1997 Fiscal Year Final Research Report Summary
The role of chemical mediators in the extruded intervertebral disc of lumbar spine
Project/Area Number |
08671658
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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 |
Orthopaedic surgery
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Research Institution | Kobe University |
Principal Investigator |
DOITA Minoru Kobe University, School of Medicine, Assistant Professor, 医学部, 助手 (60237170)
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Co-Investigator(Kenkyū-buntansha) |
HARADA Toshihiko Kobe University, School of Medicine, Lecturer, 医学部, 講師 (80228650)
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Project Period (FY) |
1996 – 1997
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Keywords | lumbar disc herniation / basic FGF / immunohistochemical study / Matrix metalloproteinase-1,3 / Interleukin-1 / cyclooxygenase-2 |
Research Abstract |
It has been recently reported that the spontaneous regression of the extruded disc materials of lumbar spine during the conservative treatment. The chemical mesiators released from those inflammatory cells, which are usually observed at the edge of extruded disc materials, may play important roles in producing matrix metalloproteases which in turn will change pain or regression of extruded disc materials. It is revealed that IL-1alpha, beta, TNF-alpha, matrix metalloproteases-1 and 3 (MMP-1,3) which play important roles in destroyin of the articular cartilage were detected in the at the edge of the extruded disc materials and IL-1alpha, beta, TNF-alpha stimulate the production of MMP-1,3 and TIMP in the disc materials. The inbalance of MMP-3 and TIMP may lead to the regression of the extruded disc materials. Prostaglandin E_2 (PGE_2) seems to play an important role in the development of the pain in inflammatory process. Cyclooxgenase-2 (COX-2) is reported to be one of the key enzymes in the process of this prostagladin synthesis. Histologically, COX-2 was localized not only in the inflammatory cells invaded into the herniated disc but also in the disc cells. This result indicates that COX-2 may play a role in the pathology of the lumbar disc herniation. By the RT-PCR,COX-2 mRNA was strongly expressed both IL-1beta and TNFalpha-stimulated disc cells for 6h incubation, while little COX-2 mRNA expression was detected in unstimulated cells. The results in this study reveal that the cells in the lumbar disc express COX-2 by the stimulation of the proinflammatory cytokines. It is, therefore, suggested that inflammatory stimulation might induce COX-2, which concerns to the pain induction of lumbar disc herniation pathophysiologically.
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