期刊
CLINICAL GENETICS
卷 69, 期 6, 页码 471-479出版社
WILEY
DOI: 10.1111/j.0009-9163.2006.00615.x
关键词
22q11 deletion Syndrome; congenital birth defects; craniofacial; neural crest cells; Collins Syndrome
资金
- NIDCR NIH HHS [R01 DE016082-04, R01 DE016082-01, R01 DE016082, R01 DE016082-03, R01 DE016082-02, R01 DE016082-05] Funding Source: Medline
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE016082] Funding Source: NIH RePORTER
The craniofacial complex is anatomically the most sophisticated part of the body. It houses all the major sensory organ systems and its origins are synonymous with vertebrate evolution. Of fundamental importance to craniofacial development is a specialized population of stem and progenitor cells, known as the neural crest, which generate the majority of the bone, cartilage, connective and peripheral nerve tissue in the head. Approximately one third of all congenital abnormalities exhibit craniofacial malformations and consequently, most craniofacial anomalies are considered to arise through primary defects in neural crest cell development. Recent advances however, have challenged this classical dogma, underscoring the influence of tissues with which the neural crest cells interact as the primary origin of patterning defects in craniofacial morphogenesis. In this review we discuss these neural crest cell interactions with mesoderm, endoderm and ectoderm in the head in the context of a better understanding of craniofacial malformations such as in Treacher Collins and 22q11 deletion syndromes.
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