2020 Fiscal Year Final Research Report
Elucidation of the mechanism of tertiary dentin formation in pulp tissue using MMP-20 knockout mice
| Project/Area Number |
19K18995
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 57030:Conservative dentistry-related
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2019-04-01 – 2021-03-31
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| Keywords | 歯髄 / 第三象牙質 |
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| Outline of Final Research Achievements |
Since the risk of tooth loss increases dramatically after pulpotomy and is directly related to healthy life expectancy, direct pulp capping to maintain pulp activity is extremely important. On the other hand, although it is an important procedure, its success rate is low and it is an issue that needs to be improved.
In this research, we conducted an experiment using MMP-20-deficient mice based on our previous research results to develop a new therapeutic agent based on the wound healing mechanism of dental pulp to improve the success rate of direct pulp capping. However, contrary to our expectation, MMP-20 is not essential for the formation of tertiary dentin. We evaluated the effect of rapamycin, an inhibitor of mTOR, in the model, and found that the repair dentin formation was reproducibly inhibited.
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| Free Research Field |
保存修復学
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| Academic Significance and Societal Importance of the Research Achievements |
歯髄を失うと歯を喪失するリスクが上昇し, ひいてはQOLや健康寿命に直結する問題であることが示されており,歯髄の活性を維持し治癒に導く直接覆髄は極めて重要な処置である.
一方, 直接覆髄の成功率はあまり高くなく, 現在用いられている直接覆髄剤が歯髄の創傷治癒機転に基づく材料ではないことは解決すべき課題である. 本研究では mTOR分子を阻害するラパマイシンを投与することで, 歯髄の創傷治癒が再現性をもって阻害された. これらの知見は歯髄炎に対する分子生物学的な標的としての可能性を示すとともに先天的な象牙質形成不全や知覚過敏などに対する新たな治療戦略を基盤構築につながるものである.
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