branching (Fig.
216). The smallest excretory channels are the intercalated ducts or the
so-called necks or isthmuses. These connect the terminal alveoli with the
 
Albumlnous cell
-  Myoepithelial
_, . cell
, .
I’
 
serous alveolus I’-ll’-31'¢°11“18!‘
secretory
 
capillary
 
Demllune
 
Myoeplthelial
cell
Basement
membrane
Mucous cells
 
Intercalated duct
 
Striated duct
 
 
Fi . 216.—Reconstruc1:ion of a terminal portion and its duct or a salivary gland (a).
(b) ross section through serous alveolus. (0) Cross section through mucous alveolus.
(d) Qross section through lntercalated duct. (a) Cross section through striated duct.
(Maximow and Bloom“)
 
excretory system. An outstanding characteristic of the intercalated
ducts is their thin Wall and relatively small diameter. They are always
surrounded by moyepithelial cells ‘(Fig 213). The cells are simple, low
cuboidal in type, remain relatively undifferentiated, and take ordinary
stains very poorly. They are of variable length depending on the type
of gland which they drain. The parotid gland has long intercalated
very short and inconspicuous (Fig. 214). In pure mucous glands the
cells abut directly upon the distal tubules of the larger excretory ducts.
 
In the parotid and submaxillary glands striated ducts (secretory ducts,
salivary tubules) intervene between the intercalated ducts and the larger
excretory ducts. These ducts are believed to secrete water and inorganic
salts which act to dissolve the antecedents secreted by the alveolar cells.
In the striated ducts the epithelial cells are regular and columnar in form
274 ORAL HISTOLOGY AND EMBRYOLOGY
 
and arranged in a single layer. The cytoplasm is finely granular and
contains a nucleus which is centrally placed. The perpendicular stria-
tions from which the cells derive their name are confined to the outer or
basal zone near the basement membrane (Figs. 215, 217). In the larger
ducts (parotid, submaxillary, major sublingual) the epithelium is colum-
nar and pseudo-stratified; a basement membrane is distinct between
epithelium and connective tissue wall. Where the ducts open into the
oral cavity the walls fuse with the mucous membrane.
 
A common feature of compound glands in general is the presence of
secretory capillaries or canaliculi which arise from the smallest excretory
ducts and penetrate between the functional cells at their boundaries (Figs.
212, 215). The purpose of secretory capillaries is to increase the drainage
capacity of alveoli composed of multiple layers of cells and, for that
reason secretory capillaries are a constant feature of mixed alveoli. The
capillaries are most effectively demonstrated with silver impregnation.
 
7. INTERSTITIAI. GONNECTIVE TISSUE; BLOOD, LYMPH
AND NERVE SUPPLY
 
The interstitial substance of the salivary glands is loose connective
tissue made up of a large number of fibers. The fibers run in all direc-
tions to form networks which surround and support the various elements.
In it are fibroblasts, macrophages, plasma and fat cells which vary in
relative number with the type of gland. Around the terminal alveoli
and ducts, located peripherally to the myoepithelial cells, the connective
tissue forms a basement membrane.
 
The salivary glands possess a rich blood supply. The larger arteries
follow the course of the excretory ducts, giving off branches which ac-
company the divisions of the ducts to the lobules; the capillaries form
dense networks on the outer surface of the basement membrane of alveoli
and ducts. The veins and lymph vessels follow the arteries in reverse order
to drain the gland. The main branches of the nerves supplying the salivary
glands also follow the course of the vessels to break up into terminal plex-
uses in the connective tissue adjacent to the alveoli. Both sympathetic and
parasympathetic fibers pass through the basement membrane and end in
varicose filaments and budlike expansions between the secretory cells.
 
8. MAJOR SALIVARY GLANDS
 
The parotid, submaxillary and sublingual glands are often classified
as the salivary glands proper. Because of their size and the volume of
saliva which they contribute they deserve special consideration. Physio-
logic investigations have been, for the most part, carried out on these
glands but conclusions which have been drawn from their study can prob-
GL.-LNDS or THE ORAL oavrrr 275
 
ably be applied with little change to the numerous smaller glands of the
oral cavity. A comparison of the anatomic features of the three large
salivary glands is presented in the accompanying table.
 
Tasnn IX
 
COMPARISON or rm: MAJOR Sanrvucr GLANDS
(Amen Cownnv)
 
 
 
   
 
 
 
 
     
   
 
   
   
 
 
   
 
SUBMAXILLARY SUBLINGUAL
 
Size and Largest; main and ac- Intermediate; well lim-Smallest; major gland
 
 
 
 
   
   
 
 
 
 
 
       
 
 
shape cessory parts both en- ited and encapsulated; and several minor
 
capsulated; compound, compound, branched, ones; no capsule; com-
 
branched, alveolar alveolar, partly tubular poxmd, b ranch e d,
tubnlo-alveolar
 
Posifion A r ound mandibular Beneath mandible (also In floor of mouth
ramus anterior to ear called submandibular
 
gland)
 
Ducts Parotid (Stenson’s)ductSubma.xi1lary (Whar- Major sublingual (Bar-
opens opposite second ton’s) duct opens on tholin’s) duct opens
upper molar; double either side of frenu- near submaxillary
layer columnar cells on lum of tongue; struc- sometimes by common
in a r k e d basement ture same aperture, also several
membrane minor sublingual
 
(Rivinian) ducts;
structure same
 
Secretory Single layer very con- Same but somewhat Rare or absent
 
ducts spicuously striated longer and may con-
eolumnar cells tain yellow pigment
 
Inter- Long, narrow, brancl1- Much shorter but similar Absent
 
calated ing made of single structure
ducts layer of flattened cells
 
59°79“?! 5610115 8-1V601i, 1111160115 Serons alveoli predom-Major gland: mucous
 
e_pithe- alveoli rare (in new- inate, some mucous al- alveoli predominate,
hum born) veoli have serous cres- many serous crescents
cents and alveoli. Minor
glands all mucous
Interstitial Fat cells most abundant Connective tissue septa
‘$188118 most abundant
Ni’-"73 Sensory: fifth nerve. Sens fifth nerve. Sensory: fifth nerve
WPP1)’ Secretary: (1) sympa- Secretory: (1) sympa-Secretory: same as sub-
thetic, superior cer- thetic, same; (2) maxillary gland
 
vical ganglion (vaso- parasympathetic,
constriction); seventh‘ nerve, chords
(2) parasympathetic, tympam, subrnamllary
ninth nerve, fitic gan- ganglion (vasod1la-
glion (vasodilation) tion)
 
 
The parotid gland (glandula parotis) is the largest of the salivary
glands. Its superficial portion is located in front of the external car on
the lateral surface of the masseter muscle and extends slightly backward
below the external auditory meatus. Its upper corner never transgresses
the zygomatic arch, the lower corner reaches into the neck as cervical
lobe (Fig. 209). The deep part of the parotid gland fills the retroman-
dibular fossa. The gland is enclosed within a strong capsule which is
tightly adherent and continuous with the connective tissue separating
lobes and lobules. Accessory parotid glands are often found alongside
 
the parotid duct.‘
 
Parotid Gland
276 our. HISTOLOGY mu mmnmzonoey
 
The parotld gland empties by the parotid duct (ductus parotideus,
Stenson’s duct) which is given off at the anterior corner of the gland,
continues forward, turns around the anterior border of the masseter
muscle, pierces the buccinator muscle and mucous membrane of the cheek
to open opposite the upper second molar. Usually a small papilla marks
the opening.
 
. 1:, yrs ‘;f'::.&v:h ‘,.
‘  ‘xi  an
 
   
 
Branching
duct
'$;':‘I".‘;‘3|. ’ - ;’V
Fig. 216.—Section through a human parotid gland.
Intercalated ' ~  *~-~—v~—
duct
Striated duct ,, new W4, A *-W’-r—‘ ' - - --— striated duct
 
Fig. 217.—I-Iigher magnification of field X in Fig. 216.
GLANDS on THE omu. csvrrr 277
 
 
 
   
 
- Albuminous
 
 
alveoll
3-Mucous
alveoli
5 ‘i id 57>‘ i« I‘ ./
.:"‘-  ‘ii. . .‘:-  ’  ‘Zn :1" i 
 
Fig. 218.—Section through a human submaxillary gland.
 
7)" Albuminous
 
Demilune _* ‘mean
 
Mixed --
alveolus
 
Interlobulsr
septum
 
Fig. 219.—Higher magnification or fleld X in Fig. 218.
 
The parotid gland of the adult is made up entirely of albuminous cells
(Fig. 216). The alveoli which form small tightly packed oval masses are
drained by long thin branching intercalated ducts; striated tubules are
conspicuous (Fig. 217).
 
The parotid gland produces a thin and watery saliva which serves for
the moistening and cleansing of the mouth cavity. It contains, besides
278 ORAL HISTOLOGY AND EMBRYOLOGY
 
Interlobular ‘
septum
 
Fig. 220.—-Section through a. human major sublingual gland.
 
 
Fig. 221.-—Higher magnification of field X in Fig. 220.
GLANDS or THE osar. oavrrr 279
 
salts and proteins, the enzyme ptyalin (amylase) which acts chemically
to hydrolize starch into simpler compounds.
 
The submaxillary gland (submandibular gland; glandula submaxillaris)
of man comprises one component of the group of glands in the floor of
the mouth sometimes designated as the alveolingual complex.‘ It is
ovoid in form, loosely encapsulated and about the size of a walnut. The
greater part of the gland is located in the submaxillary triangle behind
and below the free border of the mylohyoid muscle (Fig. 209). It is
usually divided into several large lobes by deep incisures penetrating to
the hylus. A tongue—like extension of the gland usually lies above the
mylohyoid muscle close to the sublingual glands. It, occasionally, ex-
tends forward under cover of the lesser sublingual gland, nearly to the
midline, and is designated as the secondary submaxillary gland proper.
 
The submaxillary gland including its accessory portions drains by the
submaxillary duct (Wharton’s duct) which is composed of many smaller
ducts arising in the lobules of the gland. The submaxillary duct is much
thinner than the parotid duct. The supporting stroma contains a few
longitudinal smooth muscle cells. It opens by a narrow orifice on the
summit of a small papilla, caruncula sublingualis, at the side of the
lingual frenulum at the floor of the mouth.
 
In man, the submaxillary gland is of the mixed type with albuminous
elements predominating (Fig. 218). Many purely serous alveoli are pres-
ent; infrequently occurring mucous alveoli are usually capped by demi-
lunes of serous cells. The intercalated ducts of the submaxillary gland
are relatively short (Fig. 214), but similar in structure to those of the
parotid gland (Fig. 219). The striated tubules are also structurally simi-
lar to those of the parotid but are somewhat longer (Fig. 214).
 
The secretion of the submaxillary gland contains mucin and is, conse-
quently, more viscid than that of the parotid gland. It is described as
clear and abundant. It varies, however, both in quantity and quality
with the type of stimuli.
 
The sublingual glands form a composite of one larger and several smaller
glands which open independently into the oral cavity. The larger or
major sublingual gland (Bartholinian gland) is drained by a single duct,
major sublingual duct, Bartholin’s duct. The smaller glands, Rivinian
glands, are usually 8 to 20 in number and drain by separate openings,
Rivinian ducts. The greater and lesser sublingual glands plus the supra-
mylohyoid submaxillary gland sometimes carry the inclusive designation
of “massa sublingualis.”‘
 
The sublingual gland or glands of the adult are the smallest of the units
 
comprising the salivary glands proper. The greater sublingual is nar-
row, flattened and elongated; it is situated in the floor of the mouth in
 
the sublingual fold (Fig. 209). The course of the duct which drains it
is roughly parallel to and a little lateral to the submaxillary duct. It
opens into the mouth at the side of the frenulum of the tongue on the
 
submaxillary
Gland
 
sublinguai
tion
 
Tubulo-alveolar :
terminal por- _
A Albumlnous
alveolus
septum
Demllune
Mucous
alveoli
 
fiiual Glands
 
Minor Buccal
Glands
 
Demllune .7
 
280 out HISTOLOGY AND EMBRYOLOGY
 
salivary caruncle with Wharton’s Qluct, in most cases; occasionally, how-
ever, the duct opens independently into the oral cavity near the sub-
maxillary duct.
 
Some of the ducts of Rivini which do not take part in the formation of
the larger sublingual duct, join the submaxillary duct, others open sepa-
rately into the mouth on an elevated crest of the mucous membrane, plica
sublingualis.
 
The large sublingual gland in man is a mixed gland in which the
mucous elements predominate (Figs. 220, 221, 222). Most alveoli are
purely mucous, the albuminous cells are mostly found as demilunes in
mixed alveoli. Purely serous alveoli are rare. The smaller sublingual
glands are, for the most part, mucous glands.
 
 
 
Fig. 222.--Section thro h a human sublingual gland with long tubulo-alveolar terminal
no ons. (Courtesy Army Medical Museum.)
 
10. MINOR SALIVARY GLANDS
 
The labial glands, which are located in the inner surface of the lips, are
of the mixed type. They are variable in size and closely packed in the
submuoosa where they may be easily palpated. They are not encapsu-
lated. The secretory portions may contain both serous and mucous cells
lining the same lumen but more often typical demilunes are formed. A
considerable number may contain only mucous cells (Fig. 223). The cells
have a distinct muco-albuminous character, the intercalated ducts are short.
 
The buccal glands, which are a continuation of the labial glands, bear a
marked resemblance to those of the lips. The glands which lie in the im-
mediate vicinity of the parotid duct opening, and drain in the third molar
region, are frequently designated as the molar glands (Fig. 224).
GLANDS or THE ORAL CAVITY 281
 
The glossopalatine (isthmian or faucial) glands are pure mucous glands; G1‘(’}*:;P;:‘”"°
they are located in the isthmus region and are a continuation, posteriorly,
of the lesser sublingual glands. They ascend in the mucosa of the glosse-
 
Fig. 224.—Section through a human retromolar gland.
Palatine
Glands
 
Glands of the
Tongue
 
282 ORAL HISTOLOGY AND EMBRYOLOGY
 
palatine fold. They may be confined to the anterior faucial pillar or extend
into the soft palate to fuse with the palatine glands pI‘0PeI‘- They may
also be seen on the lingual side of the retromolar area of the mandible.
The palatine glands which occupy the roof of the oral cavity can be
topographically divided into ( 1) glands of the hard palate; (2) glands of
the soft palate and uvula. They are composed of independent glandular
aggregates numbering approximately 250 in the hard palate, 100 in the
soft palate, and 12 in the uvula. In the posterior area of the hard palate
the glands lie between the mucous membrane and bone supported by a
 
Fig. 225.——'.l.‘he palatine glands. (Sicher and Tandlerfi)
 
dense framework of connective tissue characteristic of this region. Con-
tinuing backward, the lateral groups become arranged into compact rows
and take on considerable size (Fig. 225). They merge with those of the
soft palate and form a thick layer between the mucous membrane and
palatal musculature (see chapter on Mucous Membrane).
 
The structure of the palatine glands is that of long branched tubulo~
 
alveoli connecting with single ducts. The predominating cell produces
only mucus. Cells of the so-called intercalated ducts are converted into
 
mucous cells in the palatal glands, and function as part of the elongated
alveoli.
 
The glands of the tongue are of three types: serous, mucous, and mixed,
the mucous being the most numerous. The anterior lingual gland (gland
GLANDS or ran oaar. cavrrx 283
 
of Blandin-Nuhn) is located close to the inferior surface of the tongue, one
on each side of the frenulum near the apex. The structure is composed of a
group of raccmose glands embedded deeply Within the structure of the
tongue (Fig. 226). Approximately five small ducts open Imder the tongue
on the plica fimbriata. The gland is of the mixed type although chiefly
mucous in its anterior part. In its posterior part are found mucous alveoli
capped with delicate demilunes, with a distinctly serous character.
 
The glands of the base and border of the tongue are of the pure mucous
variety. The glands which are located on the surface of the tongue -bear
long mucous tubular alveoli and ill-defined ducts. In the immediate re-
gion of the vallate and foliate papillae they are replaced by the serous
glands of the gustatory papillae (glands of v. Ebner). These glands
pour a watery secretion into and serve to wash out the furrows of the
circumvallate papillae. (See chapter on Mucous Membrane.)
 
 
 
Anterior -
lingual
gland ,’
 
Fig. 226.-Longitudinal section through the tip of the tongue of a. newborn child.
Anterior lingual gland.
 
11. GLINIGAL CONSIDERATIONS
 
Pathologic disturbances of the salivary glands are relatively infrequent.
When they do occur the result may be either an increase in the flow of
saliva (sialism) or a decrease (xerostomia). Secretion is increased in
mental and nervous affections, occasionally in acute fever and during
attacks of generalized stomatitis. Injections of certain drugs, particu-
larly mercury and iodine compounds, are likely to produce an abundance
of saliva. Other than the discomfort. an abundance of saliva results in
no known harm. Disturbances that cause a reduction of saliva, however.
bring about loss of the protective action which this fluid exerts upon
284 ORAL I-IISTOLOGY AND EMBRYOLOGY
 
the teeth and oral tissues. Atrophy of the secretory elements and their
replacement by adipose tissue occurs in old age. The resulting xerostomia
may cause discomfort to a. patient wearing artificial dentures. Through
its loss the lubricating, cleansing and neutralizing power of the saliva
is forfeited. Moreover, a normal flow of saliva is a mechanical guard
against infection.
 
Inflammation is frequently the cause of disturbances in the flow of
saliva. It is common in the parotid gland, less common in the submaxil-
lary, sublingual and smaller glands. Pyogenic organisms are the chief
offenders in acute infections. Most frequently in debilitated individuals
suffering from infectious fever or general postoperative complications,
the infection may be confined to the ducts (sialodochitis) or, less fre-
quently, spread through the parenchyma of the gland (sialadenitis). In-
flammation of the glandular substance itself, when it occurs, is usually
severe. When it progresses to suppuration, surgery is indicated.
 
Glass blowers and players of wind instruments are especially subject
to infection of the salivary ducts. The heightened intraoral pressure
tends to dilate the ducts, counteract the normal outflow of saliva, and
bacteria are forced into the ducts.
 
Infection of the ducts of a salivary gland may cause a mass of dead
cells or bacterial debris to become lodged in a constricted area of the
ducts. If allowed to remain, such a mass acts as a nidus in which calcium
salts are deposited. This leads to the formation of a salivary calculus.
Salivary calculi occur most often in the submaxillary duct (90 per cent)
where they vary in size from minute particles to deposits several
centimeters in length. If they are retained their obstructive influence
invites inflammatory exacerbations afiecting the parenchymatous tissues;
or, if saliva is retained under pressure for any length of time, atrophy
and fibrosis of the gland may result. Salivary duct calculi are easily
 
detected by palpation or roentgenologic examination, and are removed
by gentle pressure or by excision. When calculi involve the glandular sub-
 
stance proper, total extirpation of the gland may be advisable.
 
Infectious parotitis (mumps) is the most common example of a virus
infection of the salivary glands. This disease shows tender swelling
of the parotid region, usually bilateral, with mild fever but no leuko-
cytosis. Tuberculosis, syphilis, and actinomycosis may occasionally affect
the salivary glands. The etiologic agents may be hematogenous or car-
ried to the glandular substance through the ducts.
 
Mikulicz’ disease is a type of granulomatous inflammation, rare in oc-
currence, which affects both the salivary and lacrimal glands, and occa-
sionally, the lips and eyelids. It makes its appearance as a symmetrical,
indolent enlargement which may last several years. A dry mouth is one
of the accompanying symptoms. Histologically, there is a lymphocytic
infiltration of the interstitial connective tissue and, if persistent, ultimate
GLANDS or THE omu. CAVITY 285
 
destruction of the parenchymatous elements.“ The blood picture re-
mains normal. It must be diflerentiated from Mikulicz’ syndrome which
is associated with such general processes as leukemia, Hodgkin’s disease,
and syphilis. A variety of tumors have been described in connection with
the salivary glands: mixed tumors, carcinoma, sarcoma, and several other
types are found of which about 75 per cent occur in the parotid. Of this
number about 95 per cent are of the mixed variety.’
 
Congenital malformations of the salivary glands may vary from atresia
of the ducts to complete aplasia of the gland. Such disturbances are more
common in the floor of the mouth in connection with the alveolingual
complex, but they are not uncommon in the parotid area. Atresia is less
common than aplasia, but when present causes disfiguring cysts or tumor-
like growths. The large sublingual gland is most frequently afiected,
giving rise to the so-called ranula, in the floor of the mouth. The glands
of Blandin-Nuhn, located in the anterior part of the tongue, are susceptible
to cystic involvement as a result of closure of their ducts. These cysts
are designated as mucous cysts or mucoceles. Mucoceles are quite com-
monly found in connection with the smaller glands of the oral cavity,
where they probably result from trauma, a mild infection of the duets with
consequent closure. They are, however, of little concern and usually disap-
pear after rupture and discharge of their contents.
 
Aberrant glands are encountered occasionally in the alveolingual area.
They are accessory glands which have become detached from the duct
system. These glands remain functional but because they-lack an excre-
tory duct, the secretion accumulates within their structure and causes
distention with cyst formation.
 
The use of rubber dam or prolonged pressure by cotton rolls can
occlude the opening of one of the salivary ducts. The resulting swelling
occurs at the time the work is in progress, and disappears soon after the
obstruction is removed and the saliva has an opportunity to discharge.
 
References
 
1. Appleton, J. L. T.: Bacterial Infection, Philadelphia, 1925, Lea &; Febiger.
 
2. Babkin, B. P.: The Physiology of the Salivary Glands, in Gordon, S. M.: Dental
Science and Dental Art, Philadelphia 1938, Lea & Febige .
 
3. Braus, H.: Anatomic des Menschen (Human Anatomy), Book 2, ed. 2, Berlin,
1934, Julius Springer.
 
4. Brawley, R. E.: Studies of pH of Normal Resting Saliva: Variations With Age
and Sex; Diurnal Variation, J. Dent. Research 15: 55, 79, 1935.
 
5. Car-malt, Churchill: Contribution to the Anatomy of the Adult Human Salivary
Glands, IV, Part 1, Geo. Cracker Special Research Fund, 1913.
 
6. Cheyne, V. D.: Efiects of Selective Salivary Gland Extirpation Upon Experimental
Dental Caries in Rat, Proc. Soc. Exper. Biol. & Med. 42: 587, 1939.
 
7. Cheyne, Virgil D., Tiecke, Richard W., and Home, Eleanor V.: A Review of
So-Called Mixed Tumors of the Salivary Glands Including an Analysis of
Fifty Additional Cases, Oral Surg., Oral Med., Oral Path. 1: 359, 1948.
 
8. Gies, W. J., and Kahn, M.: An Inquiry Into the Possible Relation of Sulfa-
cyanate to Dental Caries, Dental Cosmos 55: 40, 1913.
 
9. Hill, T. J .: Salivary Factor Which Influences Growth of L. Acidophilus and Is an
Expression of Susceptibility or Resistance to Dental Caries, J. A. D. A. 26:
 
239, 1939.
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12.
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14.
 
15.
16.
 
17.
18.
 
19.
20.
21.
 
22.
23.
24.
 
ORAL I-IISTOLOGY AND EMBRYOLOGY
 
Hill, '1‘. J.: The Influence of Saliva Upon the Growth of Oral Bacteria, J . Dent.
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Inouye, J. M.: Biochemical Studies of Salivary Mucin, J. Dent. Research 10: 7,
1930.
Langley, J . N .:
 
261, 1379.
 
Lashley, K. S.: Reflex Secretion of the Human Parotid Gland, J . Exper. Psychol.
1: 461, 1916.
 
Lehman, J. A., and Leaman, W. G.:
1940.
 
Mathews: The Physiology
Maximow, A. A., and Bloom, W.:
1942, W. B. Saunders Co.
Orban, B., and Weinmann, J. P.: Cellular Elements of Saliva and Their Possible
 
Role in Caries J. A. D. A. 26: 2008, 1939.
 
Rosemann, B.: Iihysikalische Eigenschaften und chemische Zusammenstezung
der Verdauungssiifte unter normalen und abnormen Bedingungen. Handb.
der normalen und pathologischen Physiologic (Physical Properties and
Chemical Constitution of the Digestive Juices Under Normal and Abnormal
Conditions. I. Saliva, Handbook of Normal and Pathologic Physiology),
Berlin, 1927, Julius Springer, vol. 3, p. 819.
 
Sicher, H., and Tandler, J .: Anatomie fiir Zahniirzte (Anatomy for Dentists),
Berlin, 1928 Julius Springer.
 
Stephens, D. J.,’and Jones, E.: Leukocytes in the Saliva in Normal and Ab-
normal Subjects, Proc. Soc. Exper. Biol. & Med. 31: 879, 1934.
 
Thoma, K. E.: A Contribution to the Knowledge of the Development of the
Snbmaxillary and Sublingual Salivary Glands in Human Embroys, J . Dent.
Research 1: 95, 1919.
 
Updegrafi, H., and Lewis, H. B.: A Quantitative Study
stituents of Saliva, J. Biol. Chem. 61: 633, 1924.
Youngberg, G. E.: Salivary Ammonia and Its Relation to Dental Caries, J . Dent.
 
Research 15: 247, 1936.
 
Zimmermann, K. W.: Die Speicheldriisen der Mundhiihle und die Bauch-
speicheldriise. Handb. der mikr. Anat. des Menschen (The Salivary Glands
and the Pancreas. Handbook of Human Microscopic Anatomy), Book 5,
Part 1, Berlin, 1927, Julius Springer.
 
On the Changes in Serous Cells During Secretion, J. Physiol. 2:
 
Mikulicz’s Disease, Internat. Clin. 3: 105,
 
of Secretion, Ann. New York Acad. Sc. 11: 293, 1898.
A Textbook of Histology, ed. 4, Philadelphia,
 
of Some Organic Con-
CHAPTER XI
 
ERUPTION OF THE TEETH
 
1. INTRODUCTION
2. EISTOLOGY OI‘ ERUTTION
 
a. Preemptive Phase
1:. Pre1'uncti.ona.1 Phase
c. Functional Phase
 
3. MEGEANISM OF ERUPTION
4. CLINICAL CONSIDERATIONS
 
1. INTRODUCTION
 
The human teeth develop in the jaws and do not enter the oral cavity
until the crown has matured. In the past, the term eruption was gen-
erally applied only to the appearance of the teeth in the oral cavity.
It is, however, known that the movements of the teeth do not cease when
the teeth meet their antagonists.“ 7 Movements of eruption begin at the
time of root formation and continue throughout the life span of a tooth.
The emergence through the gingiva is merely an incident in the process of
eruption. The eruption of deciduous as well as permanent teeth can be
divided into the prefunctional and functional phases. At the end of the
prefunctional phase the teeth come into occlusion. In the functional
phase the teeth continue to move to maintain a proper relation to the jaw
and to each other.
 
Eruption is preceded by a period in which the developing and growing
teeth move to adjust their position in the growing jaw.’ A knowledge
of the movements of the teeth during this preeruptive phase is necessary
for a complete understanding of eruption. Thus, the movements of the!
teeth can be divided into three phases: (1) preeruptive phase; (2) pre-
functional phase; (3) functional phase.
 
During these phases the teeth move in difierent directions.” These
movements can be termed: ( 1) axial: occlusal movement in the direction
of the long axis of the teeth; (2) drifting: bodily movement in a distal,
mesial, lingual or buccal direction; (3) tilting: movement around a trans-
verse axis; (4) rotating: movement around a longitudinal axis.
 
2. HISTOLOGY OF ERUPTION
 
During the first, preeruptive phase the enamel organ develops to its Preemptive
full size, and formation of the hard substances of the crown takes place. Pm“
 
First draft submitted by Joseph P. Weinmann.
287
288 ORAL HISTOLOGY AND EMBRYOLOGY
 
At this time the tooth germs are surrounded by the loose connective tis-
sue of the dental sac and by the bone of the tooth crypt.
 
The development of the teeth and the growth of the jaw are simulta-
neous and interdependent processes. The microscopic picture of the
growing jaw indicates that extensive growth takes place in that area of
the jaws where the alveolar crest ultimately develops (Fig. 227). The
tooth germs maintain their relationship to the growing alveolar margin
by moving occlusally and buccally.‘
 
 
 
. fxi
 
.  Anlage of
. permanent
 
tooth
 
Fig. 227.—-Cross section through lower jaw and deciduous molar or human fetus (4th
month). Tooth germ moves bucoally by excentric growth indicated by resorption at
inner surface of.’ the buccal alveolar plate and lack of apposition at the inner surface
of the lingual plate.
 
Two processes are responsible for the developing teeth attaining and
maintaining their position in the growing jaw, especially in relation to
the alveolar ridge: the bodily movement of the teeth, and the excentric
growth of the tooth germs. Bodily movement is characterized by a shift
of the entire tooth germ. It is recognized by apposition of bone behind
the moving tooth, and by resorption of bone in front of it. In excentric
growth one part of the tooth germ remains fixed: the growth gives rise
ERUPTION or ran TEETH 289
 
to a. shift of the center of the tooth germ. Excentric growth is charac-
terized solely by resorption of the bone at the surface toward which the
tooth germ grows.
 
During most of the time when the deciduous teeth develop and grow,
upper and lower jaws grow in length by apposition in the midline and
at their posterior ends. Accordingly, the growing germs of the deciduous
teeth shift in vestibular direction; at the same time the anterior teeth
move mesially, the posterior distally, into the expanding alveolar
arches." These movements of the deciduous teeth are partly bodily
movements, in part caused by excentric growth. The deciduous tooth
germ grows in length at about the same rate as the jaws grow in height.
The deciduous teeth maintain, therefore, their superficial position through-
out the preeruptive phase.
 
The permanent teeth which have temporary predecessors undergo an in-
tricate movement before they reach the position from which they emerge.
Each permanent incisor (Fig. 228) and cuspid develops at first lingually to
the deciduous tooth germ at the level of its occlusal surface.“ At the
close of the preemptive phase they are found lingual to the apical region
of their deciduous predecessors. The permanent bicuspids (Fig. 229)
begin their development lingually to and at the level of the occlusal plane
of the deciduous molars.“ Later, they are found between the divergent
roots and, at the end of the preeruptive phase, below the roots of the
deciduous molars (see chapter on Shedding). The changes in axial rela-
tionship, between deciduous and permanent teeth, are due to the occlusal
movement of the deciduous teeth and the growth of the jaw in height.
The germs of the bicuspids move by their buccally directed excentric
growth into the interradicular space of the deciduous molars.
 
The second phase of tooth movement, the prefunctional phase of erup-. pmucflom
tion, begins with the formation of the root (page 42) and is completed! P1350 01
when the teeth reach the occlusal plane. In the beginning of this phase nmptm
the crown is covered by enamel epithelium. While the crown moves toward
the surface, the connective tissue between the reduced enamel epithelium
and the oral epithelium disappears, probably by the desmolytic action
of the enamel epithelium. When the cusp of the crown approach the oral
mucosa, the oral epithelium and reduced enamel epithelium fuse. In the
center of the area of fusion the epithelium degenerates and the tip of the
cusp emerges into the oral cavity. The gradual emergence of the crown
is due to the occlusal movement of the tooth (active eruption), and also
to the separation of the epithelium from the enamel (passive eruption).
 
The reduced enamel epithelium remains in organic connection with that
part of the crown which has not yet emerged. (See section on Epithelial
Attachment.) The growth of the root or roots of a tooth occurs by simul-
taneous and correlated proliferation of Hertwig’s epithelial root sheath
and the connective tissue of the dental papilla. The proliferation of the
290 ORAL HISTOLOGY AND EMBRYOLOGY
 
epithelium takes place by mitotic division of the cells of the epithelial
diaphragm. The proliferation of the connective tissue cells is concen-
trated in the area above the diaphragm.
 
During the prefunctional phase of eruption the primitive periodontal
membrane, derived from the dental sac, is adapted to the relatively rapid
movement of the teeth. Three layers of the periodontal membrane can
be distinguished around the surface of the developing root: one, adja-
cent to the surface of the root (dental fibers); another attached to the
 
 
9 1110.
 
Fig: 228.——BuccoIingua1 sections through lower central incisors of seven consecutive
stages, from newborn infant to 9 years 01.’ age.
 
primitive alveolus (alveolar fibers) ; and a third, the intermediate plexus
(Fig. 137). The intermediate plexus’ consists mainly of precollagenous
fibers, whereas the alveolar and dental fibers are mainly collagenous.
The collagenous fibers can be traced into the intermediate plexus for a
short distance. The intermediate plexus permits continuous rebuilding
 
and rearranging of the periodontal membrane during the phase of rapid
eruption.“ 2°
ERUPTION or THE TEETH 291
 
In the region of the fundus, the dental sac differentiates into two
layers: one, close to the bone, consists of loose connective tissue, whereas
the other, adjacent to the growing end of the tooth, consists of a network
of rather thick fibers and contains a large amount of fluid in the tissue
spaces between the fibers (Fig. 230). Strong strands of fibers from the
 
‘periodontal area at the side of the root curve as a strong ligament around
the edge of the root, and then divide into a network forming spaces that
are filled with fluid. This entire structure is designated as “cushioned
hammock ligament.”-'1
 
In the prefunctional phase of eruption the alveolar ridge of the jaws
grows rapidly. To emerge from the growing jaws the deciduous teeth
must move more rapidly than the ridge increases in height. Growth of
the root is not always suflicient to meet these requirements. A rapid
formation of bone begins at the alveolar fundus Where it is laid down in
trabeculae, parallel to the surface of the alveolar fundus” (Fig. 231).
The number of trabeculae increases markedly during the prefunctional
292 om. HISTOLOGY AND EMBRYOLOGY
 
phase, and varies in difierent teeth: the smallest number of trabeculae
is found at the fundus of the molars. This variance in the number of
trabeculae seems to depend upon the distance which the teeth have to
cover during this phase of tooth eruption.
 
The germs of most permanent teeth develop in a crowded position. They
occupy, therefore, a position which difiers markedly from their ultimate-
position after emergence. The molars are tilted; the occlusal surface of
the upper molars, which develop in the maxillary tuberosity, is directed
distally and downward. The occlusal surface of the lower molars, which
develop in the base of the mandibular ramus, is directed mesially and
upward. The long axis of the upper cuspids deviates mesially. The
lower incisors are frequently rotated around their long axis. In the later
stages of the prefunctional phase of eruption these teeth undergo intri-
 
   
 
 
i\ en:-"' ”"“"-‘-”»'%’.f’v". ,. 1
 
Fig. 229.—Bucco1ingus.i sections through lower deciduous flrst molar and flrst bicuspid
or eight consecutive stages, from newborn infant to 14 years.
 
cate movements to rectify their primary position. During these tilting
and rotating movements, bone apposition takes place in those areas of the
tooth crypt from which the tooth moves away, and resorption occurs in
the areas toward which the tooth moves. In all other details, the his-
 
tologic changes correlated to eruption are identical in permanent and de-
ciduous teeth..
ERUPTION or run TEETH 293
 
The histologic findings in erupting multirootecl teeth present a picture
quite diflerent from that in single-rooted teeth. The epithelial root
sheath does not form an epithelial diaphragm, a cushioned hammock liga-
ment is absent, and the proliferating pulp protrudes beyond the root
end. The bone at the crest of the interradicular septum shows all signs
of rapid growth. Apposition of cementum is also evident at the bifurca-
tion. , _
 
After the erupting teeth have met their antagonists their movements are 1-uncuoml
not easily ascertained For a long time it was believed that functioning §h“°_°f
teeth do not erupt any longer. However, clinical observations and his- mph”
tologic findings show that the teeth continue to move throughout their life
span. The movements are in an occlusal as well as in a mesial direction.
 
..,,..... .... __ _ ...
 
 
 
 
 
 
  a l V E
*’*s..,.. /A .
3 yr. 41,5 yr. 11 yr. 14 yr.
 
Clinically, the continued active movement of teeth can be proved by
an analysis of the so-called shortened and submerged teeth (see page
322). Histologically, the changes in the alveolar bone furnish concrete
evidence for the movements of the teeth in their functional period (see
page 205).
 
During the period of growth, the occlusal movement of the teeth is.
fairly rapid. The bodies of the jaws grow in height almost exclusively at‘
the alveolar crests and the teeth have to move occlusally as fast as the
294 ORAL HISTOLOGY AND EMBRYOLOGY
 
   
   
 
 
 
- -  Prollferzttlon
zone of pulp
 
‘ §~-,-— -—-—————» Epithelial
' _-V ' diaphragm
 
 
4 m4 —-»— V — Cushioned
. hammock
ligament
 
Fig. 230.—Cushioned hammock ligament Root end or an erupting 10WeI' cuspid.
Proliferation zone of the pulp above the epithelial diaphI'a€m- Note the numerous tissue
spaces in the ligament. (slcher-.3‘)
 
I Deciduous
tooth
Bone Q  ' ’
trabeculae ,- —.’ u
at fundus ,‘ -‘ .3 Enamel
Permanent
tooth
 
trabeculae
at tundus
 
F13-. 231.—-Erupting upper deciduous cuspicl (A) and lower permanent cuspid (B),
Note formation of numerous parallel bone trebeculae at alveolar fundus. Formation of
bone trabeculae at the alveolar crest of deciduous cuspids (A) is 9. sign or rapid growth
or the maxilla in height. (Kronteldfi)
Bundle bone at
fundus
 
     
 
 
 
 
 
me5ia-l- ;  ‘.5 ‘  Bundle bone on
alveolar ‘ ‘f  distal
wall .3 "I.  ,  alveolar
r;_'.,:l - i  wall
’ 7“ Alveolar
! ; septum
First bzcuspid. 2" ’ _, _  Second bicuspm"
 
-2‘
 
~. M «
‘  \
 
L . ‘E
 
Fig‘. 232—-—1\_£[esia._l drift and vertical eruption. Meslodistal section through upper first.
and second bxcuspids. Arrow indicates direction of drifting movement. Apposition or
bundle bone at the distal, resorption of bone on the meslal surfaces or the alveoli. Ap-
 
Dosition of bundle bone at the tundus and alveolar crest. (Weinma.nn.")
 
Periodontal
membrane
 
. . Periodontal
Apposition ,
o! bundle membrane
bone
- Resorption
First __.._.. p or bone
bicuspid
- Second
J bicuspid
 
Avposition of - W - '‘
bundle bone -
 
Fig. Z33.—I-Iigher magnification of crest of interdental septum between first and
second upper bicuspids of Fig. 232. Arrows indicate direction of movement. Apposition
or bundle bone on surface of septum facing the flrst blcuspid and at alveolar crest, re-
sorption of bone on surface of septum facing the second bicuspid. (Wein1na.nn.")
296 ORAL HISTOLOGY AND EMBRYOLOGY
 
jaws grow, in order to maintain their functional position. The eruptive
movement in this period is masked by the simultaneous growth of the
jaws. _
 
The continued vertical eruption also compensates for occlusal. or m-
cisal attrition. Only in this way can the occlusal plane and the distance
between the jaws during mastication be maintaincd—a condition which
is essential for the normal function of the masticatory muscles.
 
Epithelial
rest
 
Epithelial
rest
 
Epithelial
rest
 
Epithelial
rest
 
Epithelial
rests
 
Fig. 234.—-A. Bundle bone at tundus of alveolus and in wall of canal leading blood
vessels and nerves to apical roramina. Epitl-ielial rests some distance from apex
along blood vessels and nerves. B. High magnification of epithelial rests of A.
 
The mobility of the individual teeth leads to friction at the contact
points and to increasing wear in these areas. Sharp contact of the teeth
is maintained despite the loss of substance at the proximal surfaces only
because of the continuous movement of the teeth toward the midline.
This movement is termed physiologic mesial drift.
 
Apposition of cementum continues along the entire surface of the root,
but the apposition of bone is restricted principally to the fundus, alveolar
crest, and distal Wall of the socket (Fig. 233). The mesial wall of the
ERUPTION or THE TEETH 297
 
socket shows resorption in wide areas. However, even on the mesial
 
surface of the alveolus, zones of reparative bone apposition can always
be found.
 
The tissue changes in the diiferent phases of tooth movements are sum-
marized in Table V11.
 
TABLE VII
Trssun CHANGES DURING Tm: PHASES or Tooru MOVEMENTS
 
”"‘E°"-'I°N cmuens or
OF EPITIIELIUM ————e———— 1>,1),M_
MOVEMENT TOOTH BONE
- 0ccluso-ax- Enamel organ Eccentric Growth of jaw Dental sa,
Prefihrzgrve ial; buccal growth of G
tooth germ
Prefunc- 0ccluso-ax- Fusion of re- Root growth Apposition Intermedi-
tional ial; duced enamel (trabecular ate plexus;
Phase _straighten- organ with _ bone) at fun- cushioned
of Eruption mg oral ep1thel1- due and a.1veo- hammock
tuirn; ffonnagh lar ridge ligament
on o 1 e-
lial attac -
ment. Hert-
 
wig ’s sheath;
epithelial rests
 
Functional 0ccIuso-ax- Down growth Attrition. Root Apposition Functional
Phase ial; mesial of epithelial resorption and (bundle bone) arrange-
 
of Eruption attachment shedding of at fundus and ment of
(passive erup- deciduous alveolar ridge suspensory
' tion) teeth. Ce- and distal al- apparatus
 
mentum appo- veolar wall;
sition of per- resorption at
manent teeth mesial wall
 
 
3. MECHANISM OF ERUPTION
 
Many theories have been advanced on the causes of tooth eruption}
The following factors have been eonsidered:"”' 1‘ growth of the root;?
growth of dentin; proliferation of the dental tissues; pressure from mus-p
cular action; pressure from the vascular bed in the pulp and periapieal
tissue; apposition and resorption of bone.
 
The eruptive movements of a tooth are the effect of differential growth. #
One speaks of diiferential growth if two topographically related organs,
or parts of an organ, grow at different rates of speed. Changes in the
spatial relations of such organs, or of the parts of an organ, are the in-
evitable consequence of differential growth. The ontogenesis of almost
any organ and of the whole embryo proves that diiferential growth is
one of the most important factors of morphogenesis. In the jaws, it is
the differential growth between tooth and bone which leads to the move-
ment of a tooth.
 
The most obvious eruptive “force” is generated by the longitudinal
growth of the root of the tooth. However, the different movements of
an erupting tooth cannot be explained by the development of its root?
alone. Some teeth, even while their roots develop, travel a. distance
293 ORAL HISTOLOGY AND EMBRYOLOGY
 
which is longer than the fully developed root. An auxiliary factor must
account for the additional distance. Most teeth move in different direc-
tions, for instance by tilting, rotating, drifting; the growth of the root
can only account for the axial or vertical movement. The “force” that can
explain the variety of eruptive movements is generated by the growth of
bone tissue in the neighborhood of the tooth germ.
 
1 It is also a fact that the teeth move extensively after their roots have
been fully formed. The continued growth of the cementum covering
}the root and of the surrounding bone causes the movements of the tooth
3' in this period.
 
Before the development of the root starts, the outer and inner enamel
epithelium continue from the region of the future cemento-enamel junc-
tion as a double epithelial layer, the epithelial diaphragm, which is bent
into the plane of the dental cervix. It forms a definite boundary between
the coronal pulp of the tooth germ and the underlying connective tissue
which intervenes between tooth germ and bony wall of the crypt. Thus,
 
’ growth and development of the root is possible only under active pro-
liferation of the pulpal tissue.
 
The importance of this single fact for the eruption of the tooth can
best be realized by comparing our knowledge of root development with
the long disproved, old concept of the function of Her-twig’s epithelial
root sheath. It was thought that this double layer of epithelium g_rew
into the underlying mesenchyme, punching out, as it were, part of this
tissue, isolating it and transforming it into pulpal tissue. If this were
true, the growth of the pulp would be by incorporation of new tissue
 
and therefore passive rather than active. The presence of the epithelial ‘
 
diaphragm makes an inward growth of the epithelial sheath impossible
and the pulp is “forced” to grow by multiplication of its cells and new
formation of intercellular substance ;, in other words, the pulp enlarges
by active growth, which creates the tissue pressure which can be seen
'- as the primary “force” of eruption.
1 The pressure generated by the increase in volume of the pulp in the
restricted space of the dental crypt would act against the bone in the
_bottom of the crypt and cause resorption of this bone and could not
cause an eruptive movement of the tooth germ if there were no auxiliary
structure. The auxiliary structure, which protects the bone at the bot-
'; tom of the crypt from pressure, prevents resorption of the bone, and
causes the tooth to grow or move away from the bottom of the crypt,
is the “hammock ligament.” If, by the proliferation of the growing
pulp, tissue pressure increases, this ligament is tensed, the pressure is
transmitted as traction to the bone to which the ligament is anchored,
and no pressure is directed against the bone at the bottom of the crypt.
Thus, the hammock ligament is the fixed base or plane from which the
tooth erupts because elongation of the tooth can only result in growth
toward the surface of the jaws.
ERUPTION or THE TEETH 299
 
It has been mentioned before that the growth of the root alone can-
not move a crown as far as is necessary to reach the occlusal plane. Some
teeth, for instance the cuspids, develop far from the surface of the jaws.
While all the teeth are erupting, the jaws continue to grow at their
alveolar borders. The vertical erupting movement of these teeth is aided
by growth of bone at the bottom of the crypt, lifting the growing tooth
 
with the hammock ligament toward the surface. The formation of bone 3
 
at the bottom of the crypt occurs in diiferent teeth at a different rate of
speed. Where the production of new bone is slow, new layers of bone
are laid down upon the old bone and a more or less compact bone results.
Where growth of bone is rapid, spongy bone is formed in the shape of a,
framework of trabeculae. These trabeculae develop by the growth of
small projections of bone from the old surface, which then, at a given
distance, seem to mushroom and to form new trabeculae parallel to the
 
old surface (Fig. 231). In this way, tier after tier of bone tissue develops
in the deep part of the socket.
 
The increased tissue pressure which is inevitably linked with the pro-
liferation of bone in the crypt would tend to compress the hammock liga-
ment, thereby destroying the fixed base which is essential for the normal
eruption of a tooth; finally, the bone would encroach upon tooth andj
pulp, bringing the eruption to a standstill. These consequences are pre-
vented by a peculiar structural differentiation of the hammock ligament.
Teleologically speaking, the hammock ligament is rendered incompres-
sible by the accumulation of a fluid or a semifluid substance between the
fibers and thus transformed into the “cushioned hammock ligament.”
The fluid is distributed throughout the ligament in small round drop- ,
lets. The presence of fluid in confined spaces is, of course, the cause of
the incompressibility of this ligament. The incompressibility is relative
but gives entirely sufficient protection if one considers the low intensity
of the pressure forces generated during tooth eruption. That this pres-
sure normally never reaches any higher intensity is explained by the
simple fact that reactive tissue changes immediately follow the increase
of tissue pressure and relieve it. '
 
While the hammock ligament and tooth are lifted toward the surface,
the anchoring fibers of the hammock ligament have to be continually
reconstructed. In other words, the hammock ligament has to shift its
anchoring plane toward the surface of the jaws. Details of the mech-
anism of this shift are, as yet, not known.
 
Enlargement of the root does not cease when the root is fully formed.
By continuous apposition of cementum, the root grows slightly in its
transverse diameters and more rapidly in length. Cementum apposition
is not only increased in the apical area of roots but the bifurcation of
two or three-rooted teeth is also a site of fairly intensive cementum ap-
position. It is also well known that there is continuous apposition of
bone at the fundus of the socket and at the crests of the alveolar process.
300 omu. HISTOLOGY AND EMBRYOLOGY
 
The bone apposition at the fundus and at the free border of the alveolar
process is very rapid in youth, slows down in the thirties, but normally
never ceases. Apposition at the alveolar crest, however, is found only
‘when the tissues are entirely normal. The frequency of inflammatory
changes at the gingivodental junction accounts for the fact that this
site of bone growth has been overlooked for a long time. There is also
constant apposition of bone on the distal wall of each socket while the
mesial wall shows resorption of the bone alternating with reparative
apposition.
 
Though the correlation of bone changes and movement of the teeth
is self-evident, the question still must be raised whether the bone changes
are primary and thus the cause of the movement of the teeth, or not.
The impossibility of finding any internal or external “forces” which
would account for the continuous vertical eruption and mesial drift is an
indication that the apposition of bone in the functional period plays the
same role which one can ascribe to it in the preeruptive and prefunctional
eruptive movements.
 
The apposition of bone can lead to a movement of a tooth only if the
root surface is protected against resorption. This protection is actually
given by the surface layers of uncalcified cementum, the cementoid tis-
sue, which regularly covers the surface of the cementum. The resistance
of cementoid tissues to resorption has been demonstrated repeatedly.
 
The mechanism of tooth movement in the functional period can there-
fore be described in the following way: The entire surface of the root
is protected against resorption by the growth pattern of the cementum
which shows continuous, though not even, apposition throughout the
life of the tooth. If apposition of bone occurs at the bottom of the crypt,
the" slight increase of tissue pressure can lead to a movement of the tooth
in occlusal direction only. This is because a relief of the pressure is not
possible by resorption of the root. For the normal occlusal movement
of a tooth in the functional period, the normal general growth of the
cementum and the patterned growth of the bone are of equal importance.
It is necessary to point out that only simultaneous growth of the op-
posing surfaces of cementum and bone can lead to a movement of a
 
itooth. It is therefore clear that the apposition of cementum at the apex
- can compensate only in part for the loss of tooth substance at the oc-
clusal surface, that is, for the shortening of the tooth by attrition. A con-
 
sequence of this behavior is the fact that the teeth do shorten during the
functional period.
 
In the life of every tooth there comes a time in which the “forces” of
eruption change abruptly. It is, of course, the time when the pulp is fully
grown and the root is fully formed. From now on, it is the differential
growth of bone and cementum, and not that of pulp and bone, which
causes the continued vertical movement of the tooth. The eruptive mech-
anism of multirooted teeth differs in that the shift from one to the
ERUPTION or arm: mam 301
 
other mechanism of eruption occurs much earlier, namely, as soon as the
bifurcation is fully formed, though the roots are still growing.
 
The mesial drift is caused, in principle, by similar changes of bone
and tooth which seem to be an adaptive, genetically determined process.
However, this movement is greatly complicated by the fact that extensive
bone resorption at the mesial alveolar walls has to open the space into
 
which the teeth move, while the vertical movement is not opposed by
bone.
 
Apposition of bone on the distal surface of the socket leads to an in-
crease of the interalveolar pressure. This can be relieved only by re-
sorption of bone at the mesial wall of the socket since the growing sur-
face of the bone and the entire surface of the root are protected by their
own growth, that is, by the presence of a thin layer of uncalcified ground
substance on their surface.
 
With both vertical and mesial movement of the functioning teeth, a
continual rearrangement of the principal fibers of the periodontal mem-
brane has to be postulated. Details of this process, however, are al-
 
most entirely unknown. The changes which prevent a destruction of the
ligamentous anchorage of the tooth on its mesial surface during the con-
 
tinuous mesial drift are explained by the peculiar reaction of bone to.
pressure (or during modeling resorption) which could be called “thel
law of excessive resorption.” Resorption of bone under pressure is, as '~
a rule, more extensive than necessary to relieve the pressure. The sur-'
face layers of a bone are structurally adapted to the functional needs of _
 
the particular area. If they are destroyed during resorption, the newly
exposed surface lacks this adaptation. Therefore, the resorption con-
 
tinues until room is provided for a reconstruction of a functionally ,
 
adequate new surface. This is the reason that, under normal circum-
stances, resorption is almost never a continuous process but instead oc-
curs in waves, periods of resorption alternating with periods of repara-
tive or reconstructive apposition.
 
This sequence of events can also be observed during the mesial drift
of a tooth. Some principal fibers lose their attachment during the period
of bone resorption and are then reattached, or replaced by new fibers,
which are anchored in the bone apposed during the period of repair.
Furthermore, it can be observed that bone resorption does not occur at
the same time on the entire extent of the mesial alveolar surface. In-
stead, at a given moment, areas of resorption alternate with areas of
reparative apposition. It seems that the tooth moves mesially in a com-
plicated manner. Thus, resorption occurs only in restricted areas in one
period and reconstruction occurs in the same area, while the tooth,
minutely tilting or rotating, causes resorption in another area. Only this
can account for the fact that the functional integrity of the tooth is main-
tained in spite of its continued movements.
302 ORAL HISTOLOGY AND EMBRYOLOGY
 
4. CLINICAL CONSIDERATIONS
 
The eruption of teeth is a part of general development and growth, and
therefore the progress of tooth eruption may serve as an indicator of the
physical condition of a growing individual. The time of emergence of a
tooth is readily observed by clinical examination. Considerable work has
been done in compiling data regarding this particular stage of eruption.
Table VIII illustrates that the time of emergence of all teeth varies
widely.” 5' 13 Only those cases which are not within the range of variation
may be considered abnormal. Retarded eruption is by far more frequent
than accelerated eruption and may have a local or systemic etiology.
 
Local causes, such as premature loss of deciduous teeth and closure of
the space by a shift of the neighboring teeth, may retard the eruption
of some permanent teeth. Severe acute trauma may result in an arrest of
active tooth eruption during the functional phase if the periodontal mem-
 
- brane of the tooth has been injured. Resorption of the root may ensue
 
in which event deposition of bone in the spaces opened by resorption
may lead to an ankylosis by fusion of alveolar bone and root.‘‘» 29 The
movement of such a tooth is then arrested whfle the other teeth continue
to erupt. If this disturbance takes place in the permanent dentition, a
so-called “shortened” tooth results. An ankylosed deciduous tooth may,
eventually, be covered by the rapidly growing alveolar bone. Such teeth
 
are called submerged teeth (see chapter on Shedding).
 
If the eruption of the entire deciduous or permanent dentition is delayed,
hereditary or systemic factors may be responsible. Among the systemic
causes are: disturbances of the endocrine system and nutritional defi-
ciencies. Hypothyroidism is of the former, and vitamin D deficiency of
the latter group. The eifects of hypothyroidism and vitamin D deficiency
on tooth eruption can be explained by a retardation of the growth of
teeth and bone. Delayed eruption of the teeth usually accompanies
cleidocranial dysostosis, a hereditary disease aifecting membrane bones.
 
The movements of the teeth, during eruption, are intricate and are
accomplished by minute coordination of growth of tooth, growth of the
alveolar bone, and growth of the jaws. Any break in this correlation may
affect the direction of the movements; this, in turn, may lead to an impac-
tion or embedding of a tooth. At the time the third molars develop, the jaw
has not reached its full length. Normally, the oeclusal surface of a third
lower molar turns anteriorly and upward. It is frequently prevented from
straightening out because of a lack of correlation between growth in length
of the lower jaw and tooth development. In such cases, the eruption of the
lower third molar is arrested because its crown comes in contact with the
roots of the second molar. If, at this time, the roots of the third molar are
not as yet fully developed, they will grow into the bone and may become
deformed. Cuspids, sometimes found in an oblique or horizontal position,
 
due to crowding of the teeth, may also fail to correct this malposition and
remain embedded.
TABLE VIII
 
Cnnoxonoov or THE HUMAN’ Dr.N'rI'rIoN
Logan and Kronfeld (slightly modified by McCall and Schour)
 
FORM.A'.l‘rON
ENAMEL MATRIX AMOUNT OF ENAMEL ENAMEL EMER/GENOE ROOT
 
TOOTH AND DEN,-MN MATRIX FORMED COMPLETED INTO ORAL COMPLETED
 
BEGINS AT BIRTH CAVITY
 
Central incisor 4 mo. in utero Five-sixths 1'} m0- 7% 1110- 1} )7!‘-
 
Lateral incisor 4} mo. in utero Two-thirds 21} mo. 9 mo. 2 yr.
 
Maxillary Cuspid 5 mo. in utero One-third 9 mo. 18 mo. 31 yr.
 
First molar 5 mo. in utero Cusps united 6 mo. 14 mo. 2} yr.
 
Deciduous Second molar 6 mo. in utero Cusp tips still isolated 11 mo. 24 mo. 3 yr.
 
5931310“ Central incisor 4} mo. in utero Three-flftlis 2-} mo. 6 mo. 1'} yr.
Lateral incisor 4} mo. in utero Three-fifths 3 ma. 7 mo. 1-} yr.
 
Mandibular Ouspid 5 mo. in utero One-third 9 mo. 16 mo. 3% yr.
 
First molar 5 mo. in utero Cnsps united 5-} mo. 12 mo. 2} yr.
 
Second molar 6 mo. in utero Cusp tips still isolated 10 mo. 20 mo. 3 yr.
 
7- 8 yr. 10 yr.
8- 9 yr. 11 yr.
11-12 yr. 13-15 yr.
10-11 yr. 12-13 yr.
10-12 yr. 12-14 yr.
6- 7 yr. 9-10 yr. 5-
12-13 yr. 14-16 yr.
17-21 yr. 18-25 yr.
6- 7 yr. 9 yr.
7- 8 yr. 10 yr.
9-10 yr. 12-14 yr.
10-12 yr. 12-13 yr.
11-12 yr. 13-14 yr.
6- 7 yr. 9-10 yr.
11-13 yr. 14-15 yr.
17-21 yr. 18-25 yr.
 
   
 
         
 
   
     
 
Central incisor 3 - 4 mo _-_..___.._-_..___..
Lateral incisor 10 -12 mo. .___-___.._..__-..-
Cuspid 4 - 5 mo. ________ __---___
First bicuspid 1§- 15 yr. ______________ __
Second bicuspid 2 - 2% yr. ______________ __
xFirst molar At birth Sometimes a. trace
Second molar 24- 3 yr. _--_--.._..__.._-..-
Permanent Third molar 7 - 9 yr. ___-- ____ -__..__
 
dentition Central incisor 3 - 4 mo. _______ _______-_
Lateral incisor 3 - 4 mo. ........... -----
 
Cuspid 4 - 5 mo. ...... ..--..----....
 
. First bicus id 15- 2 . .----_-_----.._..-
 
M‘“‘d‘b“1‘“' Second bicgspid 21- 2; $1. __--______-_____
 
First molar At birth Sometimes a trace
 
Second molar 21- 3 yr. _________ ..----_..
 
Third molar 8 -10 yr. .......... --_--- 1
 
ilk‘:-Isl
 
Maxillary
 
hhhmiii
_;_.
 
Iii.
 
1.!
.
 
-
 
sis‘. sis: 1.2
 
>a§=>:>a?a>~.>.
 
-oLoL~u=r.~=ooo<o inn-n.~<oL~:.~ono:o
'7‘ _..".'7‘
«swan:-seer:-‘cl vcwsucn.-::ocxn.~:u
 
 
ERUPTION on THE TEETH 303
304 ORAL HISTOLOGY AND EMBRYOLOGY
 
 
Resorptlon ** —
 
Repaired
resorption
 
Enamel -'—-
 
Resorption  ‘ 4" .
 
Alveolar
bone
 
Alveolar
bone
 
Periodontal
membrane
 
 
 
B. . D.
Fig. 235.—-Root resorption on distal surface or second lower molar caused by pressure
or erupting third molar. and repair.
 
4. Relation of germ or third molar to second molar at the beginning of pretunctional
phase of eruption. Note oblique position of the crown ot third molar.
 
B. Area. of contact between tooth erm oi third molar and root of second molar in
high magnification Resorption rea into dentin.
 
0. Relation or lower second and third molars when third molar has a.tta.ined its up~
right position.
 
D. High magnification of alveolar crest. Resorption on distal root surface is partly
repaired by apposition or cementum. (Orba.n.1')
ERUPTION or THE TEETH 305
 
Erupting teeth may cause resorption on the roots of neighboring teeth.“
This has been observed very frequently on the lower second molars, due
to the oblique position of the erupting third molar (Fig. 235). This tooth
turns its occlusal surface mesially and upward, and attains its upright
 
position only in the last stages of eruption. Therefore, its crown comes
into closest relation to the distal surface of the distal root of the second
 
molar, and exerts pressure leading to resorption of cementum and dentin
to a varying depth; it can be so extensive that the pulp may be exposed.
When the pressure is relieved during the normal movement of the wisdom
 
tooth, repair by apposition of cementum follows. Such resorption was
observed in about two-thirds of investigated jaws. A horizontal position
 
of the lower third molar might later lead to impaction. In such cases the
destruction on the root of the second molar may be severe.
 
Impacted or embedded upper third molars may cause similar resorption
of the root of the second molar. Embedded upper cuspids may exert
pressure upon the root of the lateral incisor. During the time of erup-
tion of teeth, the reduced or united enamel epithelium may undergo
changes which result in cyst formation. Such a cyst forms around the
crown of the developing tooth and is known as a dentigerous cyst. Those
which arise late may cause a noticeable swelling on the surface and are
 
sometimes known as eruptive cysts, although they are simply forms of
dentigerous cysts.
 
References
 
1. Brash, J. 0.: The Growth of the Alveolar Bone and Its Relation to the Move-
ments of the Teeth, Including Eruption, Int. J. Orthodont., Oral Surg. &
Badiogr. 14: 196, 283, 393, 487, 1928.
 
2. Brauer, J. C., and Bahador, M. A.: Variations in Calcification and Eruption of
the Deciduous and Permanent Teeth, J. A. D. A. 29: 1373, 1942.
 
3. Brodie, A. G.: Present Status of Our Knowledge Concerning Movement of the
Tooth Germ Through the Jaw, J. A. D. A. 24: 1830, 1934.
 
4. Brodie, A. G.: The Growth of Alveolar Bone and the Eruption of the Teeth,
Oral. Surg., Oral Med., Oral Path. 1: 342, 1948.
 
5. Cattell, P.: The Eruption and Growth of the Permanent Teeth, J. Dent. Research
8: 279, 1928.
 
6. Gottlieb, B.: Scheinbare Verkiirzun eines oberen Schneidezahnes (So-called
Shortening of an Upper Lateral cisor), Ztschr. f. StomatoL 22: 501, 1924.
 
7. Gottlieb, B., Orban, B., and Diamond, M.: Biology and Pathology of the Tooth
and Its Supporting Mechanism, New York, 1938, The Macmillan Co.
 
8. Gross, H.: Histologische Untersuchungen iiber das Wachstum der Kiefer-
knochen beim Menschen (Histologic Investigations of the Growth of the
Human Jaw Bone), Deutsche Zahnh. 89: 1934.
 
9. Herzberg, F., and Schour, I.: Effects of the Removal of Pulp and 1Iertwig’s
Sheath on the Eruption of Incisors in the Albino Rat, J. Dent. Research 20:
264 1941.
 
10. Hoflman’, M. M.: Experimental Alterations in the Rate of Eruption of the Rat
Incisor; Master’s Thesis, University Illinois Graduate School, 1939.
 
11. Hoffman, M. M., and Schour, I.: Quantitative Studies in the Development of
the Rat Molar, II. Alveolar Bone, Cementum and Eruption (From Birth to
500 Days), Am. J. Orthodont. & Oral Surg. 26: 856, 1940.
 
12. Kronfeld, B.: The Resorption of the Roots of Deciduous Teeth, Dental Cosmos
74: 103. 1932.
 
13. Logan, W. H. G., and Kronfeld, B.: Development of the Human Jaws and Sur-
rounding Structures From Birth to the Age of Fifteen Years, J. A. D. A.
20: 379,1933.
 
14. Logan, W. H. G.: A Histologic Study of the Anatomic Structures Forming the
Oral Cavity, J. A. D. A. 22: 3, 1935.
306
 
15.
16.
17.
18.
19.
 
.a.a.
 
23.
24.
 
25.
26.
 
27.
28.
29.
 
ORAL HISTOLOGY AND EMBRYOLOGY
 
Massler, M., and Schour, I.: Studies in Tooth Development: Theories of Erup-
tion, Am. J. Orthodont. 8: Oral Surg. 27: 552, 1941.
 
Orban, B.: Growth and Movement of the Tooth Germs and Teeth, J. A. D. A.
15: 1004, 1928.
 
Orban, B.: Resorption of Roots Due to Pressure From Erupting and Impacted
Teeth, Arch. Clin. Path. 4: 187, 1940.
 
Orban, B.: Epithelial Rests in the Teeth and Their Supporting Structures, Proc.
 
Am. A. Dent. Schools, 1928, p. 121.
 
Reichborn-Kjennerud: Ueber die Mechanik des Durchbruches der bleibenden
Ziihne beim Menschen (Mechanism of the Eruption of the Permanent Teeth
in Man), Berlin, 1934, Hermann Meusser.
 
Sicher, IL: Tooth Eruption: The Axial Movement of Continuously Growing
Teeth, J. Dent. Research 21: 201, 1942.
 
Sicher, B.: Tooth Eruption: The Axial Movement of Teeth With Limited
Growth, J. Dent. Research 21: 395, 1942.
 
Sicher, B.: Oral Anatomy, St. Louis, 1949, The G. V. Mosby Co.
 
Sicher, H., and Weinmann, J. P.: Bone Growth and Physiologic Tooth Move-
ment, Am. J. Orthodont. & Oral Surg. 30: 109, 1944.
 
Stein, G., and Weinmann, J. P.: Die physiologische Wanderung der Ziihne
Physiologic Drift of the Teeth), Ztschr. f. Stomatol. 23: 733, 1925.
 
Wassermann, F.: Personal communication.
 
Weinmann, J. P.: Das Knochenbild bei Stiirungen der physiologischen Wan-
derung der Zahne (The Bone Picture in Cases of Disturbances of the
Physiologic Movement of Teeth), Ztschr. f. Stomatol. 24: 397, 1926.
 
Weinmann, J. P.: Bone Changes Related to Eruption of the Teeth, Angle
Orthodontist 11: 83, 1941.
 
Weinmann, J. P., and Sicher, H.:
Bur 46: 3, 1946.
 
Willman, W.: An Apparent Shortening of an Upper Incisor, J. A. D. A. 17: 444,
1930.
 
(The
 
Correlation of Active and Passive Eruption,
CHAPTER XII
 
SHEDDING OF THE DECIDUOUS TEETH
 
1. IN TBODUCTION AND DEFINITION
2. PROCESS OI‘ SHZEDDING
3. CLINICAL CONSIDERATIONS
 
a. Remnants of Deciduous Teeth
b. Retained Deciduous Teeth
c. Submerged Deciduous Teeth
 
1. INTRODUCTION AND DEFINITION
 
Human teeth develop in two generations known as the deciduous and
permanent dentitions. The deciduous teeth are adapted in their number,
size and pattern to the small jaw of the early years of life. The size of
their roots, and therefore the strength of the suspensory ligament (perio-
dontal membrane), are in accordance with the developmental stage of
the masticatory muscles. They are replaced by the permanent teeth
which are larger, more numerous, and possess a stronger suspensory liga—
ment. The physiologic elimination of deciduous teeth, prior to there-
placement by their permanent successors, is called shedding.
 
2. PROCESS OF SHEDDING
 
The elimination of deciduous teeth is the result of the progressive re-
sorption of their roots by osteoclasts. In this process both cementum
and dentin are attacked (Fig. 236). The osteoclasts differentiate from
the cells of the loose connective tissue in response to the pressure exerted
by the growing and erupting permanent tooth germ. The pressure is
directed against the bone separating the alveolus of the deciduous tooth
from the crypt of its permanent successor and, later, against the root
surface of the deciduous tooth itself (Fig. 237). Because of the position
of the permanent tooth germ the resorption of the deciduous roots of the
incisors and cuspids starts at the lingual surface in the apical third (Fig.
238). The movement of the permanent germ, at this time, proceeds in
occlusal and vestibular directiori.) In later stages, the germ of the perma-
nent tooth is frequently found directly apical to the deciduous tooth (Fig.
236, A). In such cases the resorption of the deciduous root proceeds in
transverse planes, thus causing the permanent tooth to erupt later in the
exact position of the deciduous. However, the movement in vestibular
direction is frequently not complete when the crown of the permanent tooth
 
breaks through the gingiva. In such cases, the permanent tooth appears
lingual to its deciduous predecessor (Fig. 238). In the first described
 
First draft submitted by Myron S. Aisenberg.
307
308 ORAL HISTOLOGY AND Emntwonoav
 
   
 
R°s°rpfl°n area  " Resorptlon ot
 
     
 
 
 
_ root
.T* ‘'''’'''_T" Resorptlon or
Permanent cuspid ‘ ' b°“°
 
1*’.
 
‘ cementum
 
   
 
I '~ A
_....s ..
 
“°‘°’P“°'* 'S
(°3t°°°13-533) ' W .. Periodontal
Jr “ membrane
' —--——,—- Resorptlon
of bone
 
 
B.
F . 236.—Resox-ption of root of deciduous cus id during eruption of permanent successor.
Kronteld!) A. General view. B. Linguafreaorption area in higher magnification.
sauonme or DECIDUOUS TEETH 309
 
Deciduous incisor
 
deciduous tooth
and successor
 
 
 
Enamel of perma-
nent incisor
 
Dentin
 
Fig‘. 23'I.~—.A thin lamclla of bone separates permanent tooth germ from its predecessor.
310 ORAL EISTOLOGY AND EMBRYOLOGY
 
r ._ _ ,,_ W , _  /._—...~_..,
 
Deciduous incisor -—'—-~ I
 
Enamel of Der-mar
 
Root resorption .-
nent incisor
 
Dentin
 
..r'
 
Fig. 23S.—Resorption of root of deciduous incisor due to pressure of erupting successor.
SHEDDING on THE DECIDUOUS TEETH 311
 
alternative the deciduous tooth is lost before the permanent tooth erupts,
whereas in the latter the permanent tooth may erupt while the Qleciduous
tooth is still in its place.
 
In most cases, resorption of the roots of the deciduous molars begins
on the surfaces of the roots next to the interradicular septum. This is
due to the fact that the germs of the bicuspids are frequently found
between the roots of the deciduous molars (Fig. 239). In such cases,
extensive resorption of the roots can be observed long before actual shed-
ding. However, during the continued active eruption the deciduous teeth
 
_ . . --w.....gs—.
 
I
 
 
 
deciduous :3
molar  .
 
’  .,  4,!’ ‘X
~-_; g ' 1'.‘ V '
‘J \ .;'~. ' ' 3‘-:,
' " - - . _ _ ,, \'_‘
, ‘wt . ”
*4’
 
.
R8S01‘Dl-303 ;_->':.i"'* '
 
 
 
.,_,__‘L.g-'3 Repaired resorp-
 
 
 
°"' r°°t . ‘ tion of dentin
Penngrlient ,,. .. (X)
too
germ
 
Fig. 239.——Germ or lower flrst bicuspid between the roots of lower flrst deciduous molar.
Repaired resorption on the roots of the deciduous tooth (see Fig. 241).
 
move away from the growing permanent tooth germs which, for the most
part, soon come to lie apical to the deciduous molars (Fig. 240). This
change in position allows the growing bicuspid adequate space for its
development. The areas of early resorption on the deciduous molar are
then repaired by the apposition of new cementum and the alveolar bone
regenerates’ (Fig. 241). In later stages, however, the erupting bicuspids
again overtake the deciduous molars and, in most cases, their roots be-
come entirely resorbed (Fig. 242). The resorption may even proceed far
312 ORAL msronomz AND EMBRYOLOGY
 
up into the coronal dentin; occasionally, greater or less areas of the
enamel may be destroyed. The bicuspids appear with the tips of their
crowns in the place of the deciduous teeth.
 
The osteoclastic resorption which is initiated by the pressure of the
permanent tooth is the primary reason for the elimination of a deciduous
tooth. Two auxiliary factors have to be taken into consideration. These
are, first, the weakening of the supporting tissues of the deciduous tooth,
due to resorption of wide areas of its roots; and continued active and
passive eruption which seems to be accelerated during the period of
 
 
   
 
—— Second
 
deciduous
‘ molar
 
‘ Traumatic
changes In
periodontal
membrane
 
,' (x)
 
"1
 
. ‘V  Second
 
‘ bicuspld
germ
 
-'4 ' '  I . \ 1’
-. ,,_;  -,-1. ~ , ,/ ,
3» r K I / - 5”: ‘ / ' " w‘.‘.''.
.‘ . A‘ ’ f/ «r ; V: - ‘
.‘—.
 
\ / ,
 
r  p ‘A ‘Ti 2", X1! ti _
 
6
“"‘
 
Fig. 240.—Germs or bicuspids below roots of deciduous molars. Traumatic changes in
the periodontal membrane or the deciduous teeth. Z. See Fig. 243.
 
shedding. The epithelial attachment of the deciduous tooth grows down
along the cementum at this time, thus causing the clinical crown of the
tooth to be enlarged and the clinical root to which the suspensory fibers
are anchored, to be shortened. Second, the masticatory forces increase
during this period, due to the growth of the masticatory muscles, and
combine with the root resorption and eruption to initiate a vicious circle
resulting in rapid loosening of the deciduous tooth. The masticatory
stresses act as traumatic forces upon the tooth at this stage!’ 7: ¥° Due to
the loss of large parts of the suspensory apparatus the masticatory forces
SHEDDING OF THE DEGIDUOUS TEETH
 
tooth
 
Repaired
 
     
 
dentin
 
Loose connec- ‘ ' ‘
five tissue
surrounding
permanent
germ
 
313
 
cementum of
deciduous
 
resorption
 
Resorption of
 
Fig. 241.——High magniflcaton of a. repaired resorption; from area. I of Fig. 239; new
 
bone formed during rest period.
314 out. HISTOLOGY AND EMBRYOLOGY
 
4..
\
 
Deciduous molar
 
Contact between
deciduous and
permanent
 
 
 
V f
t°°th lmiaaiglliesxpgjd
 
4 _ , _ §—— New formation
Bone resorption - . ‘ »» ' of bone
 
_Fig'..242.—_—Eoots of deciduous molar completely resorbed. Dentin of deciduous tooth
iii contact with enamel of the bicuspid. Resorption of bone on one side. new formation
 
of bone on the opposite side or the bicuspid due to transmitted excentric pressure to
the bicuspid. (Grimmer!)
SHEDDING on THE nncmvous TEETH 315
 
may be transmitted to the alveolar bone not as tension but as pressure.
This leads to compression and injury of the periodontal membrane with
subsequent bleeding, thrombosis and necrosis (Fig. 243). These changes
are most frequently found in the bifurcation and interradicular surfaces
of deciduous molars. Resorption of bone and tooth substance, therefore,
occurs most rapidly in such areas, thus relieving pressure. Repair of
 
resorbed areas may be excessive and may even lead to ankylosis between
bone and tooth (Fig. 24-1).
 
Deciduous tooth
 
Necrotlc tissue
remnants
 
 
—.g .- Traumatic destruc-
‘ tion of perio-
_ ; dental membrane
Alveolar bone  " ——-—
 
 
~ '3 - Repaired
' re resorption
 
Necrotic tissue
remnants
 
51?’
 
   
 
Fig. 243.—Tx-aumatic changes of periodontal tissues. High magnification from area.
X in Fig. 240.
 
The process of shedding is not necessarily continuous. Periods of great
resorptive activity alternate with periods of relative rest.’ During the
rest periods resorption not only ceases but repair may actually occur
by apposition of cementum or bone upon the resorbed surface of cemen-
tum or dentin. Even repair of resorbed alveolar bone may take place
316 mun ms-ronoenz AND EMBRYOLOGY
 
 
Deciduous molar v \
 
 
 
 
 
Reaorption of
bone in
area. of L.
ankylosis
 
Permanent tooth . _. ‘
p.‘ ,r --
 
 
Resorptionr:  l _ . «T
 
 
a.
 
 
_L
.\ 7:
 
L43.
 
 
i<'s.«.a..'f..-4'1;
 
Fig. 244.—Ankylosl.s ot deciduous tooth as a. sequence of trauma.
4. General view.
 
B. High magnification of area. X in A.
 
{ Resorption of
cementum
 
' Ankylosis
SHEDDING or THE DECIDUOUS TEETH 317
 
durillg rest periods (Fig. 241). The phases of rest and repair are, prob-
ably, lengthened by relief of pressure upon the deciduous tooth by its
own eruptive movement. r
 
The pulp of the deciduous teeth plays a passive role during shedding.
Even in late stages the ocelusal parts of the pulp may appear almost
normal, with functioning odontoblasts (Fig. 245). However, since the
cellular elements of the pulp are identical with those of loose connective
tissue, resorption of the dentin may occur at the pulpal surface by the
 
‘W - -— Odontoblasts
 
Pu1p¢V—’—j——
 
Dentin
 
Fig. 245.—High magnification 01' the pulp of resorbed deciduous molar of Fig. 242. Pulp
of normal structure with odontoblasts.
 
differentiation of osteoclasts from the cells of the pulp. The persistence of
the pulpal tissue, and its organ.ic connection with the underlying con-
nective tissue, explain the fact that deciduous teeth show, to the last, a
fairly strong attachment even after total loss of their root (Fig. 242). In
such cases, shedding may be unduly retarded and the erupting permanent
tooth may actually come into contact with the deciduous tooth. The
masticatory forces are then transmitted to the permanent tooth” before its
suspensory ligament is fully differentiated, and traumatic injuries in the
periodontal membrane of the permanent tooth may develop (Fig. 242).
Remnants of
Deciduous
Teeth
 
Deciduous
Retained
Teeth
 
318 om. 1-nsvronocr AND EMBRYOLOGY
 
3. CLINICAL CONSIDERATIONS
 
Parts of the roots of deciduous teeth which are not in the path of erupt-
ing permanent teeth may escape resorption. Such remnants of roots,
consisting of dentin and cementum, may remain in the jaw for a con-
siderable time.‘’'‘’ In most cases, such remnants are found along the
bicuspids, especially in the region of the lower second bicuspids (Fig.
246). This can be explained by the fact that the roots of the lower second
deciduous molar are strongly curved or divergent. The mesiodistal di-
ameter of the second bicuspid is much smaller than the greatest distance
between the roots of the deciduous molar. Root remnants may later be
found deep in the jaw bone, completely surrounded by, and ankylosed to,
the bone (Fig. 247). Frequently, they become encased in heavy layers of
cellular cementum. In cases where the remnants are close to the sur-
face of the jaw (Fig. 248) they may, ultimately, become exfoliated. Pro-
gressive resorption of the root remnants and replacement by bone may
cause the disappearance of these remnants. Cysts occasionally develop
around the retained roots of deciduous teeth. They appear between the
roots of the permanent teeth.
 
 
Root remnant of - - ,,  .— — -.---.—
declduous , ~ —. Root remnant of
 
tooth “ deciduous tooth
 
Fig. 246.—Remna.nts of roots of deciduous molar embedded in the interdentai septa.
(Roentgenogram courtesy G. M. Fitzgerald, University of California.)
 
Deciduous teeth may be retained for a long time if the corresponding
permanent tooth is congenitally missing.‘ This is most frequently ob-
served in the region of the upper lateral incisor (Fig. 249, A), less fre-
quently in that of the second bicuspid, especially the lower (Fig. 249, B),
and rarely in the central lower incisor region (Fig. 2-19, 0). Also, if a
permanent tooth is embedded, its deciduous predecessor may be retained
(Fig. 249, D). This type of retained deciduous tooth is found mostly in
 
the upper cuspid region as an accompaniment of the impaction of the
permanent cuspid.
SHEDDING or THE zorzcmuous TEETH 319
 
 
 
First bicuspid second bicuapld
 
Remnant of
deciduous root
 
' - Ankylosls
 
Fig. 247.———Remna.nt of deciduous tooth embedded in, and ankylosed to, the bone.
( Schoenbauez-.5 )
320 mun HISTOLOGY AND EMBRYOLOGY
 
Interdentul papilla
 
 
31¢‘-“PW Blcusvld
 
-~——-V7 A Remnant of deciduous
tooth
 
Fig. 248.—-Remnant of deciduous tooth at alveolar crest.
SHEDDING or THE nncmuous TEETH 321
 
The fate of retained deciduous teeth varies. In some cases they persist
for many years in good functional condition (Fig. 249, A); more often,
however, resorption of the roots and continued active and passive erup-
tion cause their loosening and final loss (Fig. 249, B). The loss of retained
deciduous teeth has been explained by the assumption that such teeth may
undergo regressive changes in their pulp, dentin, cementum, and perio-
dontal membrane, thus losing their regenerative faculties which are neces-
sary to compensate for the continued injuries during function? It is, how-
ever, more probable that such teeth, because of their smaller size, are not
adapted to the strength of the masticatory forces in adult life. The roots
are narrow and short, thus rendering the area available for attachment of
principal fibers relatively inadequate. Their loss is then due to traumatism.
 
Fig. 249.—Roentgenogra.ms of retained deciduous teeth.
A. Upper lateral permanent incisor missing’. deflduous tooth retained (age 55)-
 
B. Lower second bicuspid missing, deciduous molar retained: r00tS D8-N’-1y !‘eS°1'be5~
(Courtesy M. K. Hine, University of Indiana.)
 
0'. Lower central permanent incisors missing. deciduous teeth retained.
 
D. Upper permanent cuspid embedded; deciduous cuspid retained. (Courtesy Rowe
Smith, Texarkana.)
 
If the permanent lateral incisor is missing, the -deciduous tooth is.in
many cases resorbed under the pressure of the erupting permanent cuspid.
This resorption may be simultaneous with that of the deciduous cuspid
Submerged
Deciduous
Teeth
 
322 oasr. HISTOLOGY AND EMBRYOLOGY
 
(Fig. 250). Sometimes, the permanent cuspid causes resorption of the
deciduous lateral incisor only, and erupts in its place. In such cases,
the deciduous cuspid may be retained distally to the permanent cuspid.
 
Traumatic lesions, on the other hand, may lead to ankylosis of a de-
ciduous tooth, rather than its loss. The active eruption of an ankylosed
tooth ceases and, therefore, the tooth appears shortened later on (Fig.
 
 
Fig. 250.—Upper permanent lateral incisor missing. Deciduous lateral _incisor and
deciduous cuspid are resorbed due to pressure of erupting permanent cuspid.
 
A. At the age of 11.
B. At the age of 13.
 
 
;,.‘
 
Fig. 251.—Submerging lower deciduous second molar. Second bicuspid missing.
 
(Cour-
tesy M. K. Hine, University of Indiana.)
 
251), due to continued eruption of its neighbors and the relative height
of their alveolar processes. The “shortening” of such a tooth may even
lead to its eventual overgrowth by the alveolar bone and the tooth may
become submerged in the alveolar bone.‘ The roots and crowns of such
teeth show extensive resorption and apposition of bone in the tortuous
cavities.
 
SHEDDING on THE DEGIDUOUS TEETH 323
 
Submerged deciduous teeth prevent the eruption of their per-
 
manent successors, or force them from their position. Submerged decidu-
out teeth should, therefore, be removed as soon as possible.
 
1.
 
9°
 
10.
 
.“.°’.°‘!“S'°.“"
 
References
 
Aisenberg, M. 8.: Studies of Retained Deciduous Teeth, Am. J. Orthodont. 85
 
Oral Stu‘ . 27: 179, 1941.
 
Grimmer, E. .: Trauma in an Erupting Premolar, J. Dent. Research 18: 267,
1939.
 
Kotanyi, E.: Histologische Befunde an Milchzahnreste (Histologic Findings on
Deciduous Tooth Remnants), Ztschr. f. Stomatol. 23: 516, 1925.
 
Kronfeld, R.: The Resorption of the Roots of Deciduous Teeth, Dental Cosmos
74: 103 1932.
 
Kronfeld, R.: and Weinmann, J’. P.: Traumatic Changes in the Periodontal Tissues
of Deciduous Teeth, J. Dent. Research 19: 441, 1940.
 
Noyes, F. B.: Snbmerging Deciduous Molars, Angle Orthodontist 2: 77, 1932.
 
Oppenheim, A.: Histologische Befunde beim Zahnwechsel (Histo1ogic Findings
in the Shedding of Teeth), Ztschr. f. Stomatol. 20: 543, 1922.
 
Schoenbauer, F.: Kniichern eingeheilte Milchzahnreste bei iilteren Individuen
(Ankylosed Deciduous Teeth Remnants in Adults), Ztschr. f. Stomatol. 29:
 
892 1931.
Stafne,  0.: Possible Role of Retained Deciduous Roots in the Etiology of
 
Cysts of the Jew, J. A. D. A. 24: 1489, 1937.
Weinmann, J. P., and Kronfeld, R.: Traumatic Injuries in the Jaws of Infants,
J. Dent. Research 19: 357, 1940.
CHAPTER XIII
TEMPOROMANDIBULAR JOINT
 
1. AN ATOMIC REMARKS
 
2. HISTOLOGY
 
a.. Bony Structures
 
b. Articular Pibrocartilage
c. Articular Disc
 
d. A1-ticular Capsule
 
3. CLINICAL CONSIDERATIONS
 
1. AN ATOMIC REMARKS
 
The mandibular articulation (temporomandibular joint) is a diarthrosis
between mandibular fossa and articular tubercle of the temporal bone,
and capitulum (head, condyle) of the mandible. A fibrous plate, the
articular disc, intervenes between the articulating bones.
 
The articulating surface of the temporal bone is concave in its posterior,
convex in its anterior part. The 91131 concavity, articular fossa, extends
from the squamotympanic and petrotympanic fissure in the back to the con
vex articular tubercle in front. Th latter is strongly convex in a sagittal
and slightly concave in a frontal plane. The convexity varies considerably,
the radius ranging from 5 to 15 mm. The long axes of fossa and tubercle
are directed medially and slightly posteriorly. The articular surface of
the mandibular head is, approximately, part of a cylinder the axis of
which is placed in the same direction as that of the articular surfaces on
the temporal bone. The articulating parts of the temporomandibular
joint are covered by a fibrous or fibrocartilaginous tissue and not by
hyaline cartilage, as in most other articulations of the human body. The
 
hyaline cartilage in the mandibular condyle which is present during its
growth period does not reach the surface.
 
The articular disc is an oval fibrous plate which is united around its
margin with the articular capsule (Fig. 252). It separates the articular
space into two compartments: a lower, between condyle and disc, and an
upper, between disc and temporal bone. The disc appears biconcave in
sagittal section. Its central part is thin, in rare cases perforated;
the anterior and especially the posterior borders are thickened (Fig. 253).
Fibers of the external pterygoid muscle are attached to its anterior border.
The disc serves to adapt the bony surfaces to each other, especially in a
forward position of the mandible when the convex condyle approaches the
 
aonvex articular tubercle. The disc is, at the same time, the movable
socket for the mandibular head.
 
First draft subxpitted by Donald A; Kerr.
324
TEMPOROMANDIBULAR JOINT 325
 
The articular capsule consists of an outer fibrous sac which is loose.
It IS strengthened on its lateral side by the temporomandibular ligament.‘
 
The inner synovial membrane is divided like the articular space. The
superior part reaches from the margin of the articular surfaces on the tem-
 
poral bone to the disc; the inferior extends from the disc to the neck of
the mandible.
 
2. HISTOLOGY
 
The condyle of the mandible is composed of typical cancellous bone Bony
covered by a thin layer of compact bone (Fig. 253). The trabeculae are smmm
 
grouped in such a way that they radiate from the neck of the condyle and
 
 
 
Ma.ndibula.r  ..
 
V‘
 
rossa. =. _
Articular
tubercle
 
Mandibular
head
 
Fig. 252.—Sagitta1 section through the temporomandibular joint. (Courtesy W. Bauer,‘
St. Louis University School oi‘. Dentistry.)
 
 
Fig. 253.—Sagitta1 section through the temporomandibular joint of a 28-year-old man.
(Courtesy S. W. Chase. Western Reserve University.)
326 ORAL HISTOLOGY AND EMBRYOLOGY
 
reach the cortex at right angles, thus giving maximal strength to the
condylar bone While still maintaining a light construction. In young
 
individuals the trabeculae are thin and may contain islands of hyaline
cartilage near the surface (Fig. 254, A). In older individuals these car-
 
 
   
 
 
- 3- Fibrous
. covering
 
. - .. Cartilage
V; , -I islands
 
. A! .-.1:-::. '
 
1 -§'Fibrous
‘ " covering
 
 
 
Fig. 254.—-Sections through the mandibular head.
A. Newborn infant.
R. Young adult.
 
tilaginous islands are resorbed and replaced by bone (Fig. 254, B). The
marrow spaces are large at first, but decrease in size with progressing age
by a marked thickening of the trabeculae. The marrow in the condyle
TEMPOROMANDIBULAR JOINT 327
 
is of the myeloid or cellular type; in older individuals it is sometimes
replaced by fatty marrow.
 
In young individuals the bone of the condyle is capped by a layer of
hyaline cartilage which develops as a secondary growth center in
three-month-old embryos. It is interposed between the fibrocartilage and
the bone. It may still be present in the jaw of a person in his twenties
(Fig. 254). The cartilage grows interstitially and by apposition from
the deepest layer of the covering fibrous tissue; at the same time it is,
gradually, replaced by bone on its inner surface.
 
. Ii-,,.’
 
, i . <:
k'V.‘»} ' I,‘ I‘ .
 
Fig. 255.—Higher magnification of part of the mandibular condyle of Fig. 253.
 
The bone of the mandibular fossa varies considerably from that of the
articular tubercle (Fig. 253). In the fossa it consists of a thin compact
layer; the articular tubercle is composed of spongy bone covered with a
thin layer of compact bone. In rare cases islands of hyaline cartilage are
found in the articular tubercle.
 
The condyle as well as the articular fossa and tubercle are covered by
a rather thick layer of fibrous tissue containing a. variable number of
cartilage cells. The fibrous or fibrocartilaginous covering of the man-
dibular condyle is of fairly even thickness (Fig. 255). Its superficial
layers consist of a network of strong collagenous fibers. Cartilage cells
or chondrocytes may be present and have a tendency to increase in number
with age. They can be recognized by their thin capsule which stains
heavily with basic dyes. The deepest layer of the fibrocartilage is rich in
 
 
Bone
 
Articular
Fibro-
 
cartilage
Arflcularbisc
 
ORAL HISTOLOGY AND EMBRYOLOG3.
 
chondroid cells as long as hyaline cartilage is present in the condyle; it
contains only a few thin collagenous fibers. In this zone the appositional
growth of the hyaline cartilage of the condyle takes place.
 
The fibrous layer covering the articulating surface of the temporal
bone (Fig, 256) is thin in the articular fossa and thickens rapidly on the
posterior slope of the articular tubercle (Fig. 253). In this region the
fibrous tissue shows a definite arrangement in two layers, with a small
transitional zone between them; the two layers are characterized by the
different course of the constituent fibrous bundles. In the inner zone the
fibers are at right angles to the bony surface; in the outer zone they run
parallel to that surface. As in the fibrous covering of the mandibular
condyle, a variable amount of chondrocytes is also found in the tissue on
the temporal surface. In adults the deepest layer shows a thin zone of
 
calcification.
 
Bone
 
Calcification
\ p " ~ - ' zone
 
v -- --s Inner fibrous
layer
 
-— --——a Outer fibrous
layer
 
 
Fig. 256.—Higher magnification of articular tubercle of Fig. 253
 
There is no continuous cellular lining on the free surface of the fibro-
cartilage. Only isolated fibroblasts are situated on the surface itself;
they are, generally, characterized by the formation of long flat cyto-
plasmic processes.
 
In young individuals the articular disc is composed of dense fibrous
tissue which resembles a ligament because the fibers are straight and
 
tightly packed (Fig. 257). Elastic fibers are found throughout the disc,
but only in relatively small numbers. The fibroblasts in the disc are
TEMPOROMANDIBULAR JOINT 329
 
elongated and send flat cytoplasmic wing-like processes into the inter-
stices between the adjacent bundles. The mandibular disc does not show
the usual fibrocartilaginous character of other interarticular discs. This
 
may be regarded as a functional adaptation to the high mobility and
plasticity of this disc.
 
Articular
tubercle
 
Superior articular
space
 
 
 
 
__ Articular disc
 
--- Inferior articular
space
 
- -—=  Mandibular head
 
43
 
Fig. 257.—-Higher magnification of articular disc of Fig. 253.
 
With advancing age some of the fibroblasts develop into chondroid
cells Which, later, may become real chondrocytes. Even small islands of
hyaline cartilage may be found in the discs of older persons. Chondroid
cells, true cartilage cells and hyaline ground substance develop in situ by
difierentiation of the fibroblasts. In the disc as well as in the fibrous
tissue covering the articular surfaces, this cellular change seems to
be dependent upon mechanical influences. The presence of chondrocytes
increases the resistance and resilience of the fibrous tissue.
Articulal:
capsule
 
330 ormr. HISTOLOGY AND EMBRYOLOGY
 
As in all other joints, the articular capsule consists of an outer fibrous
layer which is strengthened on the lateral surface to form the tempora-
mandibular ligament. The other parts of the fibrous capsule are thin
and loose. The inner or synovial layer is a thin layer of connective tissue.
 
'It contains numerous blood vessels which form a capillary network close
«to its inner surface. In many places larger and smaller folds or finger-
 
like processes, synovial folds and villi protrude into the articular cavity
(Fig. 258). The former concept of a continuous cellular covering of the
free synovial surface has been abandoned. Only a few fibroblasts of the
synovial membrane reach the surface and, with some histiocyte and
lymphatic‘ wandering cells, form an incomplete lining of the synovial
membrane.
 
 
 
I ‘ T synovial villl
 
Fifi 258.—Villi on the synovial capsule of ternporomandibular joint.
 
A small amount of viscous fluid, synovial fluid, is found in the articu-
lar spaces. It is a lubricant and also a nutrient to the avascular coverings
of the bones and to the disc. Its origin is not clearly established. It is
possibly in part derived from the liquefied detritus of the most super-
ficial elements of the articulating surfaces. It is not clear whether it is
a product of filtration from the blood vessels or a secretion of the cells
of the synovial membrane; possibly it is both.
TEMPOROMANDJBULAR JOINT ' 331
 
3. CLINICAL CONSIDERATIONS
 
The thinness of the bone in the articular fossa is responsible for frac-
tures if the mandibular head is driven into the fossa by a heavy blow.
In such cases injuries of the dura mater and the brain have been reported.
 
The finer structure of the bone and its fibrocartilaginous covering de-
pends upon mechanical influences. A change in force or direction of
stress, occurring especially after loss of posterior teeth, will cause struc-
tural changes. These are brought about by resorption and apposition of
bone, and by degeneration and reorganization of fibers in the covering
of the articulating surfaces and in the disc.“
 
There is considerable literature on the disturbances after loss of teeth
 
or tooth substance due to changes in the mandibular articulation.“ The
clinical symptoms are said to be: impaired hearing, tinnitus (ear buzz-
ing), pain localized to the temporomandibular joint or irradiating into
the region of ear or tongue. Many explanations have been advanced for
 
these variable symptoms: pressure on the external auditory meatus ex-
erted by the mandibular condyle which is driven deeply into the articular
fossa; compression of the auriculotemporal nerve; compression of the
chorda tympani; compression of the auditory tube; impaired function
of the tensor palati muscle. Anatomical findings do not substantiate
any one of these explanations. Probably, all the diverse symptoms are
but consequences of a traumatic arthritis in the mandibular joint.“ 2 It is
caused by an increase and a change in direction of the forces of the
masticatory muscles upon the structures of the joint.
 
References
 
1. Bauer, W.: Anatomische und mikroskopische Untersuchungen iiber das Kiefer-
gelenk Anatomical and Microscopic Investigations on the Temporo-Man-
dibular oint), Ztschr. f. Stomatol. 80: 1136, 1932.
 
2. Bauer, W. H.: Osteo-Arthritis Deformans of the Temporo-Mandibular Joint, Am.
J. Path. 17: 129, 1941.
 
3. Baecker, B.: Zur Histologie des Kiefergelenkmeniskus deg Menschen und der
 
Siiu er (Histology of the Temporo-Mandibular Disc in Man and Mammals),
Zts . f. mikr.-anat. For-sch. 26: 223, 1931.
 
Breitner, 0.: Bone Changes Resulting From Experimental Orthodontic Treatment,
Am. J. Orthodont. 26: 521 1940.
 
Cabrini, R., ‘and Erausquin,  La. Articulacion Temporomaxilar de la Rata
(Temporo-Mandibular Joint of the Rat), Rev. Odont. de Buenos Aires, 1941.
 
Cowdry, E. V.: Special Cytology, ed. 2, New York, 1932, Paul B. Hoeber, Inc.,
pp. 981-989, 1055-1075.
 
Hammer, J. Aug.: Ueber den feineren Bau der Gelenke (The Microscopic Ar-
chitecture of the Joints), Arch. f. mikr. Anat. 43: 266, 1894.
 
Marquart, W.: Zur Histologie der Synovialmembran (Histology of the Synovial
Membrane), Ztschr. f. Zellforsch. u. mikr. Anat. 12: 34, 1931.
 
Peterson, H.: Die Organe des Skeletsystems (Organs of the Skeletal System),
Moel1endorf’s Handb. d. mikr. Anat. d. Menschen. Book 2, Part 2, Berlin,
1930, Julius Springer.
 
10. Schaefler, J. P.: Morris’ Human Anatomy, ed. 10, Philadelphia, 1942, The
 
Blakiston Co.
 
11. Schafler, J.: Ueber den feineren Bau und die Entwicklung dos Knorpelgewebes
und iiber verwandte Formen der Stiitzsubstanz (On the Microscopic Struct-
ure and Development of Cartilage and Related Forms of Supporting Tissue),
Ztschr. f. wissensch. Zoo]. 80: 155, 1905.
 
S°9°.“‘.°’S"'."
332 omu. HISTOLOGY AND EMBRYOLOGY
 
12. Schaffet, J.: Die Stiitzgewebe (Supporting Tissues), Moe11endorf’s Handb. f.
mikr. Anat. d. Menschen, Book 2, Part 2, Berlin, 1930, Julius Springer.
 
13. Shapiro, H. IL, and Ti-uex, R. 0.: The Temporo-Mandibular Joint and the Auditory
Function, J. A. D. A. 30: 1147 1943.
 
14. Sicher, Harry: Temporomandibufar Articulation in Mandibular Overclosure,
J. A. D. A. 36: 131, 1948.
 
15. Sicher, Harry: Some Aspects of the Anatomy and Pathology of the Tempora-
mandibular Articulation, New York State D. J. 14: 451, 1948.
 
16. Steinhardt Gr.: Die Beanspruchun der Gelenkfliichen bei versehiedenen Bissar-
ten ( vestigations on the tresses in the Mandibular Articulation and
Their Structural Consequences), Deutsche Zahnh. in Vortr. 91: 1, 1934.
CHAPTER XIV
THE MAXILLARY SINUS
 
IN'1'RODUC'.|'.'ION
DEVELOPMENT
 
ANATOMIG REMARKS
FUNCTION
 
HISTOLOG-Y
 
CLINICAL CONSIDERATIONS
 
9‘S"'."9°!°'."
 
1. INTRODUCTION
 
The relation of the maxillary sinus to the dentition was first recognized
by Nathaniel Highmore. In his Work Carports Humawi Disquisitio Ana-
tomicafi (1651) he described the adult state of the cavity in detail, and
pointed out that his attention had been called to it because a patient had
an abscess there which was drained by the extraction of a cuspid tooth.
This proved to be one of those misleading first observations, since it is
now known that the cuspid‘ root seldom is related to this space in
such a way that its simple extraction would drain it. However, the
erroneous idea still persists that this relationship is generally true. The
molar roots most often, and the bicuspid roots less frequently, are the
dental structures which lie closest to the sinus (Fig. 259). Individual
variations are great and can be determined only by careful interpretation of
good roentgenographs.’
 
2. DEVELOPMENT
 
The maxillary sinus begins its development in about the third month-
of fetal life. It arises by a lateral evagination of the mucous membrane of
the middle nasal meatus, forming a slitlike space. In the newborn its
measurements are about 8 x 4 x 6 mm. (Fig. 260); thereafter, it grad-
ually expands by pneumatization of the body of the maxilla. The sinus
is well developed when the second dentition has erupted, but it may con-
tinue to expand, probably throughout life.5
 
3. ANATOMIG REMARKS
 
The maxillary sinus, or antrum of Highmore, is situated in the body
of the maxilla. It is pyramidal in shape; the base of the pyramid is
formed by the lateral wall of the nasal cavity; the apex extends into the
zygomatic process; the anterior wall corresponds to the facial surface
of the maxilla, and the roof to its orbital surface. The posterior wall is
formed by the infratemporal surface of the maxilla; the floor, usually,
reaches into the alveolar process (Fig. 261).
 
First draft submitted by Paul C. Kitchin in collaboration with L. F. Edwards. De-
partment of Anatomy, Ohio State University.
 
333
334 ORAL msronoev AND nmsnvonocv
 
There is a considerable variation in size, shape and position of the max-
illary sinus, not only in different individuals, but also on the two sides of
the same individual. Its average capacity in the adult is about one-half of
one fluid ounce (14.75 c.c.) with average dimensions as follows: antero-
posteriorly, 3.4 cm.; transversely, 2.3 cm.; and vertically, 3.35 cm. The
maxillary sinus communicates with a recess of the middle meatus of the
nasal cavity (semilunar hiatus) by means of an aperture, the ostium max-
illare, which is located high on its nasal or medial wall and is, therefore,
unfavorably situated for drainage (Fig. 261). An accessory ostium may
occur which is, usually, lower and thus more advantageously placed for
drainage than is the normal ostium.
 
 
 
 
Bony floor
of sinus
 
Buccal
« alveolar
plate
 
.2
, :3
 
Fig. 259.—Bucco1ingua1 ection throu h n t b‘ ‘d. ' ;
fzéom the sinusg by is thiirgpgfatenbisliione. The apex ls iepamted
 
 
Variations in the size of the maxillary sinus are explained on the basis
of the degree or extent of pneumatization of the body of the maxilla
(ho11owing—out by an air-filled pouch of the nasal cavity). In gen-
era], the greater the pneumatization the thinner the walls of the sinus
will be, since pneumatization occurs at the expense of bone. During
THE MAXILLARY sums 335
 
enlargement of the sinus various recesses or accessory fossae may form.
Thus, subcompartments or recesses may be present in the palatine, zygo-
matic, frontal and alveolar processes. The floor of the sinus may extend
downward not only between adjacent teeth but also between the roots
of individual teeth so that their apices cause elevations in the floor and
appear to protrude into the sinus. The type and number of teeth whose
 
,1. : ,,,
 
   
 
 
.7!
 
 
 
Nasal septum
 
Maxillary sinus
 
"y Inferior nasal
concha.
 
Fig. 260.—Fronta1 sections through the head.
A. Newborn infant
 
B. Nine-month-old child.
 
Compare the size of maxillary sinus.
 
apices indent the floor of the space depend upon the degree and shape of-
pneumatization. In the majority of cases the roots are covered by a. thin
layer of bone (Fig. 259). In some instances, they are covered only
by the mucous membrane which lines the cavity and by the periodontal
membrane of the root of the tooth. The floor of the sinus may be on the
336 omu. HISTOLOGY AND EMBRYOLOGY
 
 
 
 
Ethmoidal cell ‘
 
Aperture of ,- .-
lnus
 
1
 
Maxillary sinus - —-—‘
 
Nasal septum
 
Inferior nasal
concha
 
Maxtllary sinus
 
   
 
~ 3'.  ‘;bhéiF'w.;\?L( $-or‘ '
 
Fig. 261.—Rela.tion or the maxillary sinus and its opening into the nasal cavity.
A. Frontal section showing marked asymmetry between right and left sinus.
B. Relation of sinus to root apicea.
rm: MAXILLARY sINUs 337
 
same level with that of the nasal cavity, or higher or lower than that.
In some cases the sinus may be incompletely divided by osseous and mem-
branous ridges, commonly known as septa.
 
Unilateral supplemental maxillary sinuses have been observed.‘ They
occur posteriorly to the sinus proper and are, from the standpoint of origin,
overdeveloped posterior ethmoid cells. Clinically, they must be considered
as maxillary sinus.
 
4. FUNCTION
 
In the past, various functions have been ascribed to the maxillary sinus
and the other accessory nasal sinuses. It has been claimed by some, for
instance, that they aid in warming and moistening inhaled air, thus acting
as air-conditioning chambers. Others believe that the sinus plays an
important role in vocalization. However, the most probable explanation
of the development of all nasal sinuses is that bone which has lost its
mechanical function is resorbed. An example is the marrow cavity in
long bones where fatty tissue develops in the place of the disappearing
bone. The disappearance of useless bony substance in the neighborhood
of the air-filled nasal cavity leads to development of air-filled pouches
which grow into the bone and occupy the place of bony tissue which
is no longer needed to withstand mechanical stresses. The supporting
function of bone is maintained but with a minimum of material. This
is in accord with principles of economy which exist in the animal body.
 
5. HISTOLOG-Y
 
The maxillary sinus is lined by a mucosa covered with an epithelium
typical of the respiratory passages. It is thinner and more delicate than
that of the nasal cavity.
 
The lamina propria of the mucosa is fused to the periosteum of the un-
derlying bone and consists of loose bundles of collagenous fibers with
very few elastic fibers; it is only moderately vascular (Fig. 262, A).
Glands of the mucous and serous type are confined largely to that part
of the tunica propria which is located around the opening, or openings,
into the nasal cavity.
 
The epithelium is pseudostratified ciliated columnar, rich in goblet cells
(Fig. 262, B). The nuclei of the individual columnar cells are‘located at
different distances from a delicate basement membrane. Actually, each
columnar cell rests upon the basement membrane, but not all the cells
reach the surface. The goblet cells secrete mucus which moistens the
surface of the sinus mucosa. The cilia beat in such a way as to move
any surface material toward the opening communicating with the nasal
cavity, and hence act to clear the sinus cavity of inhaled substances, and
 
mucus.
6. GLINIGAI. CONSIDERATIONS
 
Pulpal infection in teeth whose root apices are in close approximation
to the floor of the sinus are dangerous because it can be a cause of sinus
Maxillary sinus
Epithelium
 
- —"- ‘ “ ‘ - Mucous membrane
‘T’ --- “F” and perlosteum
 
Incomplete bony
floor of sinus
 
 
_ _ ,_,......\‘. 7»;-w
 
 
Fig. 262.——Mucous membrane and epithelium of maxillary sinus.
 
A. Apical region of :1 second bicuspid. The lining oi.’ the sinus is continuous with the
periapicsl tissue through openings in the bony floor of the sinus.
 
B. High magnification of the epithelium of maxillary sinus. (Courtesy W. 11. Bauer.‘
St. Louis University School of Dentistry.)
 
.- - -j-—-A .g.g3;‘.I“&'
‘S
 
-2-
‘Q
 
 
es.
 
F'iE- 263.—Roentgenogrs.m or upper jaw. Maxillary sinus extends toward alveolar crest
after loss of flrst molar.
Tl-IE MAXILLARY SINUS 339
 
infection.‘= 3 Thus, the prevention of the dental type of sinusitis is pos-
sible by prevention or elimination of pulpal infection. Any root canal
operation in maxillary bicuspid or molar areas should be carried out with
particular care, in order to prevent infection of the sinus.
 
The dentist should always keep in mind that disease of the maxillary
sinus may produce referred dental pain. The superior alveolar nerves run
in narrow canals in the thin wall of the sinus and, frequently, these canals
are partly open toward the sinus. When this happens the nerves which
supply the teeth are in contact with the lining of the sinus where they
may become involved in an inflammation affecting the mucosa. In such
cases, the pain resembles pulpal pain but involves a group of teeth or
even all the teeth in one maxilla. If apices of some roots are in contact
with the lining of the sinus the affected teeth may show symptoms of
periodontitis during sinus infection. In cases where there is doubt whether
the teeth or sinus are the cause of pain, the patient should be referred to
a rhinologist before an extraction is performed.
 
In the course of an extraction a root may be forced into the sinus.
If it cannot be easily removed through the socket the patient should be
informed of the circumstances and be referred to a rhinologist. Even
if it is possible for the dentist to remove the root of the tooth, subse-
quent treatment by the sinus specialist is advisable. Any invasion of the
field of sinus surgery by the dentist operating through the alveolar wall
should be discouraged by both dental and medical professions.
 
After loss of a single maxillary molar or, more rarely, bicuspid, the
bony scar is, sometimes, hollowed out by the sinus (Fig. 263). The risk
of opening the sinus during extraction of a tooth adjacent to such an
extension has to be recognized. If a single molar remains in the maxilla
for a long time after loss of the neighboring teeth, downward extensions,‘
of the maxillary sinus may occur mesially and distally to this tooth. If [
greater force is applied in extracting such a tooth, tooth and socket are
removed together rather than extracting the tooth from its socket. To
minimize the necessary force the crown should be removed, the roots sepa-
rated and extracted singly. The expansion of the maxillary sinus (and
other sinuses) in old individuals should not be considered a process of
growth. It is rather the consequence of progressive disuse atrophy of
the bones, especially after loss of teeth, or of senile osteoporosis. The
senile expansion of sinuses strengthens the belief that they develop as
fill-ins in bones whose core is under reduced mechanical stress.
 
References
 
1. Bauer. W. ‘EL: Maxillary Sinusitis of Dental Origin, Am. J. Orthodont. & Oral Surg.
 
29: 133, 1943. _
2. Ennis, L. M., and Batson, 0.: Variations of the Maxillary Sinus as Seen in the
 
Roentgenogram, J. A. D. A. 23: 201, 1936.
3. Hofer, 0.: Dental Diseases and Their Relation to Maxillary Antrum, J. Dent.
 
Research 17: 321, 1938 (Abstract).
340 omu. HISTOLOGY AND EMBRYOLOGY
 
4. MacMilla.n, H. W.: The Relationship of the Teeth to the Maxillary Sinus; Anatomic
Factors glnderlying the Diagnosis and Surgery of This Region, J‘. A. D. A. 14.:
1635, 19 7.
 
5. Schaefier, J. I’.: The Sinus Maxillaris and Its Relations in the Embryo, Child and
Adult Man, Am. J. Anat. 10: 313, 1910.
 
6. Schaefler, J. P.: The Nose, Paranasal Sinuses, Nasolacrymal Passageways and
Olfactory Organ in Man, Philadelphia, 1920, P. B1a.kiston’s Son & Co.
 
7. Sedwick, H. .1'.: Form, Size and Position of the Maxillary Sinus at Various Ages
Studied by Means of Roentgenograms of the Skull, Am. J. Roentgenol. 32: 154,
1934.
 
8. Zuckerhandl, E.: N ormale und pathologische Anatomie der N asenhiihle und ihrer
pneumatischen Anhiinge (Anatomy of the Nasal Cavity), Leipzig, 1893.
CHAPTER XV
TECHNICAL REMARKS
 
1. INTRODUCTION
 
2. PREPARATION OF EISTOLOGIC SPI:GIM:E:N S
 
a. Dissection
 
b. Fixation
 
c. Decalciflcation
 
d. Embedding
 
e. Sectioning
 
f. staining
g. Altmann-Gersh Technique
 
3. PREPARATION OI‘ G-ROUND SECTIONS
4. PREPARATION OI‘ ORGANIC STRUCTURES IN THE ENAMEL
5. PEOTOMICROGRAPHY
 
1. INTRODUCTION
 
This chapter is intended to give the student a general idea of the prep-
aration of microscopic slides, rather than to cover fully the subject of
microscopic technique. For detailed information specialized textbooks
should be consulted." 11’ 12' 1’ The various processes to which a tissue is
subjected from the time it is taken from the body until it is ready to be
examined under the microscope, are termed microtechnique. Its object
is to prepare the specimen for examination of its microscopic structure.
 
2. PREPARATION OF I-IISTOLOGIC SPECIMENS
 
Dissection is the first step in the preparation of a specimen; the ma-
terial may be secured by a biopsy (excision during life) or at an autopsy
(postmortem examination). Pieces of tissue are cut as small as possible
to insure satisfactory fixation and impregnation. A very sharp knife
should be used to prevent tissue structures from being distorted and
squeezed.
 
Immediately after the specimen is removed and the surface washed
free of blood, it is placed in fixing solution. The object of fixing is to
preserve the tissue elements in the same condition in which they are at
the moment the reagent acts upon them, and harden or so affect them
that they will not be altered by the processes of dehydration, embedding,
staining, clearing and mounting. The amount of the fixing solution should
be at least 20 times the volume of the tissue. The fixing tissue coagulates
the protein content of the cells, thus preventing decomposition.
 
First draft submitted by Joan Launspach, research technician or the Foundation for
Dental Research, Chicago College of Dental Surgery.
 
341
 
Dissection
 
Fixation
Lciflcation
 
342 ORAL msronocr AND EMBRYOLOGY
 
There are several fixing agents in general use, the most common of
which are formalin, formalin-alcohol, Zenker-formol solution, and Bouin’s
fluid. A good and rapidly penetrating fixative for small specimens is
Zenker-formol solution, a mixture of 9 parts of potassium bichromate and
bichloride of mercury with 1 part of neutral formalin. Formalin (5 to 10
per cent) is used for large pieces of tissue, e.g., jaws. It does not de-
teriorate and it penetrates very rapidly. Formalin-alcohol fixes and dehy-
drates simultaneously, and is used mostly for surgical specimens. Bouin’s
fluid is a solution of picric acid and formalin, and is especially applicable
in studying cell outlines, but is rather slow to penetrate.
 
The length of time necessary for a fixing agent to act upon a tissue
varies according to the size of the specimen and penetrating power of the
fixative. Generally, it should be just long enough for the agent to satu-
rate the piece thoroughly without allowing it to become brittle. Small
pieces of tissue, e.g., gingiva, are left in Zenker-formol solution only 4
to 8 hours, while larger pieces such as jaws may be left in formalin for
days. In order to obtain good fixation of pulp in an intact tooth, the
surface of enamel and dentin is ground away to a thin layer of dentin
around the pulp. This process not only insures rapid and thorough pene-
tration of the fixing agent but also reduces the time of decalcification
and permits a thorough impregnation with cellodin. When fixing biopsy
specimens, the solution should be at approximately body temperature.
 
After the specimens are thoroughly fixed, they are washed in running
water for twenty-four to forty-eight hours to remove all acids and rea-
gents. Occasionally, however, special treatment is required to remove
the precipitates caused by certain agents. Example: specimens fixed in
Zenker-formol solution are treated with Lugol’s (iodine) solution and
sodium thiosulfate, and specimens fixed in formalin are placed in a mix-
ture of potassium hydroxide before staining. However, there is no need
of this if neutral formol is used.
 
Animal tissues may be classified as hard and soft, or calcified and non-
calcified. The dental histologist is particularly interested in the hard
tissues, namely, the enamel, dentin, cementum and bone. These are im-
pregnated with a variable quantity of calcium salts and cannot be see-
tioned on the microtome unless decalcified.
 
Decalcification of a tissue is the removal of its mineral content by an
acid such as nitric, hydrochloric, trichloracetic, formic, or sulfosalycilic
acid. The length of time a specimen remains in the decalcifying agent
is influenced by the choice and concentration of the acid, and the size of
the specimen; however, the shorter the time the better is the staining.
A 5 per cent solution of nitric acid seems to be most satisfactory and is,
therefore, widely used. It acts quickly without causing swelling of the
tissue or any other undue changes in its elements; it does not interfere
with the staining process to any marked degree.
 
While tissues are being decalcified they should be suspended in a large
quantity of the fluid in order that the salts dissolved may sink to the
TECHNICAL REMARKS 343
 
bottom of the jar. Occasional stirring or gentle agitation of the specimen
and heating of the acid may hasten the process of decalcification, but
great care should be taken not to injure the tissues.
 
To ascertain whether the inorganic salts have been completely removed,
the specimen can be pierced with a sharp needle or pin: when no gritty
substance is detected, the decalcification is sufficient. Roentgenographic
check-up can also be employed. After decalcification a tooth should be
as pliable as a piece of cartilage. The enamel disappears almost entirely
owing to its low percentage of organic matter. The decalcifying agent
may also be tested for calcium; the acid is changed periodically until the
test is negative.
 
Following decalcification the specimen is washed thoroughly in run-
ning water for at least 24 hours. From this point it is treated as a soft
tissue and is ready for the embedding process. It is possible, however,
to embed hard tissues first and decalcify them later: the specimen is run
through the solutions in routine fashion and, after it is blocked, the
excess celloidin is cut away and the tissue is suspended in acid until
decalcified. This takes much longer than the usual procedure and the
results are often uncertain.
 
In order that a tissue may be sectioned on the microtome it has to have
a certain rigidity to offer sufficient resistance to the cutting edge of the
knife. This may be accomplished by freezing the tissue or, as is more
commonly done, by using an embedding medium which fills the inter-
stices of the tissue. The freezing technique is employed where immediate
investigation of the specimen is required, as in the course of a surgical
operation. Some substances (fat, lipoids, etc.) are dissolved during em-
bedding: tests for such substances can be made only in frozen sections.
 
Embedding is a much more lengthy process but results are more satis-
factory. Before the specimen is embedded, i.e, impregnated with a suit-
able substance such as paraffin or celloidin, the water has to be removed
from the tissues. Paraffin embedding is more rapid and is used for small
pieces, usually soft tissue, as decalcified pieces become brittle during the
heating which is necessary in using this method. Celloidin embedding
takes longer but causes less shrinkage. This technique is more commonly
used in dental histology when large blocks of decalcified material have
to be sectioned.
 
Dehydration is accomplished by placing the specimens in ascending
alcohols (50, 70, 95, 100 per cent) for approximately one day each; the
length of time depends on the size and permeability of the specimen.
Two consecutive changes of absolute alcohol are used. As, however,
paraifin or celloidin is not soluble in alcohol it has to be replaced by a
fluid which is a solvent for the embedding medium.
 
When paraffin is selected as the embedding medium, the absolute alco-
hol is replaced by xylol or oil of cedarwood. The specimens are placed
in the solvent 12 to 24 hours, and are then placed in liquid parafiin in the
 
Embedding
Sectioning
 
344 ORAL HISTOLOGY AND EMBRYOLOGY
 
incubator (56 C.) for several hours. Finally the specimen is placed in a
form filled with molten parafiin and quickly cooled. It is then ready to
be sectioned.
 
If celloidin, a solution of nitrocellulose in absolute alcohol and ether,
is selected as the embedding medium, a mixture of equal parts of ether
and alcohol is used as a solvent in which the tissue remains for 12 hours.
It is then carried through a thin (6 per cent) and medium (121/; per
cent) into thick (25 per cent) solution of celloidin. The length of time
which is necessary for each of the solutions to penetrate the specimen
depends upon size and permeability of the tissue. Soft tissue is well
infiltrated with celloidin after three weeks while decalcified specimens
require at least six weeks; to insure thorough impregnation, it is wise
to leave teeth longer in the lower concentration of celloidin and a some-
what shorter time in the stronger concentration. When it is necessary
to “rush” a specimen the tissue in thin celloidin may be placed in a
50° C. oven in a tightly stoppered container; the embedding period is
thus shortened to two or three days. This method causes considerable
shrinkage. Small pieces of tissue may be placed directly on a fiber block
and left to harden in a desiccator filled with chloroform vapor. Large
pieces of tissue, e.g., jaws, are placed in an evaporating dish filled with
celloidin which is allowed to harden down slowly. When the celloidin
has reached the desired degree of hardness, blocks are cut out and, after
being softened in thin celloidin a few minutes, are placed on fiber blocks,
 
allowed to air dry, and then placed in 70 per cent alcohol for storage or
sectioning.
 
Tissues are sectioned by means of a microtome, ‘a machine equipped
with a knife. There are three different types of microtomes: the freez-
ing, rotary, and sliding, the use of which depends on the kind of tissue
and embedding medium used. Each is a heavy specially designed ma-
chine precisely constructed, capable of slicing prepared tissues into ex-
ceedingly thin sections. The knife is wedge-shaped and made of heavy
steel to aflord the greatest possible rigidity; it must have a very keen
edge as the slightest nick would tear a section. Sharpening a microtome
knife is one of the most important as well as the most difficult tasks of
a technician. Larger nicks are removed on a coarsely grained stone,
and a fine edge is achieved by grinding the knife on a fine hone. The
final cutting edge is obtained by stropping on a finishing leather micro-
tome strop. A much more rapid and just as satisfactory a method that
has recently been developed is the use of a grinding machine, consisting
of an ebony wheel mounted on a rotary motor. A strop, dusted with
abrasive powder, is used to put the finishing edge on the knife. The
possibility of making good sections depends upon the type of tissue,
its preparation, and the condition of the knife. Sections of 5 to 15
microns (174000 millimeter equals 1 micron) are considered thin.
TECHNICAL REMARKS 345
 
The importance of the freezing technique in preparing surgical speci-
mens has been mentioned. It is well known that, by exposing tissues
to an extreme degree of cold, they become hard and can be easily sec-
tioned with the freezing microtome. The cold is generated by means of
carbon dioxide which is sprayed onto the stage holding the specimen:
rapid evaporation produces the required temperature.
 
The rotary microtome is used only for sectioning paraffin blocks; the
knife is immovably fixed at a right angle to the block which is carried
past the sharp edge of the knife by turning a wheel. With this machine
it is possible to out long ribbons of serial sections. The ribbons are placed
in lukewarm water where the wrinkles are removed as the paraffin be-
comes soft. The desired sections are then floated onto slides smeared
with egg albumen and placed in a 37° C. oven for a few minutes. Before
staining, the paraffin is dissolved in xylol. the slides rinsed in absolute
alcohol, the sections are carried through descending concentrations of
alcohols into distilled water; then they can be stained by water-soluble
dyes.
 
A celloidin block is sectioned by a different method. For this purpose
the sliding microtome, a heavy sledgetype instrument, is used. The longi-
tudinal angle of the knife is adjusted to each specimen so that the entire
cutting edge is used in sectioning. The angle of the cutting edge of the
knife should be changed according to the hardness and density of the ma-
terial. To obtain the most satisfactory results the knife should be in an
almost horizontal position for large decalcified pieces, at an acute angle
for soft tissue. During sectioning both specimen and knife are continu-
ally moistened with 70 per cent alcohol; the sections are placed in distilled
water before staining. The celloidin is usually not removed from the
section as the stain penetrates the tissues in spite of this embedding me-
dium. However, it has to be removed from the section in the case of
specific stains, i.e., Mallory, azure-eosin, etc. For this procedure the sec-
tion is mounted on a slide smeared with egg albumen and is flooded with
oil of cloves to dissolve the celloidin; the slide is rinsed in 95 per cent
alcohol and placed in 70 per cent until ready for staining.“ When serial
sections are desired, sections are mounted on glass slides which are then
blotted and flooded with a very thin solution of collodion. After a coat-
ing is formed, the slides are marked with a diamond pencil or India ink,
and stored in 70 per cent alcohol until ready for staining.“
 
Some special staining methods can be applied only to sections of un-
decalcified teeth and bone. To obtain such sections mature enamel has
to be removed from the teeth. The tissue impregnated With celloidin is
placed in a shallow dish and covered with celloidin. The solution is
allowed to evaporate slowly until the celloidin is very hard (two to four
weeks) . A very hard knife should be used which has been sharpened and
stropped ; when checked under the microscope it has deep and even teeth
and should be clamped in the microtome at a 13° angle.
Staining
 
Altmann-Gersh
Technique
 
346 orm. ursronoev AND nmasvonoer
 
Dyes used to stain specimens for microscopic examination may be clas-
sified as basic or acid, according to their affinity for different cellular
elements. Basic dyes, sometimes called nuclear dyes, primarily stain
nuclear chromatin, basic substance of cartilage and mucus; the more
commonly used are hematoxylin, methylene blue, safranin, and carmin.
Acid dyes color the cytoplasm of the cell, uncalcified bone and dentin
matrix, some connective tissue fibers; eosin and phloxin are representative
of this group. By using combinations of the two groups, due to their
different affinities, a marked difierentiation of the cellular elements of
the specimen is possible.
 
Sections may be stained on the slide or floating in dishes; in the latter
case better differentiation is afiorded. Although the steps of the various
staining methods differ considerably, they may be arranged in the fol-
lowing order: staining, differentiating, decolorizing, dehydrating, clear-
ing and mounting.
 
Hematoxylin and eosin is one of the most commonly used combinations
of stains because it is the simplest to handle. For the differentiation of
more specialized tissues the following are recommended: Mallory stain,“
or Heidenhain’s Azan“ (modification of Mallory’s stain) for connective
tissue; the latter is more brilliant and has greater capacity for differen-
tiation; Silver Impregnation (modification of Foot’s stain by Gomori)
for connective tissue fibers and nerve elements ;’ Van Gieson’s stain, a
counterstain to hematoxylin, for differentiation of white connective tis-
sue," and Weigert’s stain for elastic tissue.“
 
After sections of tissues have been stained and differentiated, they are
dehydrated and then passed through a medium that will mix with the
dehydrating fluid as well as the reagent in which the sections are to be
mounted. These intermediary fluids are called clearing agents because
they have a high refractive index, thus rendering the sections more or
less transparent.
 
For celloidin sections a variety of clearing agents is used: terpineol
(Lilacine), carbol-xylol, oil of cloves, oil of cedar wood, oil of origanum
and beechwood creosote; for paraffin sections usually only two are used:
xylol or toluol.
 
After clearing, the sections have to be placed in some medium which
will preserve the stain and prevent the tissue from drying. Such solu-
tions are termed mounting agents: among the most common are Gum
damar, Canada balsam, and clarite. Loose celloidin sections are floated
onto the slide and straightened out with the aid of a fine camel’s hair
brush; they are carefully blotted and covered with a drop of mounting
medium and a coverslip. Weights are placed on the coverslips to prevent
the formation of air bubbles. When dry, they are carefully cleaned with
xylol and labeled with India ink.
 
The Altmann-Gersh freezing and drying technique for special micro-
chemical studies should also be mentioned. The tissues are frozen in-
TECHNICAL REMARKS 347
 
stantaneously when placed in a tube of isopentane in a Liquidair container
and are dehydrated under vacuum while still frozen, thus avoiding a re-
distribution of minerals. Fixation, alcohol dehydration, and clearing
are omitted as the dehydrated tissue can be immediately infiltrated with
paraffin and sectioned according to the usual methods. This technique
has proved valuable in the preparation of tissues for micro-incineration,
and for special micro-chemical reactions.
 
Many submicroscopic structures may be seen with the electron micro-
scope, not visible in sections prepared in the routine manner.
 
3. PREPARATION OF GROUND SECTIONS
 
Ground sections are prepared by using abrasive stones upon a tooth
or bone until the tissue is reduced to translucent thinness. It is the prin-
cipal method of examining the enamel which has so little organic material
that it disappears almost entirely when the teeth are decalcified by ordi-
nary methods. Therefore, this technique should complement the decal-
cification method. i
 
To prepare a ground section of a tooth it is first ground down on one
side on a carborundum stone which rotates at high speed on a laboratory
lathe. It is important that the tooth be kept wet constantly with cold
water to lessen the heat produced by friction and to prevent the section
from drying. If it is allowed to dry its organic constituents will shrink
and present a picture untrue to the conditions during life. The tissue is
likewise more apt to crack and break up during preparation if it becomes
dry. When the desired level is reached and the ground surface is per-
fectly plane, this surface is polished on wet ground glass and, finally, on
an Arkansas stone. The other side of the specimen is then ground down
until the section is sufficiently translucent. This second side is also
polished in the above described manner, to remove the gross scratches
produced by the carborundum stone. The finished ground sections should
have an average thickness of 25 to 50 microns and, if desired, may be
 
stained before they are dehydrated, cleared and mounted.”
 
For surface staining of ground sections the surface is well polished and
the section is covered with a 0.25 per cent H01 to decalcify it slightly;
then it is stained lightly with hematoxylin.“ By this method only the
surface of the ground section is stained and the stained layer can be
viewed with high power lenses as it is only a few microns in thickness.
This method, however, causes slight decalcification of the enamel making
a marked differentiation of rods from sheaths and cementing substance,
:3. condition not representative of normal enamel. Enamel that has been
partially decalcified by caries, or a poorly formed enamel has this
appearance.
 
If it is necessary to investigate an undecalcified tooth with the sur-
rounding soft tissue, ground sections can be made by using the petrifica-
tion method. The specimen is embedded in Kollolith-chloroform solution
348 omu. HISTOLOGY AND EMBRYOLOGY
 
or in Canada balsam”, 15 where it is left until it is sufficiently hard before
it is ground down to a desired thickness. Thin “serial” ground sections of
teeth and jaws may be cut in one operation by infiltrating the specimen
with a plastic material and using a cutting device made up of steel wheels
set at various distances."
 
4. PREPARATION OF ORGANIC STRUCTURES IN THE ENAMEL
 
The routine decalcification of whole teeth in an aqueous solution of
acid usually destroys the enamel completely. At most, merely shreds of
the organic structures remain near the cervical areas in a tooth of a
young person.
 
The organic structures may be demonstrated by C. F. Bodecker’s cel-
loidin decalcifying method.‘ When dentin is included in the specimen
sections are rarely satisfactory because this tissue becomes very brittle
as a result of the many media through which it passes. It is necessary
only for study of the organic structures in the enamel under high magni-
fication. In general, this method is erratic and a high percentage of
failures must be expected.
 
The Cape-Kitchin modification‘ 5 of Bodecker’s method is quite simple
and gives satisfactory results if the structures of the matrix are not mag-
nified more than about 500 diameters.
 
Frisbie, Nuckolls, and Saunders’ have recently developed a technique
for the successful recovery of the enamel matrix. The fresh specimen
is immediately fixed in neutral formalin for a long period of time (six
months) ; most of the dentin is then removed with a dental bur and the
tooth is placed in the fixative again for a shorter period of time, depend-
ing on the penetrability of the specimen. The completely fixed enamel
is decalcified by placing the specimen on a gauze stretched over a plat-
inum wire frame, and immersing it in a 5 per cent solution of nitric acid
in 80 per cent alcohol for 24 to 48 hours. Dehydration is begun with 70
per cent alcohol without preliminary washing. The specimen is in-
filtrated with celloidin at 56 C. for two weeks and then allowed to harden
down slowly at room temperature until the block is very hard. Section-
ing is done with a sliding microtome at 3 to 4 microns.
 
An aqueous decalcification of enamel under a cover-glass is the simplest
but the least satisfactory method for its study. It is sufficient to show
enamel lamellae, cuticle, tufts, and can be used to demonstrate gross
differences in quantity of organic structures of enamel in recently erupted
teeth and in teeth of old persons. However, the disadvantages are that
only low magnifications up to 100 diameters are possible and that the
specimens are not durable.
 
Another method of differentiating the organic from the inorganic con-
tent of the enamel is by incineration. It has been shown that the heating
of sections of human adult enamel up to 800° 0. causes a destruction of
the organic content but leaves enamel rods intact.
TECHNICAL REMARKS 349
 
5. PHOTOMICROGRAPHY
 
Photomicrographs are photographs of small microscopic objects, made
with the aid of a microscope. Most of the illustrations in this book are
such pictures. Transmitted light is the most commonly used method of
illumination as it permits the sharpest differentiation of details and the
highest magnification of tissue structures in stained decalcified sections.
 
Refiected light is used in oral histology in photographs of ground
sections of enamel and dentin. These sections should be ground per-
fectly smooth. There is no need for extreme thinness because the speci-
men is viewed only from the surface from which the light is reflected.
 
Polarized light also is useful in the study of the dental tissues. It
vibrates in a single known plane and requires special equipment and
technique. By this means it is possible to determine details of the sub-
microscopic structure of tissues, due to the differences in optical prop-
erties of various elements. Polarized light is particularly useful in the
study of calcified tissues, but is not confined to these, because fibrous and
keratinized structures also yield information when studied by this method.
 
Grenz rays are a form of exceedingly soft roentgen rays. When ground
sections of teeth are photographed in this way, slight variation in calci-
fication may be defined thus rendering this method useful in the study of
calcified structures." 13
 
A method has recently been developed by Gurney and Rapp” for
studying the fine structural details of tooth surface by adapting the Fax
Film technique used for study of metallographic surfaces. Micro-im-
pressions are made of the specimen, using a plastic film which may then
be mounted on a glass slide for a permanent preparation. Scott and
Wyckoff“ obtained similar results by shadowing collodion replicas with
vaporized metal in a high vacuum, a more complicated method. The
eifect of chemical agents on tooth structure and the changes in tooth
surfaces (caries) may be observed using these methods. When examined
under the electron microscope, many submicroscopic structures are
visible.
 
Ultraviolet light technique‘ and fluorescence light microscopy, like-
wise, have been applied in special studies of dental tissues, but have not
yet attained wide use.
 
References
 
1. Applebaum, E.. Hollander, F., and Bodecker. C. F.: Normal and Pathological
Variations in Calcification of Teeth as Shown by the Use of Soft X-rays,
Dental Cosmos 75: 1097, 1933. _
 
Bensley, R. R., and Bensley, S. 8.: Handbook of Histological and Cytological
Technique, Chicago, University of Chicago Press. _ _
 
Bodecker, C. F.: Cape-Kitchin Modification of Celloidin Deoalcifymg Method for
Dental Enamel, J. Dent. Research 16: 143, 1937. _ _ _ '
 
Bodecker, C. F.: Enamel of Teeth Decalcifled by Celloidin Decalcifying Method
and Examined by Ultra Violet Light, Dental Review 20: 317, 1906.
 
Cape, A. T., and Kitchjn, P. 0.: Histologic Phenomenon of Tooth Tissues Observed
Under Polarized Light, With a Note on Roentgen Ray Spectra of Enamel and
Dentin, J. A. D. A. 17: 193, 1930.
 
S"l“9°.l‘-"
350 ORAL HISTOLOGY AND EMBRYOLOGY
 
6. Cowdry, E. V.: Microscopic Technique in Biology and Medicine, Baltimore,
1943, Williams & Wilkins Co.
 
7. Frisbie, H. E., Nuckolls, J., and Saunders, J. B. de G. M.: Distribution of
Organic Matrix of Enamel in Human Teeth and Its Relation to Histo-
pathology of Caries, J. Am. Coll. Dent. 11: 243, 1944.
 
8. Gurney, B. R, and Rapp, G. W.: Technic for Observing Minute Changes on
Tooth Surfaces, J. Dent. Research 25: 367, 1946.
 
9. Guyer, M. F.: Animal Micrology, Chicago, 1943, University of Chicago Press.
 
10. Hotchkiss, R. D.: Microchernical Reaction Resulting in Staining of Polysac-
charide Structures in Fixed Tissue Preparation, Arch. Biochem. 16: 131,
1948.
 
11. Loosli, C. G.: Outline of Histological Methods, Chicago, University of Chicago
Press.
 
12. Mallory, F. B.: Pathological Technique, Philadelphia, 1938, W. B. Saunders Co.
 
13. McClung, C.  Microscopic Technique, New York, 1937, Paul B. I-Ioeber, Inc.,
pp. 353-401.
 
14. McLean, F. 0., and Bloom, W.: Calcification and Ossification. Calcification in
Normal Growing Bone, Anat. Rec. 78: 133, 1940.
 
15. Meyer, W.: Die Anfertigung histologicher Schlifie (Preparation of Histologic
Ground Sections), Vrtljschr. f. Zahnheilk. 41: 111, 1925.
 
16. Scott, D. B., and Wyckofi, R. W. G.: Shadowed Replicas of Tooth Surfaces,
Pub. Health Rep. 61: 697, 1946.
 
17. Sognaecs, R. F.: Preparation of Thin Serial Ground Sections of Whole Teeth
and Jaws and Other Highly Calcified and Brittle Structures, Anat. Rec.
99: 133, 1947.
 
17a. Sognnaes, R. F.: The Organic Elements of the Enamel. I, II, III, IV, J. Dent.
Research 27: 609, 1948; 28: 549, and 558, 1949; 29: 260, 1950.
 
18. Willman, M.: Technique for Preparation of Histological Sections Through Teeth
and Jaws for Teaching and Research 16: 183, 1937.
 
19. Wolf, J.: Plastische Histologie der Zahngewebe (Plastic Histology of Dental
Tissues), Deutsche Zahn-, Mund- und Kieferheilkunde 7: 265, 1940.
INDEX
 
A
 
Aberrant glands, 285
Aberrations in tooth development, 46
of the cemento-enamel junction, 165
of the epithelial attachment, 229, 230
Abrasion, 260
Accessory fossae, 335
glands, 285
parotid, 275
submaxillary, 279
nasal sinuses, 337
ostium, 334
root canals, 45, 130, 131, 132, 133, 151
Acellular cementum, 159, 160, 166
Acid dyes, 346
Acidophile granules, 87
Acrornegaly, 209
Active eruption, 23, 232, 243, 289, 311,
312, 321, 322
Addison ’s disease, 219
Adheions of the amnion, 28
Adrenal cortex, 219
Adventitial cells, 142
Age changes, 71, 115, 120, 135, 136, 174,
188, 203, 205, 229, 261
Air conditioning, 337
Albuminous alveolus, 277
cells, 263, 270, 271, 273
glands, 254, 269
Alkaline phosphatase, 122
Altmann-Gcrsh freezing-drying technique,
346
Alveolar arteries, 244
bone, 37
proper, 198, 202, 208, 259
crest, 180, 199, 200, 288, 293, 300
fibers, 178, 180
fibers, 180, 290
fundus, 291
mucosa, 216, 220, 223, 250, 251
nerve, 134
process, 23, 195, 197, 198, 300, 333
develo ment of, 197
physio ogic changes in, 203
structure of, 197
ridge, 22, 40, 43, 291
development of, 23
pseudo-alveolar, 22, 23
septum, 199 244, 295
Alveolodental ligament, 179
Ameboid wandering cell, 141, 142
Ameloblasts, 36, 37, 40, 45, 46, 47, 66,
81, 82, 83, 84, 85, 88, 90, 95, 227
development of, 87, 88
formative stage, 88
maturation stage, 88
morphogenetic stage, 87
organizing stage, 87
life cycle of, 85
polarity of, 36
Aznelogenesi, 36, 89, 90
Ammonia, 265
 
Amnion, adhesions of, 28
Amylase, 263, 279
Anatomical crown, 48, 158, 239, 259
repair, 173
root, 154, 260
Anatomy of maxillary sinus, 333
of pulp, 128
of tempcromandibular joint, 324
Angle of mandible, 202
Ankylosis, 302, 315, 316, 318, 319, 322
Anlage of permanent tooth, 39, 40, 41, 81,
84, 288
Anodontia, 46
Anterior faucial pillar, 213, 282
lingual glands, 266, 282
Antrum of Highmore, 333
Anvil, 197
Apatite crystals, 98, 113
Aperture of sinus, 336
Apex of root, 45, 129, 130, 132, 151, 162
Apical fibers, 179, 181
£oramei15145, 128, 129, 130, 132, 140,
variations of, 133
Aplasia of glands, 285
Apposition, 29, 30, 45, 48
bone, 296, 300
cementum, 296, 311
of dentin, 106
Appositiongl growth potential, 46, 106,
1 8
Arches, branchial, 14, 23
hyoid, 14, 23
mandibular, 14, 23
Argyrophié fibers, 87, 121, 134, 135, 156,
1 7
Arkansas stone, 347
Articular capsule, 324, 325, 330
cavity, 330
disc, 324. 325, 328
fibrocartilage, 329
fossa, 324, 328
tubercle, 324, 325, 327. 328, 329
Astringent chemicals, 175
Atresia, 285
Attached cementicles, 189
denticles, 148, 150
gingiva, 216, 221, 223, 249
Attrition, 73, 120, 296, 300
Auditory ossicles, 194
tube, 24, 331
Auriculotemporal nerve, 331
Autopsy, 341
Auxiliary structure, 298
Azure-eosin stain, 345
 
B
 
Bartholinian gland, 266, 279
 
Bartho1in’s duct, 279
 
Basal cells, 242
layer, 32, 85, 21:3, 217, 218, 219
processes, 212
 
351
352
 
Basement membrane, 32, 37, 40, 82, 87,
90, 121, 123, 134, 135, 211, 242,
256, 268, 270, 274, 337
 
Basic dyes, 346
lamellae, 200
 
Basket cells, 271
 
Bell stage of tooth development, 36, 39
Bifid tongue, 26
 
Bifurcation, 44, 45, 132, 133, 152, 172,
 
179, 293, 299, 301, 315
 
Biopsy, 341
Birefringence of enamel, 66, 73
of dentin, 113
Blandin-Nuhn glands, 283, 285
Bleeding, 172
Blood dyscrasias, 260
supply of gingiva, 244
of glands, 274
of periodontal membrane, 183, 184,
185
of pulp, 142, 143
Bodily movement of teeth, 288
Bone, alveolar proper, 198, 201, 202, 208
apposition, 192, 301
blood vessels of, 200-201, 203
bundle, 180, 201, 203, 206, 295, 296
calcification of, 205
cancelous, 325
cementing lines, 205
chemical composition of, 52, 205
chondroid, 197, 198
coarse fibrillar, 209
compact, 198, 325, 327
decalcification of, 203
development of, 194, 197
embryonic, 209
endochondral, 194
endocrine disturbances and, 209
fibrils in, 202, 205, 209
fibrous, 202
Haverséan systems in, 200, 201, 203, 205,
06
 
Howship’s lacunae, 203, 206
immature, 209, 210
in orthodontia, 207
internal reconstruction of, 205
intramembranous, 194, 195
lamellae of, 200, 205
basic, 200, 205
circumferential, 200, 201, 205
longitudinal 200, 201, 205
lamellated, 180, 206
lymph vessels of, 201
marrow, cellular, 202, 325
fatty, 202, 327
hemopoietic, 202
matrix of, 203, 204
physiological changes in, 203
plasticity of, 208
rarefication, 208
resorption, 192
resting lines, 200, 205, 206
reversal lines, 200, 205
Sharpey’s fibers in, 203, 205
spongy, 198, 200, 201, 205, 208, 327
trabeculae 208, 325
vitality of, 203
vitamin deficiencies and, 208
 
INDEX
 
Bottom of gingival sulcus, 224, 228, 232,
233, 234, 235, 236, 237, 238, 258
Bouin’s solution, 342
Brain vesicles, 13
Branchial arch, 14, 23, 194
clefts, 28
cysts, 25, 28
fistulae, 28
grooves, 23
pouches, 23, 24
Buccal frenula, 250
glands, 280
Buccinator muscle, 250, 276
Buccogingival lamina, 42
Bucconasal membrane, 17
Buccopharyngeal membrane, 14
Bud stage, 29, 32
Bundle bone, 180, 201, 203, 206, 295, 296
 
C
 
Calcification of dentinal ground substance,
110
globular, 123, 124
linear, 123 2
semilunar 11
of cementum,,158
of enamel, 85, 92, 99
zone 328
calcium metabolism, 85
Calculus 174
Callus, bony, 209
Canal, incisive 28
root, 129, 130, 131, 132, 133
Canaliculi, 164, 268, 274
Cancelous bone 325
Cap stage, 29, 34, 38
Capillaries of the pulp, 142, 143
Capitulum of mandible 324
Carbohydrates, 263 ’
Carborundum stone, 347
Carcinoma, 285
Caries, 78, 79, 125, 260, 264
and enamel lamellae, 78
o en Lll
aztttdck t?ate1’1'8]3 125
Carmin stain, 348
Cartilage islands, 326
Meckel’%,71%,8820, 34, 35, 40, 194, 195,
1
Caruncula stiblingualis, 279
ggvity preparation, 75,23
vum Ol'1S propnum
Celloidin decalcificatibn method, 343
C plInbed1d1ng,t.'-Z112, 131423, 344, 345
e s a ventii
alb’u,z)ni1(11ous, 363, 2617, miss, 270, 273
ame oi wan ering 41 42
basket, 271 ’ ’
chondroid, 328
clear, 219
defense, 135, 140, 141, 152
dendritic. 219
encllpthelial, 141
go et 337 338
lymphoid véandering, 141, 142
mesenehymal, 141, 142
undifferentiated, 145, 156, 182, 183,
203
INDEX
 
Ce1ls—Cont’d
mucous, 263, 267, 268, 269, 273
myoepithelial, 271, 273, 274
plasma, 142, 244, 274
resting wandering, 142
Rouget’s, 144
serous, 263, 267, 270
undifiegergtiated, 141, 142, 145, 182, 183,
0
mesegchymal, 141, 142, 145, 182, 183,
03
Cellular bone marrow, 202, 327
cementum, 149, 161, 162, 163, 167, 313
Cemental caries, 260
cuticle, 241
Cementicles, 172, 187, 189
Cementing lines, 205
substance, 53, 85, 102, 103, 123, 135,
158
Cementoblasts, 43, 47, 156, 158, 159, 167,
176, 183
Cementocytes, 163, 164, 167
Cemento-dentinal junction, 166
Cemento-enamel junction, 37, 42, 154, 164,
178, 199, 225, 229, 237, 298
aberrations of, 165
Cementogenesis, 154
Cemcntoid tissue, 157, 159, 161, 162, 167,
300
Cementum, 32, 37, 43, 129, 154
chemical composition, 154
definition, 154
development of, 154
fragments, 173
hypertrophy, 168
hyperplasia, 169, 171, 172
physical characteristics, 154
thickness of, 160
vitality, 163
Central bodies, 87
Centrioles, 88
Cervical cyst, 25
loop, 81, 83, 84, 85
Cheek, 213, 247
Choanae primary, 18
Cholesterol, 265
Chondrocranium, 194
Chondrocytes, 327
Chondroid cells, 328
Chordatympany, 259, 331
Chronology of dentition, 303
Circumferential lamellae, 200, 201
Clear cells, 219
Cleft jaw, 26
palate, 26, 27
Clefts of face, 26
Cleidocranial dysostosis, 302
Clinical crown, 239, 259, 312
root, 312
Coarse fibrillar bone, 209
Collagenous fibers, 157, 177, 290, 327
fibrils, 102, 103
submicroscopic units of, 113
Columnar epithelium, 254
Compact bone, 325, 327
Condylar growth centers, 208
Condyloid process, 202
Congenital malformations of face, 26
of salivary glands, 285
 
353
 
Contact points, 189, 259, 298
Continuous) cementum apposition, 159, 163,
2 9
Contour lines of Owen, 109
Copula, 14, 24, 25
Card, enamel, 36
Corniculate tubercle, 255
Coronal pulp, 128, 129, 298
Corrosion specimens, 132
Cortical plates, 198, 201
Course of dentmal tubules, 105
Creatinine, 263
Crescents, 270
Cribriform plate, 203
Cross striation, 54, 55, 64, 92
Cuneiform tubercle, 255
Cushioned hammock ligament, 291, 293,
294, 298
Cusp interference, 192
Cusps, dentinal, 48
Cuticle, primary, 66, 89, 241
secondary, 66, 71, 241
Cuticula dentis, 241
Cysts, 187, 192 285, 305, 318
branchial 26, 28
cervical, 25
dentigerous 305
dermoid, 28
globulomaxillary, 28
median, 28
thyroglossal duct, 26
Cytocentrum, 268, 270
 
D
 
Dead tracts, 120, 121
Decalcification, 97, 101, 203, 342, 343
Deciduous dentition, 38, 307
 
teeth, 33
 
retained, 318, 319, 320, 321
 
tooth remnants, 318, 319, 320, 321
 
traumatism in, 312, 313, 314
Defense cells, 135, 140, 141, 152, 220
Deficiency, vitamin A, 47
Deglutition, 263
Dehydration, 341
Demilunes of Gianuzzi, 270, 273, 277, 280
Dendritic cells, 219
Dental caries, 78, 79, 99, 125, 260, 264
 
and lamellae, 79
attack rate, 72
 
cervix, 298
 
crypt, 298
 
cuticle, 241, 242
 
fibers, 290
 
fluorosis, 99
 
granuloma, 192
 
lamina, 23, 27, 29, 31, 32, 33, 34, 37,
 
38, 39, 40, 41, 46, 81, 84
fate of, 42
 
lymph, 115
 
pain, 339
 
papilla, 32, 35, 36, 37, 38, 39, 40, 46, 81,
 
83, 134, 289
embryonic, 134
 
pulp, 32, 127
 
sac, 32, 36, 37, 42, 82, 83, 288, 290, 291
Denticles, 147, 148, 149, 150
 
attached, 148, 150
354
 
Dentic1es——Cont ’d
embedded, 150
false, 147, 148
free, 148, 150
 
Dentifrices, 174
Dentigerous cyst, 305
Dentin, 32, 36, 86
age changes of, 115, 120
and operative procedures, 125
apposition of, 106
appositional growth, 106
birefringence, 114
calcification of, 110, 111, 112, 122
carious, 118
chemical composition of, 52, 101
development of, 121, 137
formation, 84, 88
ground substance, 47, 101, 102, 110, 135
incremental lines in, 106, 108, 109
innervation of, 114
interglobular, 110, 111, 112
irregular, 117, 118
lines of Owen, 109
mantle, 103
matrix, 123
morphology, 101
neonatal line of, 110
physical properties of, 101
postnatal, 110
prenatal, 110
protective metamorphosis of, 117
sclerotic, 117, 118, 119, 120, 260
secondary, 116, 139, 150, 260
semilunar calcification of, 112
sensitivity of, 125
structure of, 114
submicroscopic, 111, 114
transparent, 118, 119, 120
vitality of, 115, 124
Dentinal cusps, 48
part of lamella, 67, 71, 119
tubules, 102, 103, 104, 105, 107, 164
course of, 104
number of, 105, 108
size of, 108
width of, 105
 
Dentino—cemental junction, 47, 48
Dentino-enamel junction, 37, 47, 48, 69,
70, 72, 81, 106, 110
membrane, 89, 90, 91, 95
Dentinogenesis, 122
imperfecta, 47
Denture construction, 261
Denture-bearing areas, 261
Depth of gingival pocket, 259
sulcus, 244
Dermoid cysts, 28
Desmocranium, 194
Desmolysis, 89, 289
Desmolytic stage, 89
Development of accessory root canals, 45
alveolar process, 197
ridge, 23
bifurcation, 44
branchial arches, 23
cementum, 154
cleft palate, 26, 27
dentin, 121
 
INDEX
 
Deve1opment—-Cont ’d
enamel, 81
epithelial attachment, 227
face, 13
hard palgge, 23
harelip
mandib,le, 194, 197
mandibulag arcgl, 17
maxilla 1 4 1 5
maxillaiy sinus, 333
oblique facial cleft, 27
oral cavity, 13
le§'hE.u;1auI§1’u23 22 23
paa in a 1 a. ,
processes, 18,,19, 20, 21, 23, 27
periodontal membrane, 176
primary4palate, 15, 16
pulp 13
root,’ 43, 293
salivary glands, 266
secondary palate, 19
soffthpazlgte, 23
ee
terminal bars, 91
3°” B§°°§Z‘°§s9ie
ongue
uvuls-J.,’21,26 ’ ’
Developmental Idigtiérbances, 98
Diamond penci 4
ggapthhragrn, %%i4t’he1ia1, 43, 44, 45
iar rosis
Differential growth, 17, 21, 297, 300
Diffuse calcifications, 147, 150
Disease, Addison ’s, 219
For-dyce’s 261
Hodgkin ’s, 285
Mikulicz’, 284
periodontal, 79, 152, 172, 259
Dissection, 341
Disturbances of mandibular articulation,
331
Disuse, 190, 191, 339
Dorsal lingual mucosa, 254
Duct elements of salivary gland, 273, 274
of Bartholin 266, 279
of parotid gland, 273
of Rivini, 279
of Stenson, 276
of Wharton, 275, 279
nasolacrimal 15 28
nasopalatine: 21: 28
thyroglossal, 26
Dura mater, 331
 
E
 
Ebner’s glands, 254, 257
Ectoderm, 29
Edema, 225
Elastic fibers, 135, 254, 328
stain, 346
Electron microscope, 57, 68, 74, 76, 77,
106, 115, 347
Eleidin, 214
Embedded cementicles, 189
denticles, 148, 150
Embedding, 302, 342
Enamel, 32, 50
age changes of, 71, 72
INDEX
 
Enamel——Cont ’d
 
birefringence of, 74
calcification of, 92, 93
chemical properties of, 51, 92, 93, 95
cleavage of, 75, 78
color of, 50, 51
cord, 36, 39, 81
crystallization of, 93
cuticle, 66, 227
primary, 66 67
secondary, 66, 71, 228
dentino-enamel membrane, 89, 90, 91
density of, 50
development of, 81
developmental disturbances of, 98
distribution of, 52
drops, 166, 168, 169
epithelium, 67, 289
inner, 34, 36, 37, 46, 81, 84, 85, 298
outer, 34, 36, 37, 40, 81, 32, 84, 293
reduced, 66
fissures, 78
development of, 78
formation of, 84
function of, 50
gnarled, 59
grooves, 36
hardness of, 50
Hunter-Schreger bands, 59, 60, 61
hypocalcification of, 98, 99
hypoplasia, '48, 98, 99
chronologic, 98
hereditary, 98
local, 98
multiple, 98
incremental pattern of, 61, 62
inorganic material of, 51
interprismatic substance, 55, 57
knot, 34, 36
lamellae, 67, 69, 70, 71, 78
and caries, 78
matrix, 47, 52, 85, 88, 89
formation of, 89, 93
young, 93
maturation of, 88, 89, 93, 96
calcification, 93
chemical changes in, 95
crystallization, 93
mature, 89
mottled, 68, 99
navel, 36
niche, 39, 81
of deciduous teeth, 58
organ, 29, 31, 32, 34, 35, 36, 37, 38, 40,
42, 47, 82, 93, 134, 287
contents of, 52
development of, 81
organic structure of, 52, 56
pearls, 45, 166
physical characteristics of, 50
hardness, 50
thickness, 50
translucency, 50
postnatal, 65, 66
prenatal, 65, 66
pri1smsé55337
11 P
fads’ 36,’ 53, 89, 91
calcification of, 53, 54
 
355
 
Enamel—Cont ’d
course of, 58
cross striation of, 54, 55, 64
diameter of, 53
direction of, 56, 58
in deciduous teeth, 56, 58
in permanent teeth, 56, 58
length of, 53
number of, 53
pre-enamel, 90, 91
sheath, 53, 54, 56
transverse striation of, 54, 55
spindles, 71, 73
spurs, 166
structure of, 53
submicroscopic crystals of, 74, 76
structure of, 73
Tomes’ processes, 90, 9.1
tracer studies of, 52
tufts, 58, 69, 70, 72
young enamel matrix, 93
 
Endochondral ossification, 194-197
Endocrine disturbances, 47, 208, 260
estrogenic hormones, 260
function, 187
Enzyme, 89, 158, 203, 263
Epidermoid cyst, 28
Epiglottis, 24, 255
Epimysium, 247
Epithelial attachment, 218, 223, 227, 228,
229, 230, 231, 233, 234, 235, 237,
238, 239, 312
formation of dental cuticle in, 241,
242
mode of, 239, 242
shifting of, 237, 239
structure of, 230
tears in, 231
theories of, 239
variation of, 239
width of, 233
diaphragm, 42, 129, 155, 293, 294, 298
inclusions, 28
network, 185
pearls, 21, 42, 247
pegs, 213, 227
remnants, 41, 148
rests, 129, 156, 182, 184, 185, 186, 187,
192, 296
degenerated, 186
of Malassez, 42, 156, 186
ridges, 213, 250, 251
root sheath of Hertwig, 29, 37, 42, 43,
45, 85, 129, 148, 155, 166, 186,
289, 293, 298
strands, 42
structures in periodontal membrane, 185,
186, 187
tears in, 231
 
Epithelium of mucous membrane, 211
pseudostratified ciliated columnar, 337
 
Erosion, 120
 
Eruption, chronology of, 303
direction of, 287
force of, 298
histology of, 287
mechanism of, 297, 300
of teeth, 197, 287, 302
356
 
E1-uption——Cont ’d
 
phases of, 287
 
functional, 293
pre-eruptive, 287
prefunctional, 289
 
theories of, 297
 
vertical, 167
Eruptive cyst, 305
Estrogenic hormones, 260
Ethmoidal cell, 336
Eukeratin, 52
Eustachian tube, 18, 21, 24, 33
Excementosis, 168, 169, 170, 174, 187
Excentric growth, 288
Excessive resorption, 301
Excretory system, 272, 273, 274
Exfoliation, 318
External auditory meatus, 275, 325, 331
 
pterygoid muscle, 324, 325
 
F
 
Face, clefts Of, 26
development of, 13
embryonic, 17
malformations of, 26
False denticles, 147, 148, 149, 150
median cleft, 27
Fate of dental lamina, 42
of retained deciduous teeth, 321
Fatty bone marrow, 202, 327
zone of palate, 244, 245
Faucial gland, 281
Fax film technique, 349
Fibers, argyrophil, 87, 135, 156, 157
collagenous, 135, 156, 290, 327
elastic, 220, 254, 328
of periodontal membrane, 167, 179
alveolar group, 180
apical, 181
gingival group, 179, 220
transseptal group, 179
precolla enous, 135, 156, 157, 290
principa, 167, 177, 181, 182, 191
reticular, 135
Sharpey’s 159, 161
Tomes’, 138
von Korfl:"s, 121, 122, 123, 135, 137
Fibrils, 102, 160, 205
argyroplul, 121
dentinal, 122
of bone matrix, 203
of cementum, 160
Fibrob1ast;,8135, 141, 176, 181, 271, 274,
3 .
Fibrocartilage, 197, 324, 327, 328, 329
Fibrosis, 150, 151
Fibrous covering of cartilage 326
Filiform papillae, 254, 255, 256
First branchial arch, 23
Fistula of the lower lip, 27
Fistulae, bronchial, 28
labial, 26
Fixation, 341
Fixing agents, 342
Floor of oral cavity, 251, 252, 279
of sinus, 335
Fluorescent light technique, 349
Fluoride hypocalcification, 99
 
INDEX
 
Fluorosis, dental, 99
Foramen cecum, 25, 26, 254, 255
incisivum, 26
Fordyce’s disease, 261
Fordyce spots, 250
Forebrain, 13
Foreg-ut, 14
Formalin fixation, 342
alcohol, 342
Formation, dentin, 84, 88
enamel, 84, 88
matrix, 88, 95
root, 42
pre-enamel rods, 92
Formative stage, 88
Fornix vestibuli, 220 247, 260
Fractures, healing of: 209
Free cementicles, 187, 189
denticles, 148
gingiva 216, 221, 223
gingival groove, 216, 221, 223, 237
Freezing microtome, 345
technique, 343
Frenulu (Frenulum), labial, 22
tectolabial, 23
Frenulum linguae, 279
Frequency of calcifications, 150
of denticles, 150
of pulp stones, 150
Frontal process, 14, 195
Fulcrum of tooth, 189
Function, loss of, 190
of cementum, 167
of maxillary sinus, 337
of myoepithelial cells, 271
of periodontal membrane, 176
of pulp, 127
of saliva, 263
of salivary glands, 263
Functional adaptation, 201, 329
changes of bone, 201, 203, 208, 209
of dentin, 115
integrity of tooth, 301
of periodontal membrane, 188
phase of eruption, 287, 293
polarity, reversal of 87
stresses, 103, 203, 208
Fungiform papillae, 254, 255, 256
Fusions, 46
 
G
 
Grerminal center, 255, 257
Grerminative layer, 212
Gianuzzi, demilunes of, 269, 273, 278, 280
G-ingiva, 215 216 220
attacheéi, 216, 221, 223, 224, 225, 226,
50
blood supply of, 183, 244
brushing of, 260
color of, 216
free, 216, 221, 223, 237
hornification of, 217, 218
innervation of, 221, 222
marginal, 223
massage of, 260 -
pigmentation of, 218, 219
recession of, 174, 237, 243
stippling of, 223, 224, 250
INDEX
 
Gingival epithelium, 217, 218
variations of, 218
 
fibers, 178, 179
 
margin, 223
 
papilla, 179, 259
 
pocket, 259
 
su1cus,225198, 227, 228, 232, 233, 234, 242,
 
bottom of, 228, 232, 234, 235, 236, 237,
239, 243, 259
depth of, 243, 244
formation of, 243
gingivectomy, 185
gingivitis, 79, 225
Gingivo-dental junction, 300
Glands, aberrant, 285
 
accessory, 285
 
albuminous, 254
 
aplasia of, 285
 
atresia of, 285
Bartholinian, 266, 279
Blandin-Nuhn, 283, 285
buccal, 280
 
exocrine, 263
 
faucial, 281
 
glossopalatine, 267, 268, 281
isthmian, 281
 
labial, 267, 280
 
merocrine type, 263
 
minor buccal, 280
 
sublingual 252
 
mixed, 250, é51, 267, 270
molar, 280
 
mucous, 253, 254
 
of hard palate, 244, 282
 
of major secretion, 274, 275
of maxillary sinus, 337
 
of minor secretion, 280
 
of oral cavity, 263
 
of soft palate, 282
 
of tongue, 266, 267, 282, 283
of uvula, 282
 
palatine, 266, 268, 282
parathyroid, 24, 98
 
parotid, 264, 266, 267, 276, 277
racemose, 283
 
retromolar 281
 
Rivinian, ér/9
 
salivary, 263
 
sebaceous, 214, 250, 260
sublingzual, 253, 264, 266, 268, 272, 275,
 
79
 
submandibular, 279
submaxgillgry, 264, 266, 268, 272, 275,
sweat, 214
 
thymus, 24
 
Globular calcification, 123, 124
 
processes, 15
 
Globulomaxillary cysts, 28
 
Glossitis, rhomboid, 261
 
Glossopalatine fold, 280
glands, 266, 268, 281
 
Glossopharyngeal nerve, 254, 259
Glycogen, 32
 
Glycoprotein, 268
 
Grnarled enamel 59
Gnathoschisis, 26
 
357
 
Gnomonic curves, 48
Goblet cells, 246, 337, 338
Golgi apparatus, 87
 
net, 268, 270
G-onadotropic hormones, 260
Grapurlar layer of epithelium, 212, 217
 
o omes 111 113
Grranuloma, 187, 192
Granulomatous inflammation, 284
Grenz rays 119 120 349
Grinding niachine, 314
Grooves, branchial, 23
 
enamel 36
 
lateral,’ 17
 
median, 17
 
nasal, 17
 
nasolacrimal, 14, 15
 
nasomaxillary 15 115
 
oral, 14 ’ ’
 
primary oral, 14
Ground glass, 347
 
sectionaof soft and hard tissues, 55, 240,
 
47
subitaance of Jcgmerfglém, 0157, 158
0 entin 1 1 3
 
Growth, appositional, 46, 106, 323
 
center, 48, 208, 327
 
differential, 17, 21, 297, 300
 
excentric 388
 
of dentin, 106, 297
 
of jaw, 288
 
of root, 297
 
continuous, 167
 
sutural, 209
 
of teeth, 29, 48
Grustatory papillae, 283
 
H
 
Hammer, 197
Hammock ligament, 298, 299
Hard palate, 23, 195, 215, 216, 244
development of, 23
glands of, 244, 245, 282
zones of, 244, 248
 
Hardness test, 50, 119
Harelip, 26
Haversian bone, 200, 201, 203, 205
Head of mandible, 324
 
embryonic, 14
Healin of fractures, 209
Heiden ain’s Azan stain, 346
Hematoxylin-eosin stain, 87, 346
Hemopoietic marrow, 202
Hereditary opalescent dentin, 47
 
type of hypocalcification, 99
Hertwig’s epithelial root sheath, 29, 37,
 
42, 43, 45, 46, 85, 129, 148, 155,
166, 186, 289, 298
Histiocytes, 141, 142, 146, 183, 330
Histodiflerentiation, 29, 30, 37, 46, 88
Histogenesis of salivary glands, 266
Histologic specimens, preparation of, 341
staining of, 346
 
Histology of enamel, 50
 
of eruption, 287
 
of maxillary sinus, 337
 
of saliva, 266
 
of temporomandibular joint, 325
358
 
Histophysiology of tooth development, 45
Hodgkin’s disease, 285
 
Home care, 79
 
Homogenization of Tomes ’ processes, 91
Hone, 344
 
Horizontal fibers, 179, 180
Hornification of gingiva, 217, 218, 225,
 
260
 
Howsllip’s lacunae, 182, 204, 205, 206
Hunter—Schreger bands, 59, 60, 61
Hutchinson ’s incisors, 48
 
Hyalin cartilage, 324, 326, 327
 
degeneration of pulp, 150
 
Hyoid arch, 15, 23
 
Hypercementosis, 168
 
Hyperplasia, 168, 169, 171
Hypersensitivity, 175
 
Hypertrophy, 168
 
Hypocalcification, fluoride, 98, 99
 
hereditary type of, 98, 99
systemic, 98, 99
Hypophysis, primordium of, 14
hyperfunction of, 209
 
I
 
Idiopathic cementum resorption, 172
Imbrication lines of von Ebner, 106
Pickerill, 64
 
Immature bone, 209
Impaction of teeth, 302, 318
Impregnation, 341
Incineration, 101
Incisal canal, 249
papilla, 215
Incisive canal, 28
papilla, 244, 245
suture, 195
Incremental lines in cementum, 161
in dentin, 106
of enamel, 61, 62
of Retzius, 61, 62, 64
pattern, 48, 61
Incubator, 344
Incus, 194
India ink, 345
Infectious parotitis, 284
Inferior nasal concha, 18, 20, 336
surface of the tongue, 251, 252, 253
Initiation of tooth development, 29, 30,
38, 42, 46
Inner enasrgel epithelium, 34, 36, 37, 46, 81,
 
Innervation of dentin, 114
Inter-alveolar arteries, 183
 
pressure, 301
Interarticular disc, 329
Intercalated ducts, 270, 272, 276, 277
Intercellular bridges, 83, 85, 121, 138, 212
 
spaces, 85, 212
 
secretory capillary, 268, 270, 273
 
substance, 101, 135, 158, 167
Interdental folds 223, 225
 
papilla, 216, 2233, 226
 
septum, 295, 318
Interglobular dentin, 110, 111, 112
Interlobnlar septum, 277, 278
Intermaxillary suture, 195
 
INDEX
 
Intermediate cementum, 166
 
plexus, 176, 177, 290
Internal reconstruction of bone, 205
Interodontoblastic nerve plexus, 114
Interprismatic substance, 55, 56, 89, 90,
 
92, 227
 
Interradicular septum, 179, 293, 311
 
space, 289
Interstitial growth, 327
 
lamellae, 200, 205
 
spaces, 190
 
tissue, 182, 183
 
of glands, 274
 
Intraalveolar septa, 200
Intramembranous ossification, 194
Irregular dentin, 47, 116, 117
Isopentane, 347
Isthmian glands, 281
Isthmus, 27 3
 
J
 
Jacobson’s organ, 247
Jaw, clefts, 26
 
K
 
Keratin, in enamel, 52, 66
 
Keratinous layer, 212, 217
Kerato-hyalin granules, 212
 
Kop1ik’s spots, 260
 
KorfE’s fibers, 121, 122, 123, 135, 137
Krause corpuscles, 221
 
L
 
Labial ufiistulae, 26
fren a 250
frenuluin, 22
glands, 266, 280, 281
sulcus, 23
Lacrimal glands, 284
Lacunae of cementum, 163
Lamella, dentinal part of,"67, 70, 71
fl;   
Lamina, bucco-glngival, 42
dentaI,4213,4267, 29, 31, 32, 34, 37, 38, 39,
dura, 20?:
propria, 211, 3:3, 215, 220, 244, 251, 252
successlona
vestibular, és, 34, 35, 39
Large salivary glands, 264-274
parotid, 264, 274, 275
sublingual, 264, 274-279
submaxillary, 264, 274-279
Lashley’s instrument, 264
Lagt1e‘1;:(:lede]r1;ca1 lamina, 39, 42, 81
lamina: 41
tubercle, 24
Eesser subléréguaélsglands, 279, 280, 281
eucemla
Leucocytés, 2434, 265
Liesegang’s rings, 123, 124
Life cycle of ameloblasts, 85
_sp_an of formative cells, 48
Llmltlng membrane, 135
INDEX
 
Linear calcification, 124
Lingual crypt, 255, 257
 
follicles, 255, 257
 
frenulum, 279
 
mucosa, 254
 
nerve, 254
 
tonsils, 255
Lining mucosa, 215, 247
Lip, 213, 214, 247, 250
 
development of, 23
 
furrow band, 33, 38, 42
 
lower, fistula of, 27
 
malformations of, 26
 
upper, 21, 22
 
tubercles, 22
 
Vermilion border of, 214
Longitudinal lamellae, 201
Loss of function, 190
Lugol’s iodine, 342
Lymph, dental, 115
 
follicles in tongue, 255
 
nodes, 145, 184, 244, 255, 257
 
submaxillary, 244
submental, 244
vessels in gingiva, 244
in periodontal membrane, 184
in pulp, 144, 145
 
Lymphatic wandering cells, 330
Lymphocytes, 185, 253, 266
Lymphoid tissue, 266
 
wandering cell, 141, 142
 
M
 
Macrophages, 142, 182, 203, 219, 220, 2'4
Macrostoma, 27
Malformations of the face, 26
Malformed teeth, 48
Major salivary glands, 264, 274
sublingual duct, 279
Ma.lassez’s epithelial rests, 42, 156, 185
Malleus, 194
Mallory stain, 103, 121, 345
Mandible, 195, 196, 197
development of, 194, 195, 197
Mandibular arch, 14, 19, 23, 266
development of, 17
articulation, 324-331
changes of, 331
condyle, 324, 325, 327
fossa, 324, 325, 327
growth, 18
ramus, 292
symphysis, 196, 197
Mantle dentin, 103
Margin of the gingiva, 223
Marginal gingiva, 223, 228, 259
zone of hard palate, 244, 245
Marrow spaces, 326
Massa sublingualis, 279
Massage of gingiva, 260
Masseter muscle, 276
Masticatory forces, 312, 317, 321
mucosa, 215, 216
muscles, 296, 312
 
stresses, 312 _
Maturation of enamel matrix, 89, 93, 95,
 
96
stage, 88
 
35.9
 
Mature pulp, 135
Maxilla, 27, 194, 333
development of, 194
Maxillary bone, 195
processes, 14, 15, 16, 17, 19
sinus, 333, 334, 335, 336, 338
accessory fossae 335
and lpulp infecétihn, 337, 339
deve opment o 333
epithelial lining of, 33s
floor of, 334, 335
function of, 337
histology of, 337
variation in size, 334
tuberosity, 202, 292
Measles, 260
Mechanism of eruption, 297
Mecke1’s cartilage, 19, 20, 34, 35, 40, 194,
195 197 288
Medial nasal prociess, 15, 16, 17
Median cleft 27
cysts, 28 ’
fissure, 28
groove, 17
palatme suture, 246
Meissner corpuscles, 221, 222
Melanin, 219
Melanoblasts, 219
Membrane. preformativa, 37, 121
Membranes, basement, 32, 37, 40, 82, 90,
121, 211
bucconasal, 17
meanness‘, 14
s
nasobuccal: 16
Mental ossicles, 196, 197
Merocrine type glands, 263
Mesenchymal cells, 206
undifferentiated, 141, 142, 145, 183
Mesenchyme 36
Mesial drift: 206, 300, 301
migration of teeth, 189, 206
Mesoderm 29 33
Metabolicfdisturbances, 110
Metal poisoning 260
Micro-chemical rieactions, 347
Micrognathism, 18
Micron, 344
Microscopic slides, preparation of, 341
technique, 341
Microtechnique, 341
Microtome, 343, 344
freezing 344 345
rotary, 344, 345
sliding, 344, 345
Middle ear, 24
meatus of nasal cavity, 333, 334
nasal concha, 336
Mikulicz’ disease, 284
syndrome, 285
Mineral salts, 89, 92, 204
Minor buccal glands, 280
sublingual glands,7252, 266, 280
Mitochondria 268 2 0
Mixed glands’, 267: 270
tumors, 285
Modeling resorption, 301
Molar glands, 280
360
 
Morphodiflerentiation, 29, 47
Morphogenesis, 89, 297
 
Morphogenetic pattern, 48
 
stage, 87
Morphologic structure of mucous mem-
brane, 211
 
Morphology of cementum, 149
of dentin, 102
 
Mottled enamel, 68, 99
Mounting, 341, 346
agents, 346
Mouth (see Oral cavity)
floor of, 250, 251, 252
Movements of teeth, 288, 289
Mucicarmin stain, 267, 270
Mucihematin, 270
Mucigen, 270
Mucin, 263, 267, 270, 279
Mucocele, 285
Mucogingival junction, 216, 223, 250, 253
Mucous alveolus, 277, 278
cells, 263, 267, 268, 269, 270
cysts 285
glands, 246, 253, 254, 270
membrane, 211
 
Multirooted teeth, 44, 45, 132, 172
Mumps, 284
 
Myeloid bone marrow, 327
Mylohyoid muscle, 279
Myoepithelial cell, 271, 273, 274
 
function of, 271
 
N
 
Nasal cavity, 19
 
groove, 15
 
meatus, 333
 
mucosa, 254
 
pit, 14, 15, 16
 
process, lateral, 15, 17
 
medial, 15, 17
 
septum, 18, 19, 20, 21, 335, 336
Nasmyth’s membrane, 66
Nasobuccal membrane, 16
Nasolacrimal duct, 15, 27
 
groove, 15
Nasomaxillary groove, 15
Nasopalatine duct, 21, 28, 246, 249
Neck of mandible, 325
Necrosis, 172, 204, 315
Necrotic tissue remnants, 315
Neonatal line, 62, 65, 66, 110
 
ring, 62, 65, 66
Nerve supply of glands, 274
Nerves, in dentin, 114, 115
 
in periodontal membrane, 184, 185
 
in pulp, 145
 
of gingiva, 244
N eumann ’s sheath, 106
Neuroepithelial cells, 258
Nitric acid, 342
Nitrocellulose, 344
Nitrogen, 263
Nonfunctioning teeth, 169
Nose, external, 18
Nostril, 16, 17
Notochord, 14
 
INDEX
 
Nuclear dyes, 346
Number of dentinal tubules, 105
Nutritional deficiencies, 302
 
O
 
Oblique facial cleft, 26, 27
 
fibers, 179, 180
Occlusal stress, 173
 
trauma, 190
Occlusion, 192, 242
Odontoblastic processes, 70, 103, 104, 127,
 
138, 175
 
plexus, 114
 
Odontoblasts, 36, 37, 42, 47, 86, 87, 101,
121, 135, 137, 138, 167
 
terminal branches of, 104, 106
 
variations, 139
Oil of cedarwood, 343
 
of cloves, 345
Olfactory organ, 247
 
pits, 14, 15
 
sac, 16
Ontogenesis, 297
Operculum of second branchial arch, 24,
 
25
Oral cavity, development of, 13, 197
glands of, 263
groove, 14
function of, 211
hygiene, 264
primitive, 17, 18, 81
proper, 213
 
epithelium, 32, 39, 289
 
mucosa, subdivisions of, 215
 
mucous membrane, 211
 
roof, 19, 21
 
vestibule, 42
 
development of, 23
 
Organic structures in enamel, 52
Organizing influence, 36, 37, 47
Organogenesis, 88
Orthodontic tooth movement, 192
 
treatment, 172, 192
Os incisivum, 195
Osmic acid, 271
Ossification, 194
Osteoblasts, 101, 176, 181, 182
Osteoclastic resorption, 312
Osteoclasts, 181, 182, 203, 20-1, 205, 206,
 
307, 308
 
Osteocytes, 101, 203, 204, 205
Osteodentin, 47
Osteoicl tissue, 204, 205
Oteoporosis, 208, 339
Ostium maxillare, 334
Outer enamel epithelium, 34, 35, 37, 40
Owen, contour lines of, 109
 
P
 
Palate cleft, 27
hard, 19, 23, 215, 244
development of, 22
primary, 15, 16, 17
development of, 16
primitive, 21
secondary, 19
development of, 19
soft, 21, 23, 253
INDEX
 
Palatine glands, 266, 269, 282
 
mucosa, 244, 245
 
nerves, 249
 
papilla, 22, 23, 215, 244, 245, 247
process, 18, 19, 20, 21, 23, 27, 195
 
development of, 18
 
raphe, 215, 244, 246
 
rugae, 23, 247
 
torus, 246
 
vessels, 246, 249
 
Pancreas, 260
Papilla, dental, 35, 36, 37, 38, 39, 40, 81,
83, 289
 
filiform, 254, 255
 
fungiform, 254, 255
 
incisive, 244, 246
 
interdental, 223, 226
 
palatine, 22
 
vallate, 25, 249, 255, 283
Papillary layer, 213
Paraflin, 343
Parakeratosis, 215, 217, 218
Parasynipathetic nerves, 274
Parathyroid gland, 24
Parietal layer, 146
Parotid duct, 276
 
glands, 264, 266, 267, 273, 275, 276
Parotitis infectious, 284
Pars glahra, 23
 
villosa, 23
Passive eruption, 23, 232, 233, 234, 236,
 
321
rate of, 232, 233, 234-, 235, 236, 237,
238, 243, 289
stages of, 232, 233, 234, 235, 236
 
Peg tooth, 48
Perforating canals, 201
Pericementum, 176
Pericytes, 144, 145
Perikaryon, odontoblastie, 115
Perikymata, 63, 64
Periodontal cyst, 192
diseases, 79, 152, 172
treatment of, 249
fibers, 37, 167
ligament, 176
membrane, 32, 36, 158, 167, 176, 177,
198, 206, 290, 301, 307. 315
and restorative dentistry, 191, 192
blood vessels of, 183
development of, 176
epithelial structures of, 184, 185, 186
fiber groups, 178, 179, 180, 181
function of, 176
structural elements of, 177
 
Permeability studies, 119
Pernicious anemia, 260
Petrotympanic fissure, 324
Phary-ngeal pouches, 23, 24
Pharynx, 19, 213
Phases of tooth movements, 297
Phlebolite, 149
Phosphatase, 85
Physiologic changes of, 187, 189
mesial drift, 296
movement of teeth, 189
width, 187
Pigment, 218, 219
 
361
 
Piriform aperture, 195
Plasma cells, 142, 244, 274
Plica flmbriata, 283
sublingualis, 266 280
Polarity of ameloblasts, 36, 87, 88
Polarized light, 66, 73, 75, 89, 97, 98, 111,
112, 113, 114, 349
Postmortem examination, 341
Postnatal dentin, 110
Potassium hydroxide, 342
Pouches, branchial, 23, 24
ectodermal, 14
pharyngeal, 23, 24
Rath.ke’s, 14
Precollagenous fibers, 121, 135, 156, 290
substance, 121
Predentin, 104, 121, 122
Pre-enamel, 92
rods, 81, 90
Pre-eruptive phase of tooth movement,
287, 289
Prefunctional phase of eruption, 287, 289,
290, 291, 292
 
Premaxilla, 26, 195
Prenatal dentin, 110
Prickle cell layer, 212, 217
Primary choana, 15, 16, 17, 18
enamel cuticle, 66, 67, 89, 227, 228, 241
nasal cavity, 18
oral groove, 14
palate, 15, 16, 17, 18, 19
formation of, 15
processes, development of, 18
pulp, 121, 134 _
Primitive oral cavity, 18
palate, 21
periodontal membrane, 290
Primordia of teeth, 31, 33
Principal fibers, 167, 177, 181, 182, 191,
198
 
Processes, facial, 13
frontal, 14, 195
frontonasal, 14
globular, 15
head, 13
maxillary, 14, 15, 16, 17, 19
nasal, lateral, 14, 15, 16, 17
medial, 15, 16
odontoblastic, 70, 103, 104, 127, 138
palatine, 19, 20, 27
Tomes’, 90, 91
vertical, 21
Proliferation in tooth development, 29, 33
Prophylactic treatment, 79
Prosencephalon, 13
Protective metamorphosis of dentin, 117
stage, 89
Protein content of enamel matrix, 95
Pseudo-alveolar ridge, 22, 23
Pseudopodia, 142
Pseudostratified ciliated columnar epithe-
lium, 337
Ptya].i.n, 263, 268, 279
Pulp, 84, 127
amputation, 152
anatomy of, 128
blood vessels of, 142, 143
calcifications, frequency of, 150
362
 
Pulp—-Cont’d |
 
capping, 152
 
chamber, 128, 129, 151
defense cells, 140, 141, 142
development of, 134
exposure, 151
 
fibrosis, 150
 
fibrous elements of, 135
function of, 127
 
horn, 120, 128, 151, 152
infection, 337
 
lymph vessels of, 144
necrosis, 152
 
nerves of, 145
 
primary, 121
 
primordium of, 36
 
regressive changes in, 148, 32]
stones, 128, 129, 147, 148, 149
 
frequency of, 150
 
structural elements of, 135
 
Q
Quantity of saliva, 264
 
R
 
Racemose glands, 283
Radioactive isotopes, 53
Ranula, 285
 
Raphe, 246
 
Rarefication, 208
 
Rate of passive eruption, 237
 
Rathke’s pouch, 14
 
Recessional of gingiva, 174, 237, 243
 
Reconstructive apposition, 307
 
Reduced enamel epithelium, 89, 227, 228,
242, 289
 
Referred pain, 339
Reflected light, 59, 60, 119, 349
Refractive index, 161
Regressive changes in pulp, 148
Remnant of deciduous teeth, 318
Repair, 174, 315
anatomical, 173
functional, 173, 174
of resorption, 172, 173, 174, 304
Repaired resorption, 172, 173, 174,
311, 313
 
Reparative apposition, 301
Resorption lacunae, 182
of bone, 295, 308
of cementum, 172, 173, 174
of root, 302, 304, 307, 308
Resting hnes, 200, 205
wandering cells, 142
 
Restorative dentistry, 191, 192, 259
Retained deciduous teeth, 321
fate of, 321
roots, 318
 
Retarded eruption, 302
Reticular fibers, 121, 135
layer, 213
Reticulo-endothelial system, 141, 142
Retromandibular fossa, 275
Retromolar area, 282
glands, 281
Retzius, incremental lines of, 61, 62, 64
 
304,
 
INDEX
 
Reversal lines, 200, 205, 207
 
of functional polarity, 87
Rhomboid glossitls, 26 _ _
Rhythm of enamel formation, 62, 63
Ridges, alveolar, 22, 40
 
epithelial, 213, 250
 
pseudo-alveolar, 22, 23
 
tectal, 18, 20, 21, 23
Rivinian ducts, 279
 
glands, 266, 279
Rods, enamel, 53, 54, 91
 
diameter of, 53
direction of, 58
length of, 53
number of, 53
 
in deciduous teeth, 58
 
pre-enamel, 90, 92
 
sheaths, 53, 54, 56, 92
Roentgen ray absorption test, 119, 120
 
rays, soft, Grenz ray, 119, 120
Root, 32
 
apex of, 43
 
canals, 129, 130, 131, 132, 133
 
accessory, 45
 
development, 42, 43
 
formation, 29, 42, 289
 
fracture, 173
 
resorption, 302, 304
 
sheath of I-Iertwig, 29, 37, 42, 43, 45
Rotary microtome, 345
Rouget’s cells, 144
Rugae, 247
 
Safranin, 346
Saliva, 263
antibacterial factor, 264
characteristics of, 264
chemical analysis, 264
function of, 263
histology of, 266
method of collection, 264
quantity of, 264
Salivary calculus, 284
caruncle, 280
corpuscles, 264, 266
ducts, 264
glands, 263
blood supply, 274
classification of, 267
congenital malformations, 285
duct elements, 273
function of, 263
functional activity, 269
gross features of, 267
histogenesis, 266
interstitial connective tissue in, 274
lymph supply of, 274
microscopic features of, 266
nerve supply of, 274
of major secretion, 274
of minor secretion, 280
pathologic disturbances of, 283
secretory cells of, 268
tubules, 273
Sarcoma, 285
Scalloped line, 250
Schreger-Hunter bands, 59, 60, 61
Sclerotic dentin, 117, 119, 120
INDEX
 
Sebaceous glands, 214, 250, 261
Second arch, 23, 24
Secondary dentin, 47, 116, 139, 150, 260
enamel cuticle, 66, 68, 228, 241
palate, 18, 19
development of, 18
suhmnxillary glands, 279
Secretory capillaries, 270, 271, 274
cells of salivary glands, 268
ducts, 272, 273
Sectioning, 344
Semilunar calcification of dentin, 112
hiatus, 334
Senile atrophy, 261
osteoporosis, 339
Sensitivity of dentin, 125, 260
Serial ground sections, 348
sections, 345
Serous cells, 263, 267, 270
Shadowed replica, 57, 63, 115
Sharpeygogbtgrsé 159, 161, 167, 191, 203,
‘ 4.
Sheath of Neumann, 106
Shedding of deciduous teeth, 307, 312, 315
repair during, 315
rest periods, 317
retarded, 317
role of pulp during, 317
Shift of 2§githoIial attachment, 232, 237,
Shortened teeth, 302, 322
Sialadenitis, 284
Sialism, 283
Sialodochitis, 284
Silver imzpreggation, 122, 135, 157, 161,
74 46
sinus, cervidal 24, 25, 2s
infection, 339
maxillary 333, 334, 336, 338
Sinusitis, 339
Skull, 194
Sliding microtome, 346
Sodium thiosulfate, 342
Soft palate, 21, 23, 27, 253, 282
development of, 23
glands of, 246, 282
Specialized mucosa, 215, 254
Spindles of enamel, 70, 71, 73
Spongy bone, 198, 200, 201, 208, 327
Squamotympanic fissure, 324
Stagger system, 87
Staining, 341, 346
Stapes, 194
Stellate rseeticulum, 35, 37, 40, 81, 82, 83,
Stenson’s duct, 276
Stippling, 223, 224, 225, 250
Stomatitis, 283
Stomatodeum, 14
Stratum corneum, 216, 217
germinativum, 212
intermedium, 37, 40, 81, 83, 85
lucidum, 213
Stresses, functional, 103
Striated ducts, 271, 272, 276, 277
Striations, transverse, 54, 55, 64
Strapping, 344
Structural elements of periodontal mem-
brane, 177
 
363
 
Structure of alveolar process, 198
of dentin, 114
of enamel, 53
Sublingual glands, 253, 264, 266, 268, 269,
278
mucosa, 251
sulcus, 247, 253
Submandibular gland, 279
Submaxillary duct, 279, 284
gland, 264, 266, 268, 272, 274, 275, 279
triangle, 279
Submerged tooth, 302, 322, 323
Submicroscopic crystals, 73, 74, 76
organic network, 74, 77
structure, 73, 111, 349
Submucosa, 211, 213, 215, 244, 247, 251
Subodontoblastic plexus, 114, 140, 146,
220, 221
region, 122
Successional lamina, 38
Sulcus buccalis, 266
lingualis, 266
Sulfocyanate, 266
Supernumerary teeth, 46
Supplemental maxillary sinuses, 337
Supporting bone, 198, 202, 208
cells, 256, 258
suppression, 46
Supramylohyoid submaxillary gland, 27 9
Suspensory ligament, 176
Sustentacular cells, 256, 258
Sutural growth, 209
Sweat glands, 214
Sympathetic nervous system, 145, 185, 271
Synchondrosis, 197
Syncytium, 271
Synovial fluid, 330
layer, 330
membrane, 330
villi, 330
Sytemic hypocalcification, 99
hypoplasia, 98
 
T
 
Taste buds, 254, 255, 256, 257, 258
organs, 211
pore, 256, 258
Technical remarks, 341
Tectal ridge, 18, 20, 21, 23
Tectolabial frenum, 22, 23
Teeth (see also Tooth)
bodily movement of, 287
chemical contents of, 52
congenitally missing, 318
deciduous, 33
development of, 29, 288
embedding of, 341
growth of, 29, 48
excentric, 288
histophysiology of, 45
Hutchinson’s, 48
mesial drift of, 301
physiologic movement of, 167, 189, 205
pulp infection in, 337
retained, 321
shedding of deciduous, 307, 312, 315
shortened, 302, 322
submerged, 293, 302, 322, 323
364
 
Tegmen oris, 21, 23
Temporal bone, 324, 328, 330
Temporomandibular joint, 324
pain in, 331
traumatic arthritis of, 331
ligament, 325, 330
Tensor palati muscle, 331
Terminal alveoli, 273
arborization, 140
bars, 85, 91, 93, 94, 95, 138
of ameloblasts, 85, 91, 94, 95
of odontoblasts, 138
branches of odontoblasts, 104, 106
sulcus, 25
Thrombosis, 149, 172, 315
Thymus, 24
Thyroglossal duct, 26, 254
Thyroid anlage, 26
gland, 26
Tinnitus 331
Tissue changes during tooth movements,
297
Tomes’ fibers, 103, 138
granular layer, 111, 113
processes, 90, 91
homogenization of, 91
Tongue, 19, 20, 21, 40, 215, 251, 253, 254
base of, 254
bifid, 26
development of, 23, 24, 25, 26
dorsal surface of, 254
glands of, 266, 267, 282, 283
inferior surface of, 251
papillae, of, 251
Tonsils, lingual, 255
palatine, 24
Tooth, anlage, 31
bud, 31, 33
crypt, 288, 292, 307
developmental stages of, 29
eruption, 232, 243, 298
active, 243, 289, 312, 322
chronology of, 303
life cycle of, 30
malformed, 48
mechanism of, 297
passive, 23, 232, 233, 243, 289, 312
peg, :18
theories on, 297
germ, 27, 36, 176, 197, 288
sac, 176
Transitional zone, 214
Translucency of enamel, 50
Transmitted light, 112, 119, 120, 121, 349
Transparent dentin, 117, 118, 119, 120
Transseptsl fibers, 178, 179
Transverse palatine ridges, 247
striations, 54, 55
Trauma,  190, 192, 244, 312, 315, 316,
Traumatic arthritis, 331
forces, 312
injuries, 317
lesions, 322
Traumatism, 192, 321
in deciduous teeth, 312, 313, 314, 315,
316, 317
 
INDEX
 
Trigeminal nerve, 254
 
True denticles, 147, 148
 
Tubercle of upper lip, 23
Tuberculum impar, 24, 25
 
Tuberosity, 202, 292
 
Tubules, dentinal, 105
Tubulo-alveolar terminal portion, 280
Tufts, 69
 
Tumors, dermoid, 46
 
Twinning, 46
 
U
 
Ultimo-branchial body, 24
Ultraterminal fibers, 221, 222
Ultraviolet fight technique, 349
Uncalcified cementum, 158, 162, 167, 300
Undiiferentiated mesenchymal cell, 141,
 
142 144, 145, 156, 132, 184, 203
Upper alveolar nerves, 339
Urea, 263, 265
Uvula, 19, 21, 26, 282
 
V
 
Vacuum dehydration, 347
 
Vallate papillae, 25, 254, 255, 257, 267
 
Velum palatinum, 254
 
Vermilion border, 214
 
Vertical eruption, 296, 300, 301
palatine processes, 19, 21
 
Vestibular fornix, 250, 260
lamina, 23, 34, 35, 39
mucosa, 260
 
Vestibule, 213
 
Vestibulum oris, 213
 
Virus infection, 284
 
Visceral part of skull, 194
 
Vital stains, 88, 154
 
Vitality of cementum, 163
of dentin, 115, 123, 124
 
Vitamin A deficiency, 47
D, 150, 302
 
V011 Ehner’s glands, 254, 257, 283
imbrication lines, 106
 
von Korif’s fibers, 121, 122, 123, 135, 137
 
W
 
Wandering cell, 141, 330
 
Weil’s zone, 140, 146
Wharton’s duct, 279 280
Width of dentinal tubules, 104
 
of periodontal membrane, 188
 
Wisdom tooth, 305
 
X
Xerostomia, 261, 283, 284
Xylol, 343
 
Z
 
Zenker-formol fixation, 342


Zone of calcification, 328
==Color Plates==
of Wefl, 140 146


Zygomatic arch, 275
* Development of the human fcve
process, 333
* Argyrophilie K01-fi"s fibers become transformeul into the collagenous ground substance of the dentin
* Reconstruction of the skull of a human embryo
* Salivary glands of major secretion


Zymogeu granules,


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Orban B. Oral Histology and Embryology (1944) The C.V. Mosby Company, St. Louis.

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Orban 1944: 1 Development of the Face and Oral Cavity | 2 Development and Growth of Teeth | 3 Enamel | 4 The Dentin | 5 Pulp | 6 Cementum | 7 Periodontal Membrane | 8 Maxilla and Mandible (Alveolar Process) | 9 The Oral Mucous Membrane | 10 Glands of the Oral Cavity | 11 Eruption Of The Teeth | 12 Shedding of the Deciduous Teeth | Temporomandibular Joint | The Maxillary Sinus | 15 Technical Remarks
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Pages where the terms "Historic" (textbooks, papers, people, recommendations) appear on this site, and sections within pages where this disclaimer appears, indicate that the content and scientific understanding are specific to the time of publication. This means that while some scientific descriptions are still accurate, the terminology and interpretation of the developmental mechanisms reflect the understanding at the time of original publication and those of the preceding periods, these terms, interpretations and recommendations may not reflect our current scientific understanding.     (More? Embryology History | Historic Embryology Papers)

Oral Histology and Embryology

Edited By

Balint Orban

Loyola University, School of Dentistry, Chicago, Illinois

Third Edition

With 263 Text Illustrations

Including 4 Color Plates

St. Louis

The C. V. Mosby Company

Copyright, 1944

Contributors

Myron S. Aisenberg, D.D-S.

Baltimore College of Dental Surgery University of Maryland Baltimore

Gerrit Bevelander, Ph.D.

College of Dentistry New York University New York

Leroy R. Boling, Ph.D.

School of Dentistry Washington University St. Louis

Samuel W. Chase A.B., A.M., Pl-i.D.

School of Dentistry Western Reserve University Cleveland

Harry E. Frisbie, D.D.S.

College of Dentistry University of California San Francisco

Donald A. Kerr, A.B., D.D.S., MS.

School of Dentistry University of Michigan Ann Arbor

Paul C. Kitchin, B.S., MC.Sc., D.D.S. College of Dentistry Ohio State University Columbus

Edgar B. Manley, M.Sc., B.D.S., F.D.S.R.C.S. (Eng.)

Department of Dental Pathology Medical School University of Birmingham Birmingham, England

Balint Orban, M.D., D-D.S.

School of Dentistry Loyola University Chicago

Hamilton B. G. Robinson, D.D.S., M.S,

College of Dentistry Ohio State University Columbus

Isaac Schour, D.D.S, M.S., Ph.D., D.Sc.

College of Dentistry University of lllinois Chicago

Harry Sicher, M.D., D.Sc.

School of Dentistry Loyola University Chicago

Reidar F. Sognnaes, D.M.D., Ph.D.

Harvard School of Dental Medicine Boston

B. O. A. Thomas, B.A., D.D.S., M.S., Ph.D.

School of Dentistry University of Washington Seattle

Joseph P. Weinmann, M.D.

College of Dentistry University of Illinois

Chicago

Contents

Preface To Third Edition

As we continue to revise this book. some of our practices are becoming traditions. one of which is changing a few contributors for each edition. Some of the contributors are changed because the)‘ have shifted their interest in research or teaching: some because they have retired or have given up teaching positions. It is a sad fact that some of our co-Workers have passed away. Gottlieb. Diamond. .\'uckolls have left us at a most regrettable time when their experiences in research as Well as in teaching would have aided us most.

“I have new men with us—new as contributors to this book, but well known as research men and teachers. We happily welcome them. The changes that have been made in this third edition are mainly due to their eiforts.

Many changes have been made in the chapter on "Enamel," with numerous new illustrations. The chapter on the “Glands of the Oral Cavity" was reduced and simplified, eliminating some of the rather cumbersome details. It was our aim in this revision to eliminate throughout the book statements that could be misinterpreted or cause some confusion. Twelve new illustrations, some of them composite. are replacing old ones We are grateful to our critics who have pointed out the weak spots in our text and invite all our students and their teachers to make suggestions which will improve this book. It is our hope that this material will remain a basic tool in creating better and better dentists.

Balint Orban

Chicago

Preface To First Edition

Oral histology and embryology have rapidly advanced during the last decade; an increase of detailed observations led to Widely divergent interpretations. In writing this book it was the task of the contributors to sift the material, coordinate different opinions, and present a. uniform and selected review of modern knowledge. It is hoped that the reader will realize that this presentation is in no way final but a basis for study and further investigation.

In compiling this text a new plan was adopted. The chapters were drafted by recognized authorities on the specific subject, and each author ’s manuscript was submitted to all other contributors for discussion. Some did not Write a chapter but aided the eflort considerably by their remarks and criticism. It was the task of the editor to coordinate the different viewpoints which were presented. Thus, the chapters had to be re-drafted several times, according to the suggestions made by the collaborators.

Whfle it is true that the co-workers cannot accept every detail presented in this book, the major difierences in concept were successively eliminated. We pooled our resources, selected the best illustrations from our material, and we believe that the result presents a sincere effort in scientific cooperation.

We are greatly indebted to Mr. P. M. Orlopp, research assistant and photographer of the Foundation for Dental Research, Chicago College of Dental Surgery, for his excellent work in preparing the photographic prints, and to Mrs. P. Slatter for her untiring and efficient secretarial work.

We hope that this textbook will be of help, not only to undergraduate students, but also to those who work for graduate degrees, and to the practicing dentist. Every chapter contains remarks on the clinical application of the basic biologic principles.

We dedicate this book to those who recognize that clinical procedure is based on the knowledge of normal structure.


Balint Orban

Chicago

Color Plates

  • Development of the human fcve
  • Argyrophilie K01-fi"s fibers become transformeul into the collagenous ground substance of the dentin
  • Reconstruction of the skull of a human embryo
  • Salivary glands of major secretion


Cite this page: Hill, M.A. (2024, May 3) Embryology Book - Oral Histology and Embryology (1944). Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Book_-_Oral_Histology_and_Embryology_(1944)

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