| Project/Area Number |
14571843
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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 |
FUJISAWA Takuo Okayama University, Graduate School of Medicine and Dentistry, Research Associate, 大学院・医歯学総合研究科, 助手 (20325096)
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| Co-Investigator(Kenkyū-buntansha) |
TAKIGAWA Masaharu Okayama University, Graduate School of Medicine and Dentistry, Professor, 大学院・医歯学総合研究科, 教授 (20112063)
NISHIDA Takashi Okayama University, Graduate School of Medicine and Dentistry, Research Associate, 大学院・医歯学総合研究科, 助手 (30322233)
KUBOKI Takuo Okayama University, Graduate School of Medicine and Dentistry, Professor, 大学院・医歯学総合研究科, 教授 (00225195)
MAEKAWA Kenji Okayama University, Graduate School of Medicine and Dentistry, Assistant Professor, 大学院・医歯学総合研究科, 講師 (20304313)
矢谷 博文 岡山大学, 大学院・医歯学総合研究科, 教授 (80174530)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Osteoarthritis / Mechanical Stress / Gene Therapy / Articular Cartilage / Cartilage Degradation / Apoptosis / Nitric Oxide / 軟骨細胞 / NO / 細胞増殖 / 細胞分化 / 結合組織成長因子 |
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| Research Abstract |
The purposes of this research are to clarify the mechanism of cartilage degradation in osteoarthritis (OA) and to investigate the possibility of gene therapy for articular cartlige restoration using connective tissue growth factor (CTGF).
First, we investigated the effects of CTGF/Hcs24 transduced by recombinant adenoviruses on the rabbit articular cartilage (RAC) cells in vitro. When RAC cells were infected with adenoviruses containing the CTGF/Hcs24 gene, RAC cells expressed CTGF/Hcs24 mRNA and produced CTGF/Hcs24 protein. RAC cells synthesized more proteoglycan than the control cells. These results suggest that CTGF is useful factor for cartilage repair.
Second, we establish a genuine mechanical-stress-induced OA model of the rabbit TMJ. In the experimental rabbits, repetitive forced jaw opening (RFJO) 3 hours/day for 5 days was applied. By histological assessment of the TMJ articular tissues, partial eburnation of the articular cartilage, reactive marginal proliferation of the articular cartilage chondrocytes and nested proliferation of chondrocytes in the subchondral bone area were observed at 7 days after the RFJO period. Furthermore, apoptotic chondrocytes were observed in the cartilage degradation area at 7 days after the RFJO period. And nitrotyrosine, a marker of NO production, and MMP-3, a key factor of cartilage ECM degradation, were observed where chondrocyte apoptosis was evident. These results suggest the RFJO protocol without any surgical intervention can induce evident OA-like lesions in the rabbit TMJ, and cartilage degradation in OA may be induced via chondrocytes apoptosis. This OA model may greatly contribute to the elucidation of the cartilage degradation mechanism in TMJ OA.
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