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Animal models for human craniofacial malformations.
1Dental Research Center, School of Dentistry, University of North Carolina, Chapel Hill 27599.
Journal of Craniofacial Genetics and Developmental Biology
|October 1, 1991
Summary
Ethanol and retinoic acid exposure can cause birth defects by affecting neural plate and crest cell development. These teratogens disrupt facial prominence formation, leading to conditions like holoprosencephaly and cleft lip.
Area of Science:
- Developmental Biology
- Teratology
- Craniofacial Development
Background:
- Holoprosencephaly, fetal alcohol syndrome, and retinoic acid syndrome share developmental origins.
- Neural plate and neural crest cells are critical for craniofacial development.
Purpose of the Study:
- To investigate the mechanisms of birth defects caused by ethanol and retinoic acid.
- To explore the role of medial nasal prominences (MNPs) and neural crest cells in malformation.
Main Methods:
- Animal models exposed to ethanol and 13-cis-retinoic acid.
- Analysis of neural plate and neural crest cell development.
- Studies on mouse palatal shelves in culture.
Main Results:
- Ethanol causes medial anterior neural plate deficiencies and MNP underdevelopment.
- 13-cis-retinoic acid induces neural crest cell death, leading to Treacher Collins syndrome-like malformations.
- Cleft lip etiology is multifactorial, involving MNP size, genetics, and environmental factors like hypoxia.
Conclusions:
- Teratogens like ethanol and retinoic acid disrupt critical developmental processes.
- Understanding these mechanisms can inform prevention and treatment of birth defects.
- Craniofacial malformations often involve complex interactions between genetics and environment.