| Project/Area Number |
15592050
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
補綴理工系歯学
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
MAEKAWA Kenji OKAYAMA UNIVERSITY, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Assistant Professor, 大学院・医歯学総合研究科, 講師 (20304313)
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| Co-Investigator(Kenkyū-buntansha) |
FUJISAWA Takuo OKAYAMA UNIVERSITY, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Research Assistant, 大学院・医歯学総合研究科, 助手 (20325096)
KUBOKI Takuo OKAYAMA UNIVERSITY, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Professor, 大学院・医歯学総合研究科, 教授 (00225195)
UEHARA Junji OKAYAMA UNIVERSITY, University hospital of Medicine and Dentistry, Research Assistant, 医学部・歯学部附属病院, 助手 (10379836)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2003: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Osteoarthritis / TNFα / sTNFR-I,II / 潰瘍壊死因子α / 変形性顎間節症 / 腫瘍壊死因子 / 可溶性レセプター |
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| Research Abstract |
In this study, we tried to confirm soluble tumor necrosis factor receptor(sTNFR)-I,II concentrations in synovial fluids of osteoarthritic temporomandibular joint (OA) and to investigate the expression changes of sTNFR-I,II in the articular chondrocytes under an osteoarthritis-mimicking condition.
1.sTNFR-I and -II concentrations were higher in the synovial fluids from OA patients than from asymptomatic controls.
2.sTNFR-I concentration was higher than sTNFR-II concentration in the synovial fluids from both of patients and asymptomatic controls.
3.sTNFR-I concentration in the synovial fluids was significantly related to the OA level.
4.Higher sTNFR-II concentration in the synovial fluids was associated with less pain and less restricted range of mouth opening in the osteoarthritic patients.
5.In the knee osteoarthritis rat model, both of TNFR-I and TNFR-II were found at the knee joint chondrocyte of arthritic side and control side, and in the arthritic side both of receptors were up-regulated.
6.IL-1β and/or TNFα addition to the culture medium up-regulated tnfr-I,-II gene expression levels of the cultured chondrocytes and specifically sTNFR-II protein concentration in the cultured medium.
Since IL-1β and/or TNFα addition to the culture medium up-regulated tnfr-II gene expression levels of the cultured chondrocytes and sTNFR-II protein concentration in the cultured medium, observed sTNFR-II up-regulation in the synovial fluids of the osteoarthritic patients could reflect the protective chondrocyte metabolism of the osteoarthritic joint. Even in the osteoarthritic joints, sTNFR-II could modulate inflammation and destruction of the temporomandibular articular tissues.
Therefore, novel therapies may include agents that specifically mimic the anti-inflammatory feedback mechanism of sTNFR-II in vivo. We speculate that injection into temporomandibular joint with Etanercept, a potent inhibitor of TNFα, will be effective treatment for OA.
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