Clarification of pathosis of temporomandibular joint arthrosis : analysis of abnormal glycan in synovial fluid
Project/Area Number |
18592207
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Surgical dentistry
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Research Institution | Kanazawa Medical University |
Principal Investigator |
DEMURA Noboru (2007) Kanazawa Medical University, School of Medicine, Senior Assistant Professor (60188703)
高橋 基浩 (2006) 金沢医科大学, 医学部, 助手 (30329388)
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Co-Investigator(Kenkyū-buntansha) |
SEGAMI Natsuki KANAZAWA MEDICAL UNIVERSITY, School of Medicine, Professor (40148721)
KANEYAMA Keiseki KANAZAWA MEDICAL UNIVERSITY, School of Medicine, Senior Assistant Professor (50329380)
YOSHITAKE Yoshino KANAZAWA MEDICAL UNIVERSITY, School of Medicine, Associate Professor (00150764)
出村 昇 金沢医科大学, 医学部, 講師 (60188703)
|
Project Period (FY) |
2006 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
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Budget Amount *help |
¥3,980,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥480,000)
Fiscal Year 2007: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2006: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
Keywords | temporomandibular joint arthrosis / synovial fluid / protein level / abnormal glycans / 蛋白糖鎖 / 生化学的解析 |
Research Abstract |
Clinical and experimental studies were undertaken in order to elucidate the pathosis of temporomandibular joint arthrosis by means of analysis of abnormal glycan in svnovial fluid. Clinical research was measurement of total protein and pro-inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) and their receptors in synovial fluid as well as histological and immunohistochemical evaluation of the synovial tissue obtained arthroscopically. These data were statistically compared with signs and symptoms of the patients. The arthroscopic findings (synovitis, adhesion, degenerative change; scored 0-10) were also compared with total protein levels. The results showed that only the degree of synovitis detected arthroscopically had significant correlation with the concentration levels of total protein, IL-6 and IL-8 in synovial fluid. Histologically, the degree of synovitis in synovial tissue showed significant relationship with JE in 2 items (synovial lining cell layer and inflammatory cell infiltrat
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ion) of 3 items. The genetic investigation using PCR in order to clarify the presence of bacteria in synovial fluid of TMD, showed 76% of bacteria-positive joint in TMD, and completely negative in control joints. This result will expand the research to investigate the pathosis of TMD in future. On the other hand, the anchored disc observed on MRI in closed lock patients demonstrated lower protein levels than previously reported data in internal derangements. It indicated that decreased protein level lead from unknown pathology may produce the anchored phenomenon in normal disc position Experimentally, the animal model produced by giving extrinsic overloading by using spring coils showed mild to moderate degree of synovitis as well as increased protein levels in synovial fluid. These interesting results imply that the mechanical loading may be major cause of TMD and produce the similar protein levels in synovial fluid. These results suggest that protein levels including pro-inflammatory cytokine, degradation products increases for up-regulating the intra-capsular pathology in TMD (internal derangements). Probably, the presence of bacteria may be one of the main etiology of regulating the intra-articular inflammation. In the future, the details of protein composition should be elucidated for better understanding the TMD pathology, moreover to establish the effective treatment modalities. Less
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Report
(3 results)
Research Products
(20 results)