2014 Fiscal Year Final Research Report
The role of lysine-specific gingipain in inflammatory bone loss in periodontitis.
Project/Area Number |
24592817
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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 |
Functional basic dentistry
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Research Institution | Showa University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
TAKAMI Masamichi 昭和大学, 歯学部, 教授 (80307058)
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Co-Investigator(Renkei-kenkyūsha) |
IMAMURA Takahisa 熊本大学, 大学院生命科学研究部, 准教授 (20176499)
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Research Collaborator |
AKIYAMA Tomohito 昭和大学, 歯学部, 助教 (90710319)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | 歯周病 / 破骨細胞 / プロテアーゼ |
Outline of Final Research Achievements |
Periodontitis is a chronic inflammatory disease accompanied by alveolar bone loss. Porphyromonas gingivalis, which plays a key role in the etiology of periodontitis, produces cysteine proteases called gingipains. Gingipains are classified into two groups based on their cleavage site specificity, i.e., Rgp and Kgp. We found that osteoclast differentiation induced by inflammatory cytokines such as TNF-α and IL-1β in co-cultures of mouse osteoblasts and bone marrow cells, whereas RgpB had no effect on osteoclast differentiation under the same experimental conditions. Osteoprotegerin (OPG), a protein that negatively regulates osteoclast differentiation, was degraded by Kgp. Kgp primarily cleaved death-domain-like region of OPG; the fragments containing RANKL-biding domain lost its binding capacity to RANKL. Our data suggests that degradation of OPG by Kgp is a crucial event in the progression of osteolysis in periodontitis.
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Free Research Field |
生化学
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