Biologic reaction in interface tissue of aseptic loosening THA.

基质金属蛋白酶（MMPs）和金属蛋白酶组织抑制剂（TIMPs）在组织破坏和重塑中起重要作用。本研究采用逆转录聚合酶链反应（RT-PCR）技术。MMP-1、2、3、9和TIMP-1、2在界面组织中的mRNA表达。MMP-10 mRNA表达阴性。MMP-1和MMP-3 mRNA在乳腺癌组织中普遍表达。TIMP-2 mRNA表达较TIMP-1明显增强。我们认为MMPs和TIMPs在THA无菌性松动的发生发展过程中起着重要作用，并通过免疫组化、电镜和分子生物学技术对巨噬细胞的作用进行了研究。提取总RNA后，采用RT-PCR检测IL-1a、IL-1b、TNF α、IL-8、MIP-1a、MIP-1b和MCP-1 mRNA的表达。在界面组织中经常观察到巨噬细胞包围聚乙烯碎片和巨噬细胞吞噬碎片。还常见趋化因子mRNA的表达，表明这导致巨噬细胞募集到骨-骨水泥界面组织中。巨噬细胞的活化和炎性细胞因子如IL-1和IL-8的产生可能诱导界面组织的发育。从植入物释放的碎片似乎会导致巨噬细胞活化和炎症细胞因子的产生，从而诱导细胞募集到界面组织中。这种机制可能形成一个恶性循环，导致THA松动。

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.