| Project/Area Number |
10671389
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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 |
Orthopaedic surgery
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
KATO Yoshiharu Faculty of Medicine, Tokyo Women's Medical University, 医学部, 助教授 (00143850)
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| Co-Investigator(Kenkyū-buntansha) |
WADA Hiroyoshi Faculty of Medicine, Tokyo Women's Medical University, 医学部, 助手 (80287416)
ITOH Shunichi Faculty of Medicine, Tokyo Women's Medical University, 医学部, 助手 (10307580)
久保田 元也 東京女子医科大学, 医学部・整形外科, 助手 (20246581)
金谷 幸一 東京女子医科大学, 医学部, 助手 (30277222)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2000: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Renal failure / Hemodialysis / Bone histomorphometry / Renal Osteodystrophy / Interleukin-1β / Destructive Spondyloarthropathy / β2-microglobulin / Gene Polymorphism / 慢性腎不全 / 破壊性脊椎骨関節症 / VitD3受容体 / ApoE遺伝子 / ビタミンD受容体 / ApoE / Hemodyalysis / 骨形能計測 / Uit D受容体 |
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| Research Abstract |
We evaluated 51 chronic renal failure and hemodialysis patients, who had orthopaedic surgery, by bone morphometry, cytokine expression and gene polymorphism. In bone morphometry these patients were histologically classified into three groups ; and osteitis fibrosa type, aplastic type, and osteomalacia type. Osteitis fibrosa demonstrates high turnover bone, and typical characteristic X-ray findings (rugger-jersy appearance etc.). In destructive spondyloarthropathy (DSA) patients aplastic type is more than osteitis fibrosa type and osteomalacia type. In RT-PCR cytokine studies IL- 1 β was clearly expressed in only osteitis fibrosa group (high turnover bone), and not control and other types. This finding indicates that this cytokine induce cell differentiation, growth and activity of bone forming cells in high turnover bone. We postulated that amyloid deposit (β2-microglobulin) may be responsible for the induction of DSA, and spinal osteoporosis may be responsible for the progression of DSA.We examined apoprortein E gene polymorphism type and vitamin D receptor gene polymorphism for gene predisposition of DSA.In DSA patients E3/3 type (72.5%) in apoprortein E gene polymorphism type and bb type (64.7%) in vitamin D receptor gene polymorphism are most frequent than other types, and the patients with E3/3 and bb may be related to DSA onset and progression.
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