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

Online Editor

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

Oral Histology and Embryology

Oral Histology And Embryology

Oralihstology Am)

Embryology

Edited By

Balint Orban

Loyola University, School of Dentistry, Chicago, Illinois

THIRD EDITION

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

ST. LOUIS

second Edition Reprinted June. 1950

Printed in the United States or America

Press of The C. 7. Mosby Company St. Louie 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, l\v£.Sc., B.D.S., F.D.S.R.C.S. (Eng.)

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

Balint Orban, l\l.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., l\rI.S., Ph.D.

School of Dentistry University of Washington Seattle

Joseph P. Weinmann, M.D.

College of Dentistry University of Illinois

Chicago

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.

“'9 have new men with us—neW as contributors to this book, but well known as research men and teachers. \Ve 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 C‘avit)"" was reduced and simpliﬁed, eliminating some of the rather cumber- some 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-

\\'e 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 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 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 pre- sented 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 appli- 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. BALINT ORBAN Chicago CONTENTS

CHAPTER I

DEVELOPMENT or THE FACE AND ORAL Cavxrr _

Introduction. 13; Development of the Face. 13: Development of the Sec- 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.”

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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 -

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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

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

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n./.,r...1...,. my ;. denlirjl

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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

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Irregular dentin

~ 1 in A” . Demarcation line

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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

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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._.

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

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. 286

10. 1 1. 12. 13. 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. Research 18: 214, 1939.

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 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

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 of Weﬂ, 140 146

Zygomatic arch, 275 process, 333

Zymogeu granules,

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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