Epithelial-mesenchymal interaction during tooth morphogenesis

牙齿形态发生过程中上皮-间质相互作用

• 批准号: 10671696
• 负责人: OHSHIMA Hayato
• 金额: $ 0.38万
• 依托单位: Niigata University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671696/
• 关键词: Tooth Morphogenesis; Enamel Knot; Apoptosis; glycogen; Dental Follicle; Msx-2; Mouse; Ultrastructure; エナメル器; エナメル芽細胞; エナメル質形成不全; 歯乳頭

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.

在日本文部科学省科学研究助学金(编号10671696)的财政支持下，我们澄清了以下结果。在早期形态发生过程中，相互作用的釉质结和间充质中糖原沉积的幸运被认为与它们表现出的高信号活性有关。由于糖原沉积在未来的骨部位的间充质细胞中，牙囊细胞中的糖原被认为是相关的。随着它们发育成硬组织形成细胞。釉结细胞高度增加，部分细胞高尔基体发达，有分泌颗粒样小泡。釉结细胞在帽状晚期高度降低，在钟状早期消失。釉质结中部分细胞有大的吞噬小体，包括电子致密物质，被认为是凋亡小体，这些吞噬小体在帽状晚期数量增加。此外，在体外，细胞凋亡抑制物可导致牙胚变小，釉质器官细胞密度增加。MSX-2基因的缺失阻碍了成釉细胞的凋亡，影响了成釉细胞的功能和营养供应，导致成釉细胞的坏死，导致成釉细胞发育不完全。此外，MSX-2基因缺失导致牙胚形态不规则，牙釉质脱落区消失，这是啮齿动物磨牙的特有特征。

项目成果

前田健康、大島勇人: "歯根膜ルフィニ神経終末の形態学的基礎"解剖学雑誌. 73・2. 119-134 (1998)

Ken Maeda，Hayato Oshima：“牙周膜鲁菲尼神经末梢的形态学基础”解剖学杂志 73・2（1998）。

Takayuki Futami 他6名: "Tissue response to titanium implants in the rat maxilla"Journal of Periodontology. 71・2. 288-299 (2000)

Takayuki Futami 等 6 人：“大鼠上颌骨钛种植体的组织反应”，牙周病学杂志 71・2（2000 年）。

Kayoko Nozawa-Inoue 他5名: "Immunocytochemical demonstration of heat shock protein 25 in the rat temperomandibular joint"Archives of Histology and Cytology. 62・5. 483-491 (1999)

Kayoko Nozawa-Inoue 等 5 人：“大鼠颞下颌关节中热休克蛋白 25 的免疫细胞化学演示”组织学和细胞学档案 62・5（1999）。

Ohshima, H., Maeda, T. and Takano, Y.: "The distribution and ultrastructure of class II MHC-positive cells in human dental pulp."Cell Tissue Res.. 295(1). 151-158 (1999)

Ohshima, H.、Maeda, T. 和 Takano, Y.：“人牙髓中 II 类 MHC 阳性细胞的分布和超微结构。”细胞组织研究 295(1)。

Naoko Kannari 他4名: "Class II MHC Antigen - expressing cells in the pulp tissue of human deciduos teeth prior to shedding"Archives of History and Cytology. 61・1. 1-15 (1998)

Naoko Kannari 等 4 人：“II 类 MHC 抗原 - 脱落前人类乳牙牙髓组织中的表达细胞”历史和细胞学档案 61・1（1998）。