Biologic reaction in interface tissue of aseptic loosening THA.

已有研究表明，基质金属蛋白酶(MMPs)及其组织抑制因子(TIMPs)在组织破坏和重塑中具有重要作用。我们使用逆转录-聚合酶链式反应(RT-PCR)进行研究。在界面组织中可检测到基质金属蛋白酶-1、2、3、9和TIMP-1、2的表达。未检测到基质金属蛋白酶-10mRNA的表达。主要观察到基质金属蛋白酶-1和基质金属蛋白酶-3mRNA的表达。与TIMP-1相比，TIMP-2mRNA表达明显增强。这些观察结果可能表明这四种酶协同作用导致种植体周围的不良骨丢失，从而导致THA失败。我们认为MMPs和TIMPs在THA无菌性松动的进展中起关键作用。此外，通过免疫组织化学、电子显微镜和分子生物学技术对巨噬细胞的作用进行了评估。提取总RNA后，用RT-PCR检测IL-1a、IL-1b、TNFa、IL-8、MIP-1a、MIP-1b和MCP-1的mRNA表达。界面组织中常可见被巨噬细胞包围的聚乙烯碎屑和巨噬细胞吞噬碎屑。趋化因子mRNAs的表达也很常见，这表明这导致巨噬细胞重新聚集到骨水泥界面组织中。巨噬细胞的激活和IL-1、IL-8等炎性细胞因子的产生可能诱导界面组织的发育。植入物释放的碎片似乎会导致巨噬细胞的激活和炎性细胞因子的产生，从而诱导细胞重新聚集到界面组织中。这种机制可能会形成恶性循环，加剧松动。

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.