| Project/Area Number |
17H04374
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Tokyo Dental College (2018-2019)
Matsumoto Dental University (2017) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
荒井 敦 松本歯科大学, 歯学部, 准教授 (00532772)
細矢 明宏 北海道医療大学, 歯学部, 准教授 (70350824)
小林 泰浩 松本歯科大学, 総合歯科医学研究所, 教授 (20264252)
宇田川 信之 松本歯科大学, 歯学部, 教授 (70245801)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥16,900,000 (Direct Cost: ¥13,000,000、Indirect Cost: ¥3,900,000)
Fiscal Year 2019: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2018: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2017: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
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| Keywords | 象牙芽細胞 / 第三象牙質 / 歯髄幹細胞 / ジフテリア毒素 / 細胞の枯渇実験 / フェイトマッピング解析 / 骨芽細胞 / 細胞枯渇実験 / 修復象牙質 / PTH / 骨髄間葉系幹細胞 |
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| Outline of Final Research Achievements |
Tertiary dentin formation is induced in response to dental cavity preparation for dental treatment. In this biological process, cavity preparation induces odontoblastic cell death and fewer odontoblasts are thus regenerated from dental pulp stem cells, resulting in induced reparative dentin formation. However, the relationship between odontoblastic cell death and the regulation of tertiary dentin formation is unclear. In this study, we examined the effects of odontoblastic depletion on dentinogenesis activation using genetically modified mice. We found that dentin formation increased in response to odontoblastic cell death. This result suggests that there is a dental pulp niche environment regulated by odontoblastic cell death and that this regulatory network is essential for the activation of reparative dentin formation.
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| Academic Significance and Societal Importance of the Research Achievements |
歯の修復は、失われた硬組織を補填する生体防御反応であり、臨床現場では、より早期の修復象牙質形成が求められる。しかしながら、これまで硬組織修復のメカニズムはよくわかっていなかった。本研究成果により、象牙芽細胞の細胞死が、歯髄環境に影響を及ぼし、未分化歯髄細胞画分の象牙芽細胞分化を誘導することが明らかになった。今後、以上の実験系を活用することにより、硬組織修復の促進を目指した治療法の提案に繋がることが期待される。
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