Inflammasome activation by dental calculus and prevention of periodontal tissue destruction using inflammasome inhibitor
Project/Area Number |
16K11836
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Periodontology
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Research Institution | Nagasaki University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
宮崎 敏博 長崎大学, 医歯薬学総合研究科(歯学系), 准教授 (10174161)
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: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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Keywords | 歯周炎 / 歯石 / インフラマソーム / 結晶 / 歯学 |
Outline of Final Research Achievements |
Dental calculus is known to be a risk factor for periodontitis. We previously found that calcium phosphate crystal in dental calculus activates a protein complex called nucleotide-binding domain leucine-rich repeat-containing protein 3 (NLRP3) inflammasome and induce IL-1β production in macrophages. In this study, we have shown that NLRP3 inflammasome is activated in the periodontal tissue of periodontitis patients, and dental calculus induces inflammasome dependent cell death called pyroptosis in gingival epithelia cells and these NLRP3 inflammasome activation can be restrained by inflammasome inhibitors.
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Academic Significance and Societal Importance of the Research Achievements |
歯石の病原性については古くから知られているが、これまでプラークリテンション因子としての意義が強調されてきた。本研究では、歯石中のリン酸カルシウム結晶がNLRP3インフラマソームを活性化することによる病原性を明らかにし、上皮細胞のピロトーシス誘導による付着の喪失の新たなメカニズムを解明した。これらは、スケーリングや抗菌薬の投与により無菌的になった根面においても、歯石が歯周組織の修復および再生を阻害することを意味する。歯石による NLRP3インフラマソームの活性化をインフラマソーム阻害薬で抑制することができれば、歯周炎の新たな予防薬や治療法の開発につながることが期待される。
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Report
(5 results)
Research Products
(61 results)
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[Journal Article] Localization and expression pattern of amelotin, odontogenic ameloblast-associated protein and follicular dendritic cell-secreted protein in the junctional epithelium of inflamed gingiva.2016
Author(s)
Nakayama Y, Kobayashi R, Matsui S, Matsumura H, Iwai Y, Noda K, Yamazaki M, Kurita-Ochiai T, Yoshimura A, Shinomura T, Ganss B, Ogata Y.
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Journal Title
Odontology
Volume: -
Issue: 3
Pages: 329-337
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Salivary pathogen and serum antibody to assess the progression of chronic periodontitis: a 24-mo prospective multicenter cohort study2016
Author(s)
Morozumi T, Nakagawa T, Nomura Y, Sugaya T, Kawanami M, Suzuki F, Takahashi K, Abe Y, Sato S, Makino-Oi A, Saito A, Takano S, Minabe M, Nakayama Y, Ogata Y, Kobayashi H, Izumi Y, Sugano N, …., Yoshimura A, Hara Y, ….
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Journal Title
Journal of Periodontal Research
Volume: 印刷中
Issue: 6
Pages: 768-778
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Presentation] Hydroxyapatite crystal particles induce cell death in the HSC-2 oral epithelial cell line2017
Author(s)
Ziauddin SM, A. Yoshimura, J L Montenegro Raudales, Y. Ozaki, T. Kaneko, K. Higuchi, C. Shiraishi, A. Kuramoto, Y. Takamori, Y. Yamashita, H. Kobayashi, T. Ukai, Y. Hara
Organizer
16th International Congress of Periodontology of the International Academy of Periodontology
Related Report
Int'l Joint Research
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[Presentation] 炎症性骨吸収における破骨細胞形成への T 細胞と骨膜構成細胞の関与2017
Author(s)
小林弘樹,鵜飼 孝,中村弘隆,高森(藏本)明子,高森雄三,山下恭徳,泉 聡史,小山美香,白石千秋,吉村篤利,原 宜興
Organizer
日本歯科保存学会2017年度春季学術大会
Related Report
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