Journal
ACTA HISTOCHEMICA
Volume 109, Issue 1, Pages 1-14Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.acthis.2006.05.009
Keywords
adhesion; ankyloglossia and cleft palate; basal lamina; cell fate tracking; craniofacial malformation; medial edge epithelium; midfacial morphogenesis
Categories
Funding
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE013085] Funding Source: NIH RePORTER
- NIDCR NIH HHS [5R01DE013085] Funding Source: Medline
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Formation of the palate, the organ that separates the oral cavity from the nasal cavity, is a developmental process characteristic to embryos of higher vertebrates. Failure in this process results in palatal cleft. During the final steps of palatogenesis, two palatal shelves outgrowing from the sides of the embryonic oronasal. cavity elevate above the tongue, meet in the midline, and rapidly fuse together. Over the decades, multiple mechanisms have been proposed to explain how the superficial mucous membranes disappear from the contact line, thus allowing for normal midline mesenchymal confluence. A substantial body of experimental evidence exists for cell death, cell migration, epithelial-to-mesenchymal transdifferentiation (EMT), replacement through new tissue intercalation, and other mechanisms. However, the most recent use of gene recombination techniques in cell fate tracking disfavors the EMT concept, and suggests that apoptosis is the major fate of the midline cells during physiological. palatal fusion. This article summarizes the benefits and drawbacks of histochemical, and molecular toots used to determine the fates of cells within the palatal midline. Mechanisms of normal disintegration of the midline epithelial seam are reviewed together with pathologic processes that prevent this disintegration, thus causing cleft palate. (C) 2006 Elsevier GmbH. All rights reserved.
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