| Budget Amount *help |
¥4,300,000 (Direct Cost: ¥4,300,000)
Fiscal Year 1996: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1995: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Research Abstract |
It had been clearly demonstrated that matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase (TIMPs) had important roles for tissue destruction and remodeling. we used the reverse-transcriptinal polymerase chain reaction (RT-PCR) for this study. We could detect the mRNA of MMP-1,2,3,9 and TIMP-1,2 in interface tissue. The mRNA of MMP-10 could not be detected. MMP-1 and MMP-3mRNA were observed commonly. TIMP-2mRNA were well observed, compared to TIMP-1. These observations may indicated all four enzymes cooperatively caused the undesirable bone loss around implants, and consequently resulted in failed THA.We considered that the MMPs and TIMPs play one of the critical roles for the progression of aseptic loosening of THA.Also the roles of macrophages was assessed by immunohistochemistry, electron microscopy, and molecular biological techniques. After extraction of total RNA,we used the RT-PCR to examine the expression of mRNA for IL-1a, IL-1b, TNFa, IL-8, MIP-1a, MIP-1b and MCP-1. Polyethylene debris surrounded by macrophages and phagocytosis of debris by macrophages were frequently observed in the interface tissue. Expression of chemokine mRNAs was also commonly seen, suggesting that this led to recruitment of macrophages into the bone-cement interface tissue. Macrophage activation and the production of inflammatory cytokines like IL-1 and IL-8 might induce the development of interface tissue. Debris released from implants appear to causes activation of macrophages and the production of inflammatory cytokines that induce cellular recruitment into interface tissue. This mechanism might form a vicious cycle that aggravates THA loosening.
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