Elsen L, Carels C E L
Afdeling Prothetische Tandheelkunde, School voor Tandheelkunde, Mondziekten en Kaakchirurgie van de Katholieke Universiteit Leuven, België.
Ned Tijdschr Tandheelkd. 2008 Feb;115(2):71-7.
Although the molecular cascades that control craniofacial development are still largely unknown, the generation of mutant animal models and the identification of gene mutations that cause human craniofacial syndromes have recently given significant insight into how the unique structure of the head develops. Craniofacial structures are formed from the prechordal mesoderm, the craniofacial ectoderm as well as the neural crest cells which develop on the dorsal side of the neural tube. Normal craniofacial morphology as well as normal (in number and in morphology) tooth organs develop as a consequence of complex interactions between these embryonic tissues. A series of inductive and reciprocal signals between the epithelium and mesenchyme determine the growth, the form and the ultimate differentiation of tissues and organs. Genetic research has shown the involvement of numerous developmental genes encoding a variety of transcription factors, growth factors and receptors. Mutations have been associated with, among others, non-syndromal forms of cleft palate, agenesis of tooth organs and abnormalities in the cranial bones.
尽管控制颅面发育的分子级联反应在很大程度上仍不为人知,但突变动物模型的建立以及导致人类颅面综合征的基因突变的鉴定,最近为头部独特结构的发育方式提供了重要见解。颅面结构由原索前中胚层、颅面外胚层以及在神经管背侧发育的神经嵴细胞形成。正常的颅面形态以及正常(数量和形态上)的牙器官是这些胚胎组织之间复杂相互作用的结果。上皮和间充质之间一系列诱导性和相互性信号决定了组织和器官的生长、形态以及最终分化。遗传学研究表明,众多编码各种转录因子、生长因子和受体的发育基因参与其中。突变与多种情况有关,包括非综合征性腭裂、牙器官发育不全以及颅骨异常。