Project/Area Number |
18K17072
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 57030:Conservative dentistry-related
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Research Institution | Nagasaki University |
Principal Investigator |
|
Project Period (FY) |
2018-04-01 – 2023-03-31
|
Project Status |
Completed (Fiscal Year 2022)
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Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2021: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2020: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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Keywords | 歯周病 / 咬合性外傷 / 破骨細胞 / 破骨細胞前駆細胞 / RANKL / 慢性歯周炎 / 静止期破骨細胞前駆細胞 / TRAP染色 / 骨代謝 |
Outline of Final Research Achievements |
It has been reported that osteoclast progenitor cells (QOP), which remain in the quiescent phase, circulate in the body, rapidly accumulate locally during alveolar bone resorption, and differentiate into osteoclasts. Since osteoclasts appear in a relatively short period of time during alveolar bone resorption due to traumatic occlusion, QOP that has already undergone RANKL prestimulation in tissues other than periodontal tissues may be involved. . The purpose of this study was to investigate the involvement of QOP in alveolar bone resorption due to traumatic occlusion. QOP was found to be involved in alveolar bone resorption in mice with occlusal trauma. It was suggested that QOP accumulated locally during traumatic occlusion and was involved in rapid bone resorption.
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Academic Significance and Societal Importance of the Research Achievements |
歯周病は殆どの成人が罹患する可能性がある慢性炎症性疾患である。本研究では、この歯周病の増悪因子の一つである咬合性外傷のメカニズムの一端として、破骨細胞分化因子であるRANKL刺激を受けている破骨細胞前駆細胞が既に生体内で循環していることで、未分化の単球マクロファージ系の前駆細胞よりも破骨細胞への分化が迅速に進むことを示した。 外傷付与後、根分岐部歯根膜組織は硝子様変性し、分岐部中隔は穿下性の骨吸収が起こる。出される血管内皮増殖因子により、破骨細胞の形成が促進されることが示された。歯周病の増悪因子による組織破壊のメカニズムの一端が示されることで、歯周病治療のみならず学術的社会的意義を示せた。
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