Abnormal Development - Cleft Palate: Difference between revisions
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* ''' | * '''Constitutive activation of hedgehog signaling adversely affects epithelial cell fate during palatal fusion'''{{#pmid:29981310|PMID29981310}} "Cleft palate is one of the most common craniofacial congenital defects in humans. It is associated with multiple genetic and environmental risk factors, including mutations in the genes encoding signaling molecules in the {{sonic hedgehog}} ({{Shh}}) pathway, which are risk factors for cleft palate in both humans and mice. However, the function of Shh signaling in the palatal epithelium during palatal fusion remains largely unknown. Although components of the Shh pathway are localized in the palatal epithelium, specific inhibition of Shh signaling in palatal epithelium does not affect palatogenesis. ...In this study, we discovered that constitutive activation of Hh signaling in the palatal epithelium results in submucous cleft palate and persistence of the medial edge epithelium (MEE). Further investigation revealed that precise downregulation of Shh signaling is required at a specific time point in the MEE during palatal fusion. Upregulation of Hh signaling in the palatal epithelium maintains the proliferation of MEE cells. This may be due to a dysfunctional p63/Irf6 regulatory loop. The resistance of MEE cells to apoptosis is likely conferred by enhancement of a cell adhesion network through the maintenance of p63 expression." | ||
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* '''Regulation of the Epithelial Adhesion Molecule CEACAM1 Is Important for Palate Formation'''{{#pmid:23613893|PMID23613893}} "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'''{{#pmid:22022457|PMID22022457}} "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'''{{#pmid:21246652|PMID21246652}} "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'''{{#pmid:20436469|PMID20436469}} "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'''{{#pmid:17693063|PMID17693063}} "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." | |||
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== Textbooks == | == Textbooks == |
Revision as of 10:18, 22 October 2018
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LA42 Cleft Palate
LA42 Cleft palate is the new ICD-11 classification within clefts of lip, alveolus or palate. Below is also the earlier ICD-10 coding information.
LA42 Cleft palate - is a fissure type embryopathy that affects the soft and hard palate to varying degrees.
- LA4Y Other specified clefts of lip, alveolus or palate
- LA4Z Clefts of lip, alveolus or palate, unspecified
International Classification of Diseases ICD-10 |
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Introduction
International Classification of Diseases (ICD-10) - Q35 Cleft palate Incl.: fissure of palate palatoschisis Excl.: cleft palate with cleft lip (Q37.-)
Cleft palate has many different causes and in humans occurs more frequently in females (57%) than in males (43%).[1] 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.
A major contribution to the palate comes from the neural crest 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:
- maxillary components of the first pharyngeal arch (lateral)
- frontonasal prominence (midline)
The secondary palate can also be divided in two anatomical parts:
- anterior hard palate - ossified
- maxilla
- palatine bones
- posterior soft palate - muscular
- tensor veli palatini (swallowing)
- palatoglossus (swallowing)
- palatopharyngeus (breathing)
- levator veli palatini (swallowing)
- musculus uvulae (uvula movement)
Palate Links: palate | cleft lip and palate | cleft palate | head | Category:Palate |
Some Recent Findings
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More recent papers |
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This table allows an automated computer search of the external PubMed database using the listed "Search term" text link.
More? References | Discussion Page | Journal Searches | 2019 References | 2020 References Search term: Cleft Palate <pubmed limit=5>Cleft Palate</pubmed> |
Older papers |
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Textbooks
- 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
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- Links: Movies | Ultrasound
Clinical Images
Incomplete Cleft Palate
Involving only the soft palate and uvula.[8]
Complete Cleft Palate
Completely involving the secondary palate.[8]
Surgical repair of the palate (palatoplasty).[8]
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 |
Veau Classification
The historic Veau System (1931)[9] classifies orofacial clefting into four classes (Veau Class I - IV) according to whether the secondary and/or primary palates are affected and by laterality.
- Incomplete cleft, soft palate only (no unilateral/bilateral designation)
- Hard and soft palate, secondary palate only (no unilateral/bilateral designation)
- Complete unilateral cleft including lip (primary and secondary palates)
- Complete bilateral cleft
Cleft Palate Genetics
Cleft Palate Only Genes[11] | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Links: OMIM Orofacial Cleft with or without cleft palate
Statistics
- 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)
Australian Palate Abnormalities (2002-2003)[13] |
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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).
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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.
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Australian Palate Abnormalities (2002-2003) |
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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).
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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.
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Ten most frequently reported Birth Anomalies
- Hypospadias (More? Male movie | Genital Abnormalities - Hypospadia)
- Obstructive Defects of the Renal Pelvis (More? Renal System - Abnormalities)
- Ventricular Septal Defect (More? Cardiovascular Abnormalities - Ventricular Septal Defect)
- Congenital Dislocated Hip (More? Musculoskelal Abnormalities - Congenital Dislocation of the Hip (CDH))
- Trisomy 21 or Down syndrome - (More? Trisomy 21)
- Hydrocephalus (More? Hydrocephalus)
- Cleft Palate (More? Palate_Development)
- Trisomy 18 or Edward Syndrome - multiple abnormalities of the heart, diaphragm, lungs, kidneys, ureters and palate 86% discontinued (More? (More? Trisomy 18)
- 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)
- 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)
Cleft Risk Variants - Two genes were identified from a recent genome-wide study.[6]
- 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
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.[14]
Cleft Palate Repair
Surgical repair of the palate is described as palatoplasty and is often carried out between 6 to 12 months of age but also during later periods (12 to 18 months). In developing countries, this may be repaired significantly later in childhood or even go unprepared.
Surgical Repair Techniques
Some Types of Surgical Repair Techniques[15]
- von Langenbeck's bipedicle flap technique
- Veau-Wardill-Kilner Pushback technique
- Bardach's two-flap technique
- Furlow Double opposing Z-Plasty
- Two-stage palatal repair
- Hole in one repair
- Raw area free palatoplasty
- Alveolar extension palatoplasty (AEP)
- Primary pharyngeal flap
- Intravelar veloplasty
- Vomer flap
- Buccal myomucosal flap
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
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Face Development
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
Neural Crest
- Mesenchyme invaded by neural crest generating connective tissue components
- cartilage, bone, ligaments
- arises from midbrain and hindbrain region
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.[16]
Embryonic Palate
Human primary palate
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- 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
Head Growth
- continues postnatally - fontanelle allow head distortion on birth and early growth
- bone plates remain unfused to allow growth, puberty growth of face
Adult
Animal Models
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 (E13.5) Palatal Shelf Wnt5a, Osr2 and Pax9 Expression.[18]
Mouse ruga pattern (E16) | Mouse - Spry1 cleft palate |
Cleft palate in newborn mice.[19]
- Links: Mouse Development | Bone Morphogenetic Protein | Wnt | Pax
Molecular
MMP25[20]
Image - Mouse E13.5 Bmp7 palate[21]
Image - palate Bmp7 palate[21]
Image - palate detail Bmp7 palate[21]
- Links: Bone Morphogenetic Protein
References
- ↑ Kosowski TR, Weathers WM, Wolfswinkel EM & Ridgway EB. (2012). Cleft palate. Semin Plast Surg , 26, 164-9. PMID: 24179449 DOI.
- ↑ Li J, Yuan Y, He J, Feng J, Han X, Jing J, Ho TV, Xu J & Chai Y. (2018). Constitutive activation of hedgehog signaling adversely affects epithelial cell fate during palatal fusion. Dev. Biol. , 441, 191-203. PMID: 29981310 DOI.
- ↑ Mima J, Koshino A, Oka K, Uchida H, Hieda Y, Nohara K, Kogo M, Chai Y & Sakai T. (2013). Regulation of the epithelial adhesion molecule CEACAM1 is important for palate formation. PLoS ONE , 8, e61653. PMID: 23613893 DOI.
- ↑ Nelson ER, Levi B, Sorkin M, James AW, Liu KJ, Quarto N & Longaker MT. (2011). Role of GSK-3β in the osteogenic differentiation of palatal mesenchyme. PLoS ONE , 6, e25847. PMID: 22022457 DOI.
- ↑ San Miguel S, Serrano MJ, Sachar A, Henkemeyer M, Svoboda KK & Benson MD. (2011). Ephrin reverse signaling controls palate fusion via a PI3 kinase-dependent mechanism. Dev. Dyn. , 240, 357-64. PMID: 21246652 DOI.
- ↑ 6.0 6.1 Beaty TH, Murray JC, Marazita ML, Munger RG, Ruczinski I, Hetmanski JB, Liang KY, Wu T, Murray T, Fallin MD, Redett RA, Raymond G, Schwender H, Jin SC, Cooper ME, Dunnwald M, Mansilla MA, Leslie E, Bullard S, Lidral AC, Moreno LM, Menezes R, Vieira AR, Petrin A, Wilcox AJ, Lie RT, Jabs EW, Wu-Chou YH, Chen PK, Wang H, Ye X, Huang S, Yeow V, Chong SS, Jee SH, Shi B, Christensen K, Melbye M, Doheny KF, Pugh EW, Ling H, Castilla EE, Czeizel AE, Ma L, Field LL, Brody L, Pangilinan F, Mills JL, Molloy AM, Kirke PN, Scott JM, Scott JM, Arcos-Burgos M & Scott AF. (2010). A genome-wide association study of cleft lip with and without cleft palate identifies risk variants near MAFB and ABCA4. Nat. Genet. , 42, 525-9. PMID: 20436469 DOI.
- ↑ Welsh IC, Hagge-Greenberg A & O'Brien TP. (2007). A dosage-dependent role for Spry2 in growth and patterning during palate development. Mech. Dev. , 124, 746-61. PMID: 17693063 DOI.
- ↑ 8.0 8.1 8.2 8.3 Freitas JA, das Neves LT, de Almeida AL, Garib DG, Trindade-Suedam IK, Yaedú RY, Lauris Rde C, Soares S, Oliveira TM & Pinto JH. (2012). Rehabilitative treatment of cleft lip and palate: experience of the Hospital for Rehabilitation of Craniofacial Anomalies/USP (HRAC/USP)--Part 1: overall aspects. J Appl Oral Sci , 20, 9-15. PMID: 22437671
- ↑ Veau V. Paris: Masson & Cie; Division Palatine. (1931).
- ↑ Rastogi MV & LaFranchi SH. (2010). Congenital hypothyroidism. Orphanet J Rare Dis , 5, 17. PMID: 20537182 DOI.
- ↑ Dixon MJ, Marazita ML, Beaty TH & Murray JC. (2011). Cleft lip and palate: understanding genetic and environmental influences. Nat. Rev. Genet. , 12, 167-78. PMID: 21331089 DOI.
- ↑ P. Lancaster and E. Pedisich, Congenital Malformations Australia 1981-1992, ISSN 1321-835.
- ↑ 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.
- ↑ De-Regil LM, Fernández-Gaxiola AC, Dowswell T & Peña-Rosas JP. (2010). Effects and safety of periconceptional folate supplementation for preventing birth defects. Cochrane Database Syst Rev , , CD007950. PMID: 20927767 DOI.
- ↑ Agrawal K. (2009). Cleft palate repair and variations. Indian J Plast Surg , 42 Suppl, S102-9. PMID: 19884664 DOI.
- ↑ Foppiano S, Hu D & Marcucio RS. (2007). Signaling by bone morphogenetic proteins directs formation of an ectodermal signaling center that regulates craniofacial development. Dev. Biol. , 312, 103-14. PMID: 18028903 DOI.
- ↑ Diewert VM & Lozanoff S. (1993). A morphometric analysis of human embryonic craniofacial growth in the median plane during primary palate formation. J. Craniofac. Genet. Dev. Biol. , 13, 147-61. PMID: 8227288
- ↑ Almaidhan A, Cesario J, Landin Malt A, Zhao Y, Sharma N, Choi V & Jeong J. (2014). Neural crest-specific deletion of Ldb1 leads to cleft secondary palate with impaired palatal shelf elevation. BMC Dev. Biol. , 14, 3. PMID: 24433583 DOI.
- ↑ Jiang YH, Pan Y, Zhu L, Landa L, Yoo J, Spencer C, Lorenzo I, Brilliant M, Noebels J & Beaudet AL. (2010). Altered ultrasonic vocalization and impaired learning and memory in Angelman syndrome mouse model with a large maternal deletion from Ube3a to Gabrb3. PLoS ONE , 5, e12278. PMID: 20808828 DOI.
- ↑ Brown GD & Nazarali AJ. (2010). Matrix metalloproteinase-25 has a functional role in mouse secondary palate development and is a downstream target of TGF-β3. BMC Dev. Biol. , 10, 93. PMID: 20809987 DOI.
- ↑ 21.0 21.1 21.2 Kouskoura T, Kozlova A, Alexiou M, Blumer S, Zouvelou V, Katsaros C, Chiquet M, Mitsiadis TA & Graf D. (2013). The etiology of cleft palate formation in BMP7-deficient mice. PLoS ONE , 8, e59463. PMID: 23516636 DOI.
Journals
- The Cleft Palate-Craniofacial Journal Homepage | Available issues
Reviews
Indian J Plast Surg. 2009 October; 42(Suppl):Cleft Lip and Palate Issue
Funato N, Nakamura M & Yanagisawa H. (2015). Molecular basis of cleft palates in mice. World J Biol Chem , 6, 121-38. PMID: 26322171 DOI.
Bush JO & Jiang R. (2012). Palatogenesis: morphogenetic and molecular mechanisms of secondary palate development. Development , 139, 231-43. PMID: 22186724 DOI.
Meng L, Bian Z, Torensma R & Von den Hoff JW. (2009). Biological mechanisms in palatogenesis and cleft palate. J. Dent. Res. , 88, 22-33. PMID: 19131313 DOI.
Dudas M, Li WY, Kim J, Yang A & Kaartinen V. (2007). Palatal fusion - where do the midline cells go? A review on cleft palate, a major human birth defect. Acta Histochem. , 109, 1-14. PMID: 16962647 DOI.
Ferguson MW. (1988). Palate development. Development , 103 Suppl, 41-60. PMID: 3074914
Hay ED. (1995). An overview of epithelio-mesenchymal transformation. Acta Anat (Basel) , 154, 8-20. PMID: 8714286
Articles
Steding G & Jian Y. (2010). The origin and early development of the nasal septum in human embryos. Ann. Anat. , 192, 82-5. PMID: 20149609 DOI.
Xiong W, He F, Morikawa Y, Yu X, Zhang Z, Lan Y, Jiang R, Cserjesi P & Chen Y. (2009). Hand2 is required in the epithelium for palatogenesis in mice. Dev. Biol. , 330, 131-41. PMID: 19341725 DOI.
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Cite this page: Hill, M.A. (2024, April 16) Embryology Abnormal Development - Cleft Palate. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Cleft_Palate
- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G