Palate Development

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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 | 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

Search term: Cleft Palate

Ningbei Yin, Tao Song, Jiajun Wu, Bo Chen, Hengyuan Ma, Zhenmin Zhao, Yongqian Wang, Haidong Li, Di Wu Unilateral Microform Cleft Lip Repair: Application of Muscle Tension Line Group Theory. J Craniofac Surg: 2015; PMID: 25723667 Philip M Kluin, Anton W Langerak, Jannetta Beverdam-Vincent, Willemina Rr Geurts-Giele, Lydia Visser, Bea Rutgers, Ed Schuuring, Joop Van Baarlen, King H Lam, Kees Seldenrijk, Robby E Kibbelaar, Peter de Wit, Arjan Diepstra, Stefano Rosati, Max M van Noesel, C Michel Zwaan, Jarmo Cb Hunting, Mels Hoogendoorn, Ellen J van der Gaag, Joost W J van Esser, Eveline de Bont, Hanneke C Kluin-Nelemans, Rik H Winter, Jerome R Lo Ten Foe, Adri Gm van der Zanden Paediatric nodal marginal zone B cell lymphadenopathy of the neck: a Haemophilus influenzae driven immune disorder? J. Pathol.: 2015; PMID: 25722108 Hilda Razzaghi, April Dawson, Scott D Grosse, Alexander C Allori, Russell S Kirby, Richard S Olney, Jane Correia, Cynthia H Cassell Factors associated with high hospital resource use in a population-based study of children with orofacial clefts. Birth Defects Res. Part A Clin. Mol. Teratol.: 2015, 103(2);127-43 PMID: 25721952 Deepa Aggarwal, Barbara Warmerdam, Katrina Wyatt, Shabbir Ahmad, Gary M Shaw Prevalence of birth defects among American-Indian births in California, 1983-2010. Birth Defects Res. Part A Clin. Mol. Teratol.: 2015, 103(2);105-10 PMID: 25721951 C S Loozen, W Maarse, G T R Manten, L Pistorius, C C Breugem The accuracy of prenatal ultrasound in determining the type of orofacial cleft. Prenat. Diagn.: 2015; PMID: 25721357

Search term: Palate Embryology

Satoshi Kokai, Eiji Fukuyama, Yutaka Sato, Jui-Chin Hsu, Yuzo Takahashi, Kiyoshi Harada, Takashi Ono Comprehensive treatment approach for bilateral cleft lip and palate in an adult with premaxillary osteotomy, tooth autotransplantation, and 2-jaw surgery. Am J Orthod Dentofacial Orthop: 2015, 147(1);114-26 PMID: 25533078

[Early morphogenesis of ciliated cells in human oral cavity]. Ontogenez: 2014, 44(6);389-95 PMID: 25438588

Hao Sun, Yi Wang, Chaofan Sun, Qingsong Ye, Weiwei Dai, Xiuying Wang, Qingchao Xu, Sisi Pan, Rongdang Hu Root morphology and development of labial inversely impacted maxillary central incisors in the mixed dentition: A retrospective cone-beam computed tomography study. Am J Orthod Dentofacial Orthop: 2014, 146(6);709-16 PMID: 25432251 Jasmien Roosenboom, Peter W Hellings, Valerie A Picavet, Emmanuel P Prokopakis, Yasmine Antonis, Joseph Schoenaers, Vincent Vander Poorten, Peter Claes, Greet Hens Secondary Cleft Rhinoplasty: Impact on Self-Esteem and Quality of Life. Plast. Reconstr. Surg.: 2014, 134(6);1285-1292 PMID: 25415095 Haiyan Zhu, Aiming Wang, Hairong Zhang, Chunyan Ji, Xiaohua Zhan [Genotype and phenotype study of two patients with 22q11.2 deletion syndrome]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi: 2014, 31(5);623-7 PMID: 25297596


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.


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


Ventral aspect of hard palate of human embryo of 80 mm

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.[8]

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


Links: Bone Morphogenetic Protein


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)[9]

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.

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.[11]
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


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)


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.[12]


  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 PMID: 23613893 | 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 PMID: 22022457 | 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 PMID: 21246652
  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 PMID: 20436469
  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 PMID: 17693063
  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 PMID: 18028903
  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 PMID: 8227288
  8. 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 PMID: 24433583 | BMC Dev Biol.
  9. P. Lancaster and E. Pedisich, Congenital Malformations Australia 1981-1992, ISSN 1321-835.
  10. 10.0 10.1 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 PMID: 21331089
  11. Maynika V Rastogi, Stephen H LaFranchi Congenital hypothyroidism. Orphanet J Rare Dis: 2010, 5;17 PMID: 20537182 | Orphanet J Rare Dis.
  12. 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 PMID: 20927767



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 PMID: 22186724

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 PMID: 19131313

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 PMID: 16962647

M W Ferguson Palate development. Development: 1988, 103 Suppl;41-60 PMID: 3074914

E D Hay An overview of epithelio-mesenchymal transformation. Acta Anat (Basel): 1995, 154(1);8-20 PMID: 8714286


Gerd Steding, Yutao Jian The origin and early development of the nasal septum in human embryos. Ann. Anat.: 2010, 192(2);82-5 PMID: 20149609

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 PMID: 19341725

Search PubMed

Search Pubmed: palate development | cleft palate development |

Additional Images



  • 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.
  • Transforming Growth Factor-beta - (TGFβ) factors induces both epithelial mesenchymal transition and/or apoptosis during palatal medial edge seam disintegration.

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Cite this page: Hill, M.A. (2015) Embryology Palate Development. Retrieved March 3, 2015, from

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© Dr Mark Hill 2015, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G