Epithelial-mesenchymal interaction during tooth morphogenesis

我们澄清了以下结果，由日本文部科学省科学研究补助金（编号10671696）的财政支持。在早期形态发生过程中，糖原在相互作用的釉结和间充质中沉积的运气被认为与它们表现出的高信号活性有关。由于在未来骨部位的间充质细胞中观察到糖原沉积，因此牙囊细胞中的糖原指示相关。随着它们发育成硬组织形成细胞。釉节细胞高度增加，部分细胞具有发达的高尔基体和分泌颗粒样小泡。釉结细胞在帽状期晚期高度降低，钟状期早期消失。釉结中的一些细胞具有大的吞噬体，其中包括电子致密物质，被认为是凋亡小体，这些吞噬体在帽状晚期数量增加。此外，凋亡抑制剂在体外诱导牙胚体积减小，成釉器细胞密度增加。Msx-2基因的缺失抑制了成釉器的凋亡，影响了成釉器的功能和营养供应，导致成釉细胞坏死，导致成釉不完全。Msx-2基因的缺失导致牙胚形态不规则，无釉区消失，这是啮齿动物磨牙的特征。

We clarified the following results, by the financial support of a Grant-in-Aid for Scientific Research (no. 10671696) from the Ministry of Education, Science, Sports, and Culture, Japan. The luck of glycogen deposits in the interacting enamel knot and mesenchyme during early morphogenesis was thought to be associated with their demonstrated high signaling activities. Since glycogen deposits was seen in the mesenchymal cells at future bone sites, the glycogen in the dental follicle cells was indicative to be associated. with their development into hard-tissue-forming cells. Enamel knot cells were increased in height and some cells possessed a developed Golgi apparatus and secretary granule-like vesicles. Enamel knot cells were decreased in height during the late cap stage, and they disappeared during the early bell stage. Some cells in the enamel knot possessed large phagosomes including electron-dense material which were thought to be apoptotic bodies and these phagosomes were increased in number during the late cap stage. Furthermore, the apoptosis inhibitor induced the decreased size of the tooth germ and increased cell density of the enamel organ in vitro. The deficiency of Msx-2 gene prevented the apoptosis of enamel organ and influenced both the function of enamel organ and the nutritional supply to induce the necrosis of ameloblasts, resulting in imperfect amelogenesis. Furthermore, the deficiency of Msx-2 gene induced the irregular shape of tooth germ and the disappearance of the enamel free area which is the peculiar features of rodent molars.