Epithelial-mesenchymal interaction during tooth morphogenesis

我们澄清了以下结果，得到了科学研究补助金（no. 5）的财政支持。10671696)，来自日本文部科学省。在早期形态形成过程中，糖原沉积在相互作用的牙釉质结和间质中被认为与它们表现出的高信号活动有关。由于糖原沉积在未来骨部位的间充质细胞中，因此牙滤泡细胞中的糖原表明与之相关。随着它们发育成硬组织形成细胞。牙釉质结细胞高度增高，部分细胞高尔基体发达，具有秘书颗粒样囊泡。珐琅质结细胞在帽期晚期高度降低，在钟期早期消失。牙釉质结内的一些细胞具有包括电子致密物质的大吞噬体，这些吞噬体被认为是凋亡小体，在帽期晚期这些吞噬体的数量增加。细胞凋亡抑制剂可诱导牙胚缩小，牙釉质器官细胞密度增加。Msx-2基因的缺失阻止了牙釉质器官的凋亡，影响了牙釉质器官的功能和营养供应，诱导成釉细胞坏死，导致成釉不完全。此外，Msx-2基因缺失导致齿胚形状不规则，无牙釉质区消失，这是啮齿动物磨牙特有的特征。

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.