| Project/Area Number |
16K11837
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Periodontology
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| Research Institution | Nagasaki University |
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Principal Investigator |
UKAI Takashi 長崎大学, 病院(歯学系), 准教授 (20295091)
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| Co-Investigator(Kenkyū-buntansha) |
原 宜興 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (60159100)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 咬合性外傷 / 破骨細胞 / 骨細胞 / HMGB1 / 外傷性咬合 / マウス / 骨吸収 / アポトーシス / HMGB-1 / RANKL |
|---|
| Outline of Final Research Achievements |
When the tooth is subjected to a strong traumatic force such as bad occlusal condition, the bone around the tooth is likely to be resorbed. This is also one of the factors that exacerbate periodontal disease. In this study using mice, when traumatic force was applied to teeth, cells in the periodontal ligament which is the tissue surrounding the teeth, and osteocytes in the bone, were released the high mobility group box-1 (HMGB1) when they were damaged. It was confirmed that the expression of increased. When this HMGB1 was suppressed, bone resorption could be inhibited, albeit slightly.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の研究で歯に外傷力が加わった場合の骨吸収メカニズムの一端を明らかにすることができた。また、HMGB1を抑制することで骨吸収を抑制できたことより、これまでとは違うアプローチでの歯周病治療の治療薬の開発に応用可能ではないかと考えられる。また、同じく骨吸収を引き起こす関節リウマチや骨粗鬆症などの疾患の治療にも応用できる可能性があり、今後の研究の発展が期待される。
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