1996 Fiscal Year Final Research Report Summary
Biologic reaction in interface tissue of aseptic loosening THA.
Project/Area Number |
07457330
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Orthopaedic surgery
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Research Institution | Nagoya University |
Principal Investigator |
ISHIGURO Naoki Nagoya University School of Medicine, Lecturer, 医学部, 講師 (20212871)
|
Co-Investigator(Kenkyū-buntansha) |
IWAHORI Yusuke Nagoya University School of Medicine, Assistant, 医学部, 医員
IWATA Hisashi Nagoya University School of Medicine, Professor, 医学部, 教授 (90023796)
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Project Period (FY) |
1995 – 1996
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Keywords | THA / cytokines / macrophage / TIMP / MMP / interface tissue |
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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Research Products
(10 results)