| Project/Area Number |
10671696
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Niigata University |
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Principal Investigator |
OHSHIMA Hayato Niigata University, Faculty of Dentistry, Associate Professor, 歯学部, 助教授 (70251824)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE-NOZAWA Kayoko Niigata University, Faculty of Dentistry, Assistant Professor, 歯学部, 助手 (90303130)
KAWANO Yoshiro Niigata University, Faculty of Dentistry, Assistant Professor, 歯学部, 助手 (60303129)
MAEDA Takeyasu Niigata University, Faculty of Dentistry, Professor, 歯学部, 教授 (40183941)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | 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 |
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| Research Abstract |
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.
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