Greene R M, Pratt R M
J Embryol Exp Morphol. 1976 Oct;36(2):225-45.
Research on development of the secondary palate has, in the past, dealt primarily with morphological aspects of shelf elevation and fusion. The many factors thought to be involved in palatal elevation, such as fetal neuromuscular activity and growth of the cranial base and mandible, as well as production of extracellular matrix and contractile elements in the palate, are mostly based on gross, light microscopic, morphometric or histochemical observations. Recently, more biochemical procedures have been utilized to described palatal shelf elevation. Although these studies strongly suggest that palatal extracellular matrix plays a major role in shelf movement, interpretation of these data remains difficult owing to the complexity of tissue interactions involved in craniofacial development. Shelf elevation does not appear to involve a single motive factor, but rather a coordinated interaction of all of the abovementioned developmental events. Further analysis of mechanisms of shelf elevation requires development of new, and refinement of existing, in vitro procedures. A system that enables one to examine shelf elevation in vitro would allow more meaningful analysis of the relative importance of the various components in shelf movement. Much more is known about fusion of the palatal shelves, owing in large part to in vitro studies. Fusion of the apposing shelves, both in vivo and in vitro, is dependent upon adhesion and cell dealth of the midline epithelial cells. Adhesion betweeen apposing epithelial surfaces appears to involve epithelial cell surface macromolecules. Further analysis of palatal epithelial adhesion should be directed towards characterization of those cell surface components responsible for this adhesive interaction. Midline epithelial cells cease DNA synthesis 24-36 h before shelf elevation and contact, become active in the synthesis of cell surface glycoproteins, and subsequently manifest morphological signs of necrosis. Death of the midline epithelial cells is thought to involve a programmed, lysosomal-mediated autolysis...
过去，关于继发腭发育的研究主要集中在腭突抬高和融合的形态学方面。许多被认为与腭突抬高有关的因素，如胎儿神经肌肉活动、颅底和下颌骨的生长，以及腭部细胞外基质和收缩成分的产生，大多基于大体、光学显微镜、形态计量学或组织化学观察。最近，更多的生化方法被用于描述腭突抬高。尽管这些研究强烈表明腭部细胞外基质在腭突移动中起主要作用，但由于颅面发育中组织相互作用的复杂性，对这些数据的解释仍然困难。腭突抬高似乎不涉及单一的驱动因素，而是上述所有发育事件的协调相互作用。对腭突抬高机制的进一步分析需要开发新的体外方法并完善现有方法。一个能够在体外检查腭突抬高的系统将允许对腭突移动中各种成分的相对重要性进行更有意义的分析。由于体外研究，人们对腭突融合的了解要多得多。在体内和体外，相对的腭突融合都依赖于中线上皮细胞的黏附与死亡。相对的上皮表面之间的黏附似乎涉及上皮细胞表面大分子。对腭上皮黏附的进一步分析应针对负责这种黏附相互作用的细胞表面成分的特征描述。中线上皮细胞在腭突抬高和接触前24 - 36小时停止DNA合成，开始活跃合成细胞表面糖蛋白，随后表现出坏死的形态学迹象。中线上皮细胞的死亡被认为涉及程序性的、溶酶体介导的自溶……
