Talk:Palate Development

About Discussion Pages

On this website the Discussion Tab or "talk pages" for a topic has been used for several purposes: References - recent and historic that relates to the topic Additional topic information - currently prepared in draft format Links - to related webpages Topic page - an edit history as used on other Wiki sites Lecture/Practical - student feedback Student Projects - online project discussions. Links: Pubmed Most Recent | Reference Tutorial | Journal Searches Glossary Links Glossary: A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | Numbers | Symbols | Term Link Cite this page: Hill, M.A. (2024, April 30) Embryology Palate Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Palate_Development

2011

Histomorphological study of palatal shelf elevation during murine secondary palate formation

Dev Dyn. 2011 May 26. doi: 10.1002/dvdy.22670. Yu K, Ornitz DM. Source Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri. kyu@wustl.edu; dornitz@wustl.edu.

Abstract

During mammalian secondary palate development, the palatal shelves undergo dramatic morphological changes to elevate from a vertical to a horizontal plane in the oral-nasal cavity. We found that E14.5 mouse embryos displayed marked variations in shelf morphology that represent various intermediate states of the elevation process. With these variations, we reconstructed the sequence of shelf morphological changes that take place during the elevation process and discovered distinct patterns in different regions along the anterior-posterior (AP) axis. Moreover, our study revealed that during the elevation process, shelf morphological changes are accompanied by tongue morphological changes, which also show distinct characteristics along the AP axis. We further discuss how to divide the palate along the AP axis based on morphological criteria. Our study provides a framework that recognizes variation in timing of palatal morphogenesis along the AP axis that will aid in the investigation of the mechanisms regulating palatal shelf elevation. Developmental Dynamics, 2011. © 2011 Wiley-Liss, Inc.

Copyright © 2011 Wiley-Liss, Inc.

• In mammals, after bulging out bilaterally from the maxillary process, the palate shelves grow rapidly away from the maxilla along the side of the tongue.
• Formation of the secondary palate requires the palatal shelves to undergo a process called shelf elevation or shelf reorientation
• palate shelves move from lateral of the tongue to above the dorsum of the tongue and change their orientation in the oral-nasal cavity from vertical to horizontal.
• the opposing horizontal shelves contact each other at the midline of the oral-nasal cavity
• A midline epithelial seam (MES) is then formed by fusion of the medial edge epithelia (MEE) of the opposing palatal shelves.

PMID: 21618642 http://www.ncbi.nlm.nih.gov/pubmed/21618642

http://onlinelibrary.wiley.com/doi/10.1002/dvdy.22670/abstract

Ephrin reverse signaling controls palate fusion via a PI3 kinase-dependent mechanism

Dev Dyn. 2011 Feb;240(2):357-64. doi: 10.1002/dvdy.22546.

San Miguel S, Serrano MJ, Sachar A, Henkemeyer M, Svoboda KK, Benson MD.

Department of Biomedical Sciences, Texas A&M Health Science Center Baylor College of Dentistry, Dallas, Texas. Abstract

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. These data describe both a novel role for ephrins in palate morphogenesis, and a previously unknown mechanism of ephrin signaling. Developmental Dynamics 240:357-364, 2011. © 2011 Wiley-Liss, Inc.

Copyright © 2011 Wiley-Liss, Inc.

PMID: 21246652 http://www.ncbi.nlm.nih.gov/pubmed/21246652

2010

Epidemiologic factors causing cleft lip and palate and their regularities of occurrence in Estonia

Stomatologija. 2010;12(4):105-108.

Jagomagi T, Soots M, Saag M.

Department of Stomatology, Faculty of Medicine, University of Tartu, Kastani 16, Tartu 50410, Estonia. triin.jagomagi@ortodontia.ee.

Abstract OBJECTIVES. To study epidemiological factors causing development of cleft lip and palate and their occurrence regularities. MATERIALS AND METHODS. This study included 583 cleft lip and palate patients and the information for statistical analyses was gathered from Tartu University Hospital. RESULTS. 19% of the patients had a cleft lip (CL), 39% of the patients had a cleft palate (CP), and 42 % of the patients had a cleft lip and palate (CLP). The ratio for different cleft types CL: CLP: CP was 1:2:2. In unilateral CLP and CL cases, the left side was affected 2.2 times more frequently than the right side. Boys had a CLP nearly 2.1 times more often than girls. CP was more common for girls (60%) than for boys (40%). 30% of children had multiple malformations. 2.6% of children with clefts were born premature, half of which had accompanying developmental anomalies. The average birth weight for cleft child was ~ 3400 grams. 6.8% of children with clefts had a birth weight below 2.5 kg. In case of children with clefts, the mother's age exceeded 30 years in 1/4 of cases and father's age in 1/3 of cases. Both parents were older than 30 years in 66% of the cases. 1/5 of both parents were older than 30 years. 1/3 of mothers of children with clefts had suffered psychological stress, 1/5 of mothers had done hard physical work. 1/5 of mothers had an exposure to teratogenic toxic substances. 15% of them received medications during the first trimester of pregnancy. 15% of mothers had experienced hormonal disorders. CONCLUSIONS. As a result of the study we found a high occurrence rate of CP (CL: CLP: CP - 1:2:2), which is similar to the studies conducted in Finland and Sweden. The reasons for this ratio need further research.

PMID: 21266834 http://www.ncbi.nlm.nih.gov/pubmed/21266834

A genome-wide association study of cleft lip with and without cleft palate identifies risk variants near MAFB and ABCA4

Nat Genet. 2010 Jun;42(6):525-9. Epub 2010 May 2.

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, Arcos-Burgos M, Scott AF.

Johns Hopkins University, School of Public Health, Baltimore, Maryland, USA. tbeaty@jhsph.edu Erratum in:

Nat Genet. 2010 Aug;42(8):727. Scott, James M [corrected to Scott, John M]. Abstract 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. Stratifying trios into European and Asian ancestry groups revealed differences in statistical significance, although estimated effect sizes remained similar. Replication studies from several populations showed confirming evidence, with families of European ancestry giving stronger evidence for markers in 8q24, whereas Asian families showed stronger evidence for association with MAFB and ABCA4. Expression studies support a role for MAFB in palatal development.

PMID: 20436469 http://www.ncbi.nlm.nih.gov/pubmed/20436469

Matrix metalloproteinase-25 has a functional role in mouse secondary palate development and is a downstream target of TGF-β3

BMC Dev Biol. 2010 Sep 1;10:93.

Brown GD, Nazarali AJ.

Laboratory of Molecular Biology, College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5C9, Canada. Abstract BACKGROUND: Development of the secondary palate (SP) is a complex event and abnormalities during SP development can lead to cleft palate, one of the most common birth disorders. Matrix metalloproteinases (MMPs) are required for proper SP development, although a functional role for any one MMP in SP development remains unknown. MMP-25 may have a functional role in SP formation as genetic scans of the DNA of human cleft palate patients indicate a common mutation at a region upstream of the MMP-25 gene. We report on the gene expression profile of MMP-25 in the developing mouse SP and identify its functional role in mouse SP development.

RESULTS: MMP-25 mRNA and protein are found at all SP developmental stages in mice, with the highest expression at embryonic day (E) 13.5. Immunohistochemistry and in situ hybridization localize MMP-25 protein and mRNA, respectively, to the apical palate shelf epithelial cells and apical mesenchyme. MMP-25 knockdown with siRNA in palatal cultures results in a significant decrease in palate shelf fusion and persistence of the medial edge epithelium. MMP-25 mRNA and protein levels significantly decrease when cultured palate shelves are incubated in growth medium with 5 μg/mL of a TGF-β3-neutralizing antibody.

CONCLUSIONS: Our findings indicate: (i) MMP-25 gene expression is highest at E12.5 and E13.5, which corresponds with increasing palate shelf growth downward alongside the tongue; (ii) MMP-25 protein and mRNA expression predominantly localize in the apical epithelium of the palate shelves, but are also found in apical areas of the mesenchyme; (iii) knockdown of MMP-25 mRNA expression impairs palate shelf fusion and results in significant medial edge epithelium remaining in contacted areas; and (iv) bio-neutralization of TGF-β3 significantly decreases MMP-25 gene expression. These data suggest a functional role for MMP-25 in mouse SP development and are the first to identify a role for a single MMP in mouse SP development.

PMID: 20809987

Antenatal determinants of oro-facial clefts in Southern Nigeria

Afr Health Sci. 2010 Mar;10(1):31-9.

Omo-Aghoja VW, Omo-Aghoja LO, Ugboko VI, Obuekwe ON, Saheeb BD, Feyi-Waboso P, Onowhakpor A.

Department of Oral and Maxillofacial Surgery, Central Hospital, Sapele, Nigeria. Abstract OBJECTIVES: Cleft lip with or without cleft palate, is the most common serious congenital anomaly that affects the orofacial regions. The management and care of the cleft patient constitutes a substantial proportion of the workload of the Nigerian maxillofacial surgeon and allied specialties. Yet, there are no specific programmes targeted at this group. We believe that the findings of this study is capable of identifying useful interventions for designing programs that will lead to a reduction in the burden of orofacial cleft in Nigeria.

METHODS: It was a transverse cross-sectional study that was undertaken at the Maxillofacial Units of the University of Benin Teaching Hospital and the Central Hospital, Benin City respectively. The prevalence and antenatal determinants of cleft lip and palate were determined.

RESULTS: Cleft lip and palate were often encountered in clinical practice in Benin City with a prevalence of 1.35%. The results showed that orofacial clefts were commoner in females and that the combined unilateral cleft lip and palate was the commonest entity encountered amongst the cases. The following risk factors were associated with the risk of development of cleft lip and palate: Paternal age >40 years, maternal age >35 years, genetic/family history, low socio-economic status, alcohol consumption and indulgence in the intake of herbal medications in pregnancy.

CONCLUSION: Public health education programmes and advocacy activities geared towards raising awareness of the identified risk factors for the development of cleft lip and or cleft palate would go a long way to obviate the occurrence and reduce the burden.

PMID: 20811522

2009

One-stage palate repair improves speech outcome and early maxillary growth in patients with cleft lip and palate

J Physiol Pharmacol. 2009 Dec;60 Suppl 8:37-41.

Pradel W, Senf D, Mai R, Ludicke G, Eckelt U, Lauer G.

Department of Oral and Maxillofacial Surgery, University Hospital Carl Gustav Carus, Dresden Technical University, Dresden, Germany. winnie.pradel@uniklinikum-dresden.de Abstract There are several types of palatal surgery; each cleft centre chooses its own technique based on experience and treatment philosophy. The aim of this study was to compare speech outcome and maxillary growth in children with cleft lip and palate deformity after palate repair with either a one-stage or a two- stage procedure and to identify the better treatment protocol. In 24 children, speech outcome was assessed regarding resonance, nasal escape, compensatory articulations, facial grimace, and spontaneous speech. In addition, plaster models of 15 children were compared. In 12 children, a two-stage procedure was performed (group A): at the age of 9-12 months, an intravelar veloplasty for repair of the soft palate, and at the age of 24-36 months a bipedicled flap closure of the hard palate. In 12 children, the same techniques were used in a one-stage procedure, at the age of 9-12 months (group B). The children of group B showed less altered resonance and less nasal emission at 4 years of age compared to the children of group A. At 6 years, the children of group A had improved their speech skills, but they did not equal the results of group B. In the study models of group A at age 6 years, the transverse dimension (anterior and posterior width of the dental arch) was smaller than in the models of group B. The one-stage repair of cleft palate at the age of 9-12 months seems to have a more positive influence on speech development and early maxillary growth than the two-stage procedure.

PMID: 20400790 http://www.ncbi.nlm.nih.gov/pubmed/20400790

2007

A dosage-dependent role for Spry2 in growth and patterning during palate development

Mech Dev. 2007 Sep-Oct;124(9-10):746-61. Epub 2007 Jul 10.

Welsh IC, Hagge-Greenberg A, O'Brien TP.

Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853, USA.

Abstract 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. We show that excessive cell proliferation in the Spry2-deficient palate is accompanied by the abnormal progression of shape changes and movements required for medially directed shelf outgrowth and midline contact. Expression of the FGF responsive transcription factors Etv5, Msx1, and Barx1, as well as the morphogen Shh, is restricted to specific regions of the developing palate. We detected elevated and ectopic expression of these transcription factors and disorganized Shh expression in the Spry2-deficient palate. Mice carrying a targeted disruption of Spry2 fail to complement the craniofacial phenotype characterized in Spry2 deletion mice. Furthermore, a Spry2-BAC transgene rescues the palate defect. However, the BAC transgenic mouse lines express reduced levels of Spry2. The resulting hypomorphic phenotype demonstrates that palate development is Spry2 dosage sensitive. Our results demonstrate the importance of proper FGF signaling thresholds in regulation of epithelial-mesenchymal interactions and cellular responses necessary for coordinated morphogenesis of the face and palate.

PMID: 17693063