Toll样受体及炎症小体在无菌性松动发病过程中的作用

无菌性松动是导致关节置换术失败的最常见的原因,磨损微粒诱导的骨溶解在其中起到了主导作用。磨损微粒产生后被假体周围的细胞吞噬,释放各种促炎因子和化学物质,抑制成骨细胞并激活破骨细胞,导致骨溶解。然而对于磨损微粒识别并激活细胞的具体机制仍不清楚。目前研究发现磨损微粒能激活Toll样受体和炎症小体,引起促炎因子的释放导致骨溶解的形成,提示Toll样受体及炎症小体可能参与了无菌性松动的发病过程。但是,对于Toll样受体是如何被激活,以及TLR信号通路与下游信号通路之间是如何相互联系等问题,目前仍未得到明确的解释。未来进一步探讨不同材料的磨损微粒激活Toll样受体和炎症小体的机制以及目前的临床药物能否针对Toll样受体或炎症小体发挥治疗作用等将有助于阐明人工关节假体无菌性松动的发病机制。

Role of Toll-like receptors and inflammasome in aseptic loosening

Aseptic loosening, ascribes to particle-induced osteolysis, is the most common reason for total joint arthroplasty failure. Wear particles, liberated from the surface of prostheses, mediate the expression of inflammatory cytokines in macrophages and increase the osteoclastogenesis. However, it remains unclear how macrophages can recognize wear particles and be induced by wear particles. Recently, a number of studies have demonstrated that Toll-like receptors and inflammasome may play a critical role in osteolysis. However, the mechanism of activation of Toll-like receptors and the relationship between TLR pathway and downstream signaling pathways still remain unclear. It will be beneficial to understand the pathogenesis of aseptic loosening by exploring these mechanisms. This article highlights the role of Toll-like receptors and inflammasome in aseptic loosening, which is helpful to the development of therapies that prevent wear particle-induced aseptic loosening.