Palate Development

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Introduction

Human Embryo Face (Week 7, Carnegie stage 18, 44 - 48 days, CRL 13 - 17 mm)

The palate anatomically separates the nasal cavity from the oral cavity and structurally has a bony (hard) anterior component and a muscular (soft) posterior component ending with the uvula. The oral side of the palate is covered with a squamous stratified (pluristratified) epithelium. The surface of the hard palate of most mammalian species is further thrown into a series of transversal palatal ridges or rugae palatinae. Both the palatal ridge number and arrangement are also species specific.


Neural crest has a major contribution to the palate development and there are a number of molecular, mechanical and morphological steps in involving the fusion of contributing structures including a key epithelial to mesenchymal transition. In palate formation there are two main and separate times and events of development, during embryonic (primary palate) and an early fetal (secondary palate). This separation of events into embryonic and fetal period corresponds closely to the classification of associated palate abnormalities.


The primary palate is formed by two parts:

  1. maxillary components of the first pharyngeal arch (lateral)
  2. frontonasal prominence (midline)


The secondary palate can also be divided in two anatomical parts:

  1. anterior hard palate - ossified (contributions from the maxilla and palatine bones).
  2. posterior soft palate - muscular.


Palate Links: Palate Development | Cleft Lip and Palate | Cleft Palate | Head Development | Category:Palate


Head Links: Introduction | Medicine Lecture | Medicine Lab | Science Lecture | Science Lab | Craniofacial Seminar | Mouth | Palate | Tongue | Placodes | Skull Development | Head and Face Movies | Abnormalities | Category:Head
Historic Embryology  
1910 Skull | 1910 Skull Images | 1921 Human Brain Vascular | 1923 Head Subcutaneous Plexus | 1919 21mm Embryo Skull | 1920 Human Embryo Head Size | 1921 43 mm Fetal Skull | Historic Disclaimer

Some Recent Findings

Ultrasound - Cleft Lip
  • Regulation of the Epithelial Adhesion Molecule CEACAM1 Is Important for Palate Formation[1] "Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at various developmental stages before, during, and after palate fusion using GeneChip® microarrays. Ceacam1 was one of the highly up-regulated genes during palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was present in prefusion palatal epithelium and was degraded during fusion. ...These results suggest that CEACAM1 has roles in the initiation of palatal fusion via epithelial cell adhesion."
  • Role of GSK-3β in the Osteogenic Differentiation of Palatal Mesenchyme[2] "Here, we identify a critical role for GSK-3β in palatogenesis through its direct regulation of canonical Wnt signaling. These findings shed light on critical developmental pathways involved in palatogenesis and may lead to novel molecular targets to prevent cleft palate formation."
  • Ephrin reverse signaling controls palate fusion via a PI3 kinase-dependent mechanism [3] "Secondary palate fusion requires adhesion and epithelial-to-mesenchymal transition (EMT) of the epithelial layers on opposing palatal shelves. This EMT requires transforming growth factor β3 (TGFβ3), and its failure results in cleft palate. Ephrins, and their receptors, the Ephs, are responsible for migration, adhesion, and midline closure events throughout development. Ephrins can also act as signal-transducing receptors in these processes, with the Ephs serving as ligands (termed "reverse" signaling). We found that activation of ephrin reverse signaling in chicken palates induced fusion in the absence of TGFβ3, and that PI3K inhibition abrogated this effect. Further, blockage of reverse signaling inhibited TGFβ3-induced fusion in the chicken and natural fusion in the mouse. Thus, ephrin reverse signaling is necessary and sufficient to induce palate fusion independent of TGFβ3."
  • A genome-wide association study of cleft lip with and without cleft palate identifies risk variants near MAFB and ABCA4[4] "Case-parent trios were used in a genome-wide association study of cleft lip with and without cleft palate. SNPs near two genes not previously associated with cleft lip with and without cleft palate (MAFB, most significant SNP rs13041247, with odds ratio (OR) per minor allele = 0.704, 95% CI 0.635-0.778, P = 1.44 x 10(-11); and ABCA4, most significant SNP rs560426, with OR = 1.432, 95% CI 1.292-1.587, P = 5.01 x 10(-12)) and two previously identified regions (at chromosome 8q24 and IRF6) attained genome-wide significance."
  • A dosage-dependent role for Spry2 in growth and patterning during palate development[5] "The formation of the palate involves the coordinated outgrowth, elevation and midline fusion of bilateral shelves leading to the separation of the oral and nasal cavities. Reciprocal signaling between adjacent fields of epithelial and mesenchymal cells directs palatal shelf growth and morphogenesis. Loss of function mutations in genes encoding FGF ligands and receptors have demonstrated a critical role for FGF signaling in mediating these epithelial-mesenchymal interactions. The Sprouty family of genes encode modulators of FGF signaling. We have established that mice carrying a deletion that removes the FGF signaling antagonist Spry2 have cleft palate."
More recent papers
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This table shows an automated computer PubMed search using the listed sub-heading term.

  • Therefore the list of references do not reflect any editorial selection of material based on content or relevance.
  • References appear in this list based upon the date of the actual page viewing.

References listed on the rest of the content page and the associated discussion page (listed under the publication year sub-headings) do include some editorial selection based upon both relevance and availability.

Links: References | Discussion Page | Pubmed Most Recent | Journal Searches


Search term: Cleft Palate


Dave T Gerrard, Andrew A Berry, Rachel E Jennings, Karen Piper Hanley, Nicoletta Bobola, Neil A Hanley
An integrative transcriptomic atlas of organogenesis in human embryos.
Elife: 2016, 5;


Dionísia Aparecida Cusin Lamônica, Mariana Jales Felix da Silva-Mori, Camila da Costa Ribeiro, Luciana Paula Maximino
Receptive and expressive language performance in children with and without Cleft Lip and Palate. [Desempenho de linguagem receptiva e expressiva em crianças com e sem Fissura Labiopalatina.]
Codas: 2016;


J C Talmant, J C Talmant, J P Lumineau
[Secondary treatment of cleft lip and palate]. [Traitement secondaire des fentes labio-palatines.]
Ann Chir Plast Esthet: 2016;


Samuel Taylor-Alexander
Ethics in Numbers: Auditing Cleft Treatment in Mexico and Beyond.
Med Anthropol Q: 2016;


Araci Malagodi de Almeida, Terumi Okada Ozawa, Arthur César de Medeiros Alves, Guilherme Janson, José Roberto Pereira Lauris, Marilia Sayako Yatabe Ioshida, Daniela Gamba Garib
Slow versus rapid maxillary expansion in bilateral cleft lip and palate: a CBCT randomized clinical trial.
Clin Oral Investig: 2016;

Search term: Palate Embryology
Boris Groisman, Juan Gili, Lucas Giménez, Fernando Poletta, María Paz Bidondo, Pablo Barbero, Rosa Liascovich, Jorge López-Camelo
Geographic clusters of congenital anomalies in Argentina.
J Community Genet: 2016;


Mahmood Khaksary Mahabady, Mohammad Reza Gholami, Hossein Najafzadeh Varzi, Abolfazl Zendedel, Mona Doostizadeh
Protective effect of quercetin on skeletal and neural tube teratogenicity induced by cyclophosphamide in rat fetuses.
Vet Res Forum: 2016, 7(2);133-8


Adauê Oliveira, Cássia Amaral
Rapid Maxillary Expansion without Posterior Anchorage.
Int J Orthod Milwaukee: 2016, 27(1);73-6


Lucie Rochard, Stefanie D Monica, Irving T C Ling, Yawei Kong, Sara Roberson, Richard Harland, Marnie Halpern, Eric C Liao
Roles of Wnt pathway genes wls, wnt9a, wnt5b, frzb and gpc4 in regulating convergent-extension during zebrafish palate morphogenesis.
Development: 2016, 143(14);2541-7


Petra Celá, Marcela Buchtová, Iva Veselá, Kathy Fu, Jean-Philippe Bogardi, Yiping Song, Amanda Barlow, Paul Buxton, Jirina Medalová, Philippa Francis-West, Joy M Richman
BMP signaling regulates the fate of chondro-osteoprogenitor cells in facial mesenchyme in a stage-specific manner.
Dev. Dyn.: 2016, 245(9);947-62

Textbooks

Pharyngeal arch cartilages.jpg
  • The Developing Human: Clinically Oriented Embryology (8th Edition) by Keith L. Moore and T.V.N Persaud - Moore & Persaud Chapter Chapter 10 The Pharyngeal Apparatus pp201 - 240.
  • Larsen’s Human Embryology by GC. Schoenwolf, SB. Bleyl, PR. Brauer and PH. Francis-West - Chapter 12 Development of the Head, the Neck, the Eyes, and the Ears pp349 - 418.

Movies

Face 001 icon.jpg
 ‎‎Face Development
Page | Play
Palate 001 icon.jpg
 ‎‎Palate (oral view)
Page | Play
Palate 002 icon.jpg
 ‎‎Palate (front view)
Page | Play
Tongue 001 icon.jpg
 ‎‎Tongue
Page | Play
Fetal week 10 palate icon.jpg
 ‎‎Fetal Palate
Page | Play
Cleft lip 02.jpg
 ‎‎Cleft Lip 15 Week
Page | Play
Cleft lip 01.jpg
 ‎‎Cleft Lip 18 Week
Page | Play


Links: Movies | Ultrasound

Development Overview

  • week 4 - pharyngeal arch formation, first pharngeal arch contributes mandible and maxilla.
  • week 6 - 7 - primary palate formation maxillary processes and frontonasal prominence.
  • week 9 - secondary palate shelves fuse, separating oral and nasal cavities.

Embryonic Period

  • (week 4) - pharyngeal arch formation in rostrocaudal sequence (1, 2, 3, 4 and 6)
  • First pharyngeal arch - upper maxillary (pair) and lower mandibular prominences
  • Late embryonic period - maxillary prominences fuse with frontonasal prominence forming upper jaw (maxilla and upper lip)


Fetal Period

  • palatal shelves elevation
  • palatal shelves midline fusion
Fetal week 10 palate icon.jpg
 ‎‎Fetal Palate
Page | Play

Pharyngeal Arch Development

Major features to identify for each: arch, pouch, groove and membrane. Contribute to the formation of head and neck and in the human appear at the 4th week. The first arch contributes the majority of upper and lower jaw structures.

  • Pharynx - begins at the buccopharyngeal membrane (oral membrane), apposition of ectoderm with endoderm (no mesoderm between).

Pharyngeal arch structure cartoon.gifStage13 pharyngeal arch excerpts.gif

  • branchial arch (Gk. branchia= gill)
  • arch consists of all 3 trilaminar embryo layers
  • ectoderm- outside
  • mesoderm- core of mesenchyme
  • endoderm- inside

Neural Crest

  • Mesenchyme invaded by neural crest generating connective tissue components
  • cartilage, bone, ligaments
  • arises from midbrain and hindbrain region

Face Development

Stage16-18 face animation.gif

Begins week 4 centered around stomodeum, external depression at oral membrane

5 initial primordia from neural crest mesenchyme

  • single frontonasal prominence (FNP) - forms forehead, nose dorsum and apex
  • nasal placodes develop later bilateral, pushed medially
  • paired maxillary prominences - form upper cheek and upper lip
  • paired mandibular prominences - lower cheek, chin and lower lip

Frontonasal Process

The frontonasal process (FNP) forms the majority of the superior part of the early face primordia. It later fuses with the maxillary component of the first pharyngeal arch to form the upper jaw. Failure of this fusion event during the embryonic period leads to cleft lip. Under the surface ectoderm the process mesenchyme consists of two cell populations; neural crest cells, forming the connective tissues; and the mesoderm forming the endothelium of the vascular network.

A chicken developmental model study has identified a specific surface region, the Frontonasal Ectodermal Zone (FEZ), initially induced by bone morphogenetic proteins that appears to regulate the future growth and patterning of the frontonasal process. The specific frontonasal ectodermal zone was located in the frontonasal process ectoderm flanking a boundary between Sonic hedgehog (Shh) and Fibroblast growth factor 8 (Fgf8) expression domains.[6]

Embryonic Palate

Human primary palate

  • develops between embryonic stages 15 and 18.[7]
  • fusion in the human embryo between stage 17 and 18, from an epithelial seam to the mesenchymal bridge.
Stage17-18 Primary palate.gif


EM Links: Image - stage 16 | Image - stage 17 | Image - stage 18 | Image - stage 19 | Palate Development

Fetal Palate

Secondary palate, fusion in the human embryo in week 9. This requires the early palatal shelves growth, elevation, and fusion. There are many fusion events occurring during this period between each palatal shelf, to the primary palate, and also to the nasal septum.

palatal shelf elevation | secondary palate

Fetal palate growth graph.

Fetal Palate Growth (second trimester)[8]

Bailey141.jpg

Ventral aspect of hard palate of human embryo of 80 mm

Soft Palate

The soft palate mechanism of closure has not yet been determined, with several existing theories. A recent study[9] of embryos from the late embryonic-early fetal period (54 to 74 days post-conception) has identified the timing of soft palate closure.

  • 57 days - Late embryonic (Carnegie stage 23), epithelial seam present throughout the soft palate
  • 64 days - Early fetal (Week 9), epithelium only persists in the most posterior regions of the soft palate


Head Growth

  • continues postnatally - fontanelle allow head distortion on birth and early growth
  • bone plates remain unfused to allow growth, puberty growth of face


Animal Palate

Mouse Palate

  • E11 - protrude from bilateral maxillary processes
  • E12.5 - secondary palatal development begins
  • E12.5-E14 - grow vertically along the developing tongue
  • E14.5 - they elevate, meet, and fuse at the midline, to form an intact palate shelf, reflex opening and closing movements of the mouth
  • E15.5 - palatal fusion is complete, mesenchymal condensation followed by osteogenic differentiation occurs.

Mouse palate gene expression 01.jpg

Mouse (E13.5) Palatal Shelf Wnt5a, Osr2 and Pax9 Expression.[10]

Mouse ruga pattern.jpg Mouse - Spry1 cleft palate.jpg
Mouse ruga pattern (E16) Mouse - Spry1 cleft palate
Links: Mouse Development | Bone Morphogenetic Protein | Wnt | Pax

Dog Palate

Dog day0-cleft palate.jpg

Newborn dog with cleft palate

Molecular


Links: Bone Morphogenetic Protein

Abnormalities

Note there are specific pages for both Cleft Lip and Palate and Cleft Palate.

Clinical Images

Cleft Lip/Palate

Cleft Palate

Cleft Palate - Australia (1981-1992)[11]

The way in which the upper jaw forms from fusion of the smaller upper prominence of the first pharyngeal arch leads to a common congenital defect in this region called "clefting", which may involve either the upper lip, the palate or both structures.

Australian Palate Abnormalities (2002-2003)
Cleft lip with or without cleft palate (9.2 per 10,000 births) ICD-10 Q36.0, Q36.1, Q36.9, Q37.0–Q37.5, Q37.8, Q37.9
A congenital anomaly characterised by a partial or complete clefting of the upper lip, with or without clefting of the alveolar ridge or the hard palate. Excludes a midline cleft of the upper or lower lip and an oblique facial fissure (going towards the eye).
  • 17% of the affected pregnancies were terminated in early pregnancy or resulted in fetal deaths. Most of the fetal deaths or terminations of pregnancy (95%) had multiple abnormalities.
  • more commonly seen in males than in females.
  • babies born before 25 weeks of gestation, 150 per 10,000 births had this anomaly. Most babies (80.0%) were born at term with a birthweight of 2,500 grams or more.
  • Maternal age group was not associated with the anomaly.
  • Rates significantly higher among Indigenous women than non Indigenous women.
Cleft palate without cleft lip (8.1 per 10,000 births) ICD-10 Q35.0–Q35.9
A congenital anomaly characterised by a closure defect of the hard and/or soft palate behind the foramen incisivum without a cleft lip. This anomaly includes sub-mucous cleft palate, but excludes cleft palate with a cleft lip, a functional short palate and high narrow palate.
  • overall rate has increased to 9.1 when the rate was estimated using data from the four states that include TOP data. The reported number of fetal deaths or early terminations of pregnancy with this anomaly was small and these deaths or terminations could be due to other associated anomalies.
  • proportion of females with this anomaly was higher (56.9%) than males.
  • 52.7 per 10,000 babies born before 25 weeks of gestation.
  • 83.0% were born at term and most of the babies (82.7%) had a birthweight of 2,500 grams or more.
  • Women aged 40 years or older and women born in South Central America or the Caribbean region had the highest rates of affected births.
  • Multiple births had a significantly higher rate of affected babies than singleton births.
  • Rates did not differ significantly by Indigenous status or areas of residence.
Links: Palate Development | Head Development | Gastrointestinal Tract - Abnormalities | ICD-10 GIT | Australian Statistics
Reference: Abeywardana S & Sullivan EA 2008. Congenital Anomalies in Australia 2002-2003. Birth anomalies series no. 3 Cat. no. PER 41. Sydney: AIHW National Perinatal Statistics Unit.
Global Orofacial Cleft Rate (1950 - 2015)
This data is from a study of the published data (1950 - 2015)[12]
Continent Orofacial cleft rate /1,000 live births (95% confidence interval)
Asia 1.57 (1.54-1.60)
North America 1.56 (1.53-1.59)
Europe 1.55 (1.52-1.58)
Oceania 1.33 (1.30-1.36)
0.99 (0.96-1.02)
Africa 0.57 (0.54-0.60)
  • American Indians 2.62 per 1,000 live births (highest prevalence rates)
  • Japanese 1.73
  • Chinese 1.56
  • Whites 1.55
  • Blacks 0.58 (lowest prevalence rates)


International Classification of Diseases - Cleft Palate

Cleft lip and cleft palate (Q35-Q37)

Use additional code (Q30.2), if desired, to identify associated malformations of the nose. Excludes Robin's syndrome ( Q87.0 )


Q37 Cleft palate with cleft lip
Q37.0 Cleft hard palate with bilateral cleft lip
Q37.1 Cleft hard palate with unilateral cleft lip
Cleft hard palate with cleft lip NOS
Q37.2 Cleft soft palate with bilateral cleft lip
Q37.3 Cleft soft palate with unilateral cleft lip
Cleft soft palate with cleft lip NOS
Q37.4 Cleft hard and soft palate with bilateral cleft lip
Q37.5 Cleft hard and soft palate with unilateral cleft lip
Cleft hard and soft palate with cleft lip NOS
Q37.8 Unspecified cleft palate with bilateral cleft lip
Q37.9 Unspecified cleft palate with unilateral cleft lip
Cleft palate with cleft lip NOS

Embryonic Human Cleft Palate

Stage16 cleft palate.jpg
Stage16 (ventral view)

Cleft Lip

Bilateral cleft palate
  • International Classification of Diseases code 749.1 for isolated cleft lip and 749.2 for cleft lip with cleft palate.
  • Australian national rate (1982-1992) 8.1 - 9.9 /10,000 births.
  • Of 2,465 infants 6.2% were stillborn and 7.8% liveborn died during neonatal period.
  • rate similar in singleton and twin births.

Cleft Palate

An 8 month old infant with an extensive cleft palate associated with Bamforth- Lazarus syndrome.[14]
Cleft palate
  • International Classification of Diseases code 749.0
  • Australian national rate (1982-1992) 4.8 - 6 /10,000 births.
  • Of 1,530 infants 5.5% were stillborn and 11.5% liveborn died during neonatal period.
  • slightly more common in twin births than singleton.

(Data: Congenital Malformations Australia 1981-1992 P. Lancaster and E. Pedisich ISSN 1321-8352)




Links: Development Animation - Palate 1 | Development Animation - Palate 2 | OMIM Orofacial Cleft with or without cleft palate

Search Pubmed Now: cleft lip | cleft palate

Cleft Risk Variants

Two genes were identified from a recent genome-wide study.[4]

  • MAFB is expressed in the mouse palatal shelf.
  • ABCA4 is a member of a superfamily of transmembrane proteins, and mutations in ABCA4 play a major role in the etiology of Stargardt disease and related retinopathies. Gene produces an ATP-binding cassette (ABC) superfamily trans-membrane protein


Links: OMIM - MAFB | OMIM - ABCA4


Ten most frequently reported Birth Anomalies

  1. Hypospadias (More? Development Animation - Genital Male External | Genital Abnormalities - Hypospadia)
  2. Obstructive Defects of the Renal Pelvis (More? Renal System - Abnormalities)
  3. Ventricular Septal Defect (More? Cardiovascular Abnormalities - Ventricular Septal Defect)
  4. Congenital Dislocated Hip (More? Musculoskelal Abnormalities - Congenital Dislocation of the Hip (CDH))
  5. Trisomy 21 or Down syndrome - (More? Trisomy 21)
  6. Hydrocephalus (More? Hydrocephalus)
  7. Cleft Palate (More? Palate_Development)
  8. Trisomy 18 or Edward Syndrome - multiple abnormalities of the heart, diaphragm, lungs, kidneys, ureters and palate 86% discontinued (More? (More? Trisomy 18)
  9. Renal Agenesis/Dysgenesis - reduction in neonatal death and stillbirth since 1993 may be due to the more severe cases being identified in utero and being represented amongst the increased proportion of terminations (approximately 31%). (More? Renal System - Abnormalities)
  10. Cleft Lip and Palate - occur with another defect in 33.7% of cases.(More? Palate Development | Head Development)

(From the Victorian Perinatal Data Collection Unit in the Australian state of Victoria between 2003-2004)

Folate

A recent study of periconceptional folate supplementation using the Cochrane Pregnancy and Childbirth Group's Trials Register (July 2010) identified no statistically significant evidence of any effects on prevention of cleft palate and cleft lip at birth.[15]

References


  1. Junko Mima, Aya Koshino, Kyoko Oka, Hitoshi Uchida, Yohki Hieda, Kanji Nohara, Mikihiko Kogo, Yang Chai, Takayoshi Sakai
    Regulation of the epithelial adhesion molecule CEACAM1 is important for palate formation.
    PLoS ONE: 2013, 8(4);e61653

    | PLoS One.


  2. Emily R Nelson, Benjamin Levi, Michael Sorkin, Aaron W James, Karen J Liu, Natalina Quarto, Michael T Longaker
    Role of GSK-3β in the osteogenic differentiation of palatal mesenchyme.
    PLoS ONE: 2011, 6(10);e25847

    | PLoS One.


  3. Symone San Miguel, Maria J Serrano, Ashneet Sachar, Mark Henkemeyer, Kathy K H Svoboda, M Douglas Benson
    Ephrin reverse signaling controls palate fusion via a PI3 kinase-dependent mechanism.
    Dev. Dyn.: 2011, 240(2);357-64

  4. 4.0 4.1
    Terri H Beaty, Jeffrey C Murray, Mary L Marazita, Ronald G Munger, Ingo Ruczinski, Jacqueline B Hetmanski, Kung Yee Liang, Tao Wu, Tanda Murray, M Daniele Fallin, Richard A Redett, Gerald Raymond, Holger Schwender, Sheng-Chih Jin, Margaret E Cooper, Martine Dunnwald, Maria A Mansilla, Elizabeth Leslie, Stephen Bullard, Andrew C Lidral, Lina M Moreno, Renato Menezes, Alexandre R Vieira, Aline Petrin, Allen J Wilcox, Rolv T Lie, Ethylin W Jabs, Yah Huei Wu-Chou, Philip K Chen, Hong Wang, Xiaoqian Ye, Shangzhi Huang, Vincent Yeow, Samuel S Chong, Sun Ha Jee, Bing Shi, Kaare Christensen, Mads Melbye, Kimberly F Doheny, Elizabeth W Pugh, Hua Ling, Eduardo E Castilla, Andrew E Czeizel, Lian Ma, L Leigh Field, Lawrence Brody, Faith Pangilinan, James L Mills, Anne M Molloy, Peadar N Kirke, John M Scott, James M Scott, Mauricio Arcos-Burgos, Alan F Scott
    A genome-wide association study of cleft lip with and without cleft palate identifies risk variants near MAFB and ABCA4.
    Nat. Genet.: 2010, 42(6);525-9


  5. Ian C Welsh, Aaron Hagge-Greenberg, Timothy P O'Brien
    A dosage-dependent role for Spry2 in growth and patterning during palate development.
    Mech. Dev.: 2007, 124(9-10);746-61


  6. Silvia Foppiano, Diane Hu, Ralph S Marcucio
    Signaling by bone morphogenetic proteins directs formation of an ectodermal signaling center that regulates craniofacial development.
    Dev. Biol.: 2007, 312(1);103-14


  7. V M Diewert, S Lozanoff
    A morphometric analysis of human embryonic craniofacial growth in the median plane during primary palate formation.
    J. Craniofac. Genet. Dev. Biol.: 1993, 13(3);147-61


  8. A R BURDI
    SAGITTAL GROWTH OF THE NASOMAXILLARY COMPLEX DURING THE SECOND TRIMESTER OF HUMAN PRENATAL DEVELOPMENT.
    J. Dent. Res.: 1965, 44;112-25


  9. Adrian Danescu, Melanie Mattson, Carly Dool, Virginia M Diewert, Joy M Richman
    Analysis of human soft palate morphogenesis supports regional regulation of palatal fusion.
    J. Anat.: 2015, 227(4);474-86


  10. Asma Almaidhan, Jeffry Cesario, Andre Landin Malt, Yangu Zhao, Neeti Sharma, Veronica Choi, Juhee Jeong
    Neural crest-specific deletion of Ldb1 leads to cleft secondary palate with impaired palatal shelf elevation.
    BMC Dev. Biol.: 2014, 14;3

    | BMC Dev Biol.

  11. P. Lancaster and E. Pedisich, Congenital Malformations Australia 1981-1992, ISSN 1321-835.

  12. Vipawee Panamonta, Suteera Pradubwong, Manat Panamonta, Bowornsilp Chowchuen
    Global Birth Prevalence of Orofacial Clefts: A Systematic Review.
    J Med Assoc Thai: 2015, 98 Suppl 7;S11-21

  13. 13.0 13.1
    Michael J Dixon, Mary L Marazita, Terri H Beaty, Jeffrey C Murray
    Cleft lip and palate: understanding genetic and environmental influences.
    Nat. Rev. Genet.: 2011, 12(3);167-78


  14. Maynika V Rastogi, Stephen H LaFranchi
    Congenital hypothyroidism.
    Orphanet J Rare Dis: 2010, 5;17

    | Orphanet J Rare Dis.


  15. Luz Maria De-Regil, Ana C Fernández-Gaxiola, Therese Dowswell, Juan Pablo Peña-Rosas
    Effects and safety of periconceptional folate supplementation for preventing birth defects.
    Cochrane Database Syst Rev: 2010, (10);CD007950


Journals

Reviews

Indian J Plast Surg. 2009 October; 42(Suppl):Cleft Lip and Palate Issue


Jeffrey O Bush, Rulang Jiang
Palatogenesis: morphogenetic and molecular mechanisms of secondary palate development.
Development: 2012, 139(2);231-43


L Meng, Z Bian, R Torensma, J W Von den Hoff
Biological mechanisms in palatogenesis and cleft palate.
J. Dent. Res.: 2009, 88(1);22-33


Marek Dudas, Wai-Yee Li, Jieun Kim, Alex Yang, Vesa Kaartinen
Palatal fusion - where do the midline cells go? A review on cleft palate, a major human birth defect.
Acta Histochem.: 2007, 109(1);1-14


M W Ferguson
Palate development.
Development: 1988, 103 Suppl;41-60


E D Hay
An overview of epithelio-mesenchymal transformation.
Acta Anat (Basel): 1995, 154(1);8-20

Articles


Gerd Steding, Yutao Jian
The origin and early development of the nasal septum in human embryos.
Ann. Anat.: 2010, 192(2);82-5


Wei Xiong, Fenglei He, Yuka Morikawa, Xueyan Yu, Zunyi Zhang, Yu Lan, Rulang Jiang, Peter Cserjesi, Yiping Chen
Hand2 is required in the epithelium for palatogenesis in mice.
Dev. Biol.: 2009, 330(1);131-41

Search PubMed

Search Pubmed: palate development | cleft palate development |

Additional Images

Historic

Terms

Palate Development (expand to see terms)  
  • cleft - An anatomical gap or space occuring in abnormal development in or between structures. Most commonly associated with cleft lip and cleft palate. Term is also used to describe the external groove that forms between each pharyngeal arch during their formation.
  • cleft lip - An abnormality of face development leading to an opening in the upper lip. Clefting of the lip and or palate occurs with 300+ different abnormalities. Depending on many factors, this cleft may extend further into the oral cavity leading to a cleft palate. In most cases clefting of the lip and palate can be repaired by surgery.
  • cleft palate - An abnormality of face development leading to an opening in the palate, the roof of the oral cavity between the mouth and the nose. Clefting of the lip and or palate occurs with 300+ different abnormalities. In most cases clefting of the lip and palate can be repaired by surgery. Palate formation in the embryo occurs at two distinct times and developmental processes called primary and secondary palate formation. This leads to different forms (classifications) and degrees of clefting.
  • epithelial mesenchymal transition - (EMT, epitheliomesenchymal transformation) conversion of an epithelium into a mesenchymal (connective tissue) cellular organization.
  • epitheliomesenchymal transformation - (epithelial mesenchymal transition) conversion of an epithelium into a mesenchymal (connective tissue) cellular organization.
  • medial edge epithelial - (MEE) opposing palatal shelves adhere to each other to form this epithelial seam.
  • palate - The roof of the mouth (oral cavity) a structure which separates the oral from the nasal cavity. Develops as two lateral palatal shelves which grow and fuse in the midline. Initally a primary palate forms with fusion of the maxillary processes with the nasal processes in early face formation. Later the secondary palate forms the anterior hard palate which will ossify and separate the oral and nasal cavities. The posterior part of the palate is called the soft palate (velum, muscular palate) and contains no bone. Abnormalities of palatal shelf fusion can lead to cleft palate.
  • palatogenesis - The process of palate formation, divided into primary and secondary palate development
  • pharyngeal arch - (branchial arch, Greek, branchial = gill) These are a series of externally visible anterior tissue bands lying under the early brain that give rise to the structures of the head and neck. In humans, five arches form (1,2,3,4 and 6) but only four are externally visible on the embryo. Each arch has initially identical structures: an internal endodermal pouch, a mesenchymal (mesoderm and neural crest) core, a membrane (endoderm and ectoderm) and external cleft (ectoderm). Each arch mesenchymal core also contains similar components: blood vessel, nerve, muscular, cartilage. Each arch though initially formed from similar components will differentiate to form different head and neck structures.
  • philtrum - (infranasal depression, Greek, philtron = "to love" or "to kiss") Anatomically the surface midline vertical groove in the upper lip. Embryonically formed by the fusion of the frontonasal prominence (FNP) with the two maxillary processes of the first pharyngeal arch. Cleft palate (primary palate) occurs if these three regions fail to fuse during development. Fetal alcohol syndrome is also indicated by flatness and extension of this upper lip region.
  • T-box 22 - (TBX22) a transcription factor that cause X-linked cleft palate and ankyloglossia in humans. Tbx22 is induced by fibroblast growth factor 8 (FGF8) in the early face while bone morphogenic protein 4 (BMP4) represses and therefore restricts its expression. (More? OMIM - TBX22)
  • Transforming Growth Factor-beta - (TGFβ) factors induces both epithelial mesenchymal transition and/or apoptosis during palatal medial edge seam disintegration.
  • uvula - (Latin = a little grape) a pendulous posterior end of soft palate used to produce guttural consonants. First named in 1695.
  • Van der Woude syndrome - common syndromic cause of clefting (2% of cleft lip and palates). Van der Woude syndrome 1 1q32.2 Van der Woude syndrome 2 1p36.11
  • velopharyngeal insufficiency - (VPI) associated with cleft palate repair, describes the velum and lateral and posterior pharyngeal walls failing to separate the oral cavity from the nasal cavity during speech.
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Cite this page: Hill, M.A. (2016) Embryology Palate Development. Retrieved August 27, 2016, from https://embryology.med.unsw.edu.au/embryology/index.php/Palate_Development

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© Dr Mark Hill 2016, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G