2022 Fiscal Year Final Research Report
Analysis of the periodontal pocket epithelium barrier destruction mechanism caused by dental calculus and periodontopathic bacteria
Project/Area Number |
20K18540
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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 |
Ziauddin SM 長崎大学, 医歯薬学総合研究科(歯学系), 客員研究員 (80868141)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 歯石 / 歯周病原細菌 / 上皮 |
Outline of Final Research Achievements |
It is known that calculus aggravates periodontal disease, but the mechanism has not been elucidated. In this study, we have clarified that calcium phosphate crystals in dental calculus activate the NLRP3 inflammasome to induce IL-1β production in macrophages, and induce inflammasome-dependent cell death called pyroptosis in gingival epithelial cells that enhances the permeability of the epithelial cell sheet. These results suggest that calculus particles are involved in the destruction of the gingival epithelial barrier and the exacerbation of inflammation in the periodontal tissue.
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Free Research Field |
歯周病学
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Academic Significance and Societal Importance of the Research Achievements |
歯周病患者では歯石沈着により症状が悪化することは広く知られているが、歯石はプラークリテンション因子と考えられ、歯石自体の為害作用はあまり知られていない。本研究では、歯石中のリン酸カルシウム結晶が、NLRP3インフラマソームの活性化を介して歯周組織の破壊と歯周組炎症拡大に関与することを示したものであり、学術的に重要な意味を持つと同時に、今後の新たな歯周病の診断、治療法の開発へ寄与することが期待される。
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