The success of total joint replacements has led to consistent growth in the use of arthroplasty in progressively younger patients. However, more than 10 percent of patients require revision surgeries due to implant failure caused by osteolytic loosening. These failures are classified as either aseptic or septic and are associated with the presence of particulate wear debris generated by mechanical action between implant components. Aseptic loosening results from chronic inflammation caused by activation of resident immune cells in contact with implant wear debris. In contrast, septic loosening is defined by the presence of chronic infection at the implant site. However, recent findings suggest that subclinical biofilms may be overlooked when evaluating the cause of implant failure, leading to a misdiagnosis of aseptic loosening. Many of the inflammatory pathways contributing to periprosthetic joint infections are also involved in bone remodeling and resorption. In particular, wear debris is increasingly implicated in the inhibition of the innate and adaptive immune response to resolve an infection or prevent hematogenous spread. This review examines the interconnectivity of wear particle- and infection-associated mechanisms of implant loosening, as well as biomaterials-based strategies to combat infection-related osteolysis.

全关节置换术的成功导致越来越年轻的患者使用关节置换术的持续增长。然而，由于溶骨性松动导致种植体失败，超过 10% 的患者需要进行翻修手术。这些故障被归类为无菌或脓毒症，并且与植入部件之间的机械作用产生的颗粒磨损碎片的存在有关。无菌性松动是由与植入物磨损碎片接触的常驻免疫细胞激活引起的慢性炎症引起的。相比之下，脓毒性松动的定义是植入部位存在慢性感染. 然而，最近的研究结果表明，在评估种植体失败的原因时可能会忽略亚临床生物膜，从而导致误诊为无菌性松动。许多导致假体周围关节感染的炎症通路也参与骨重塑和吸收。特别是，磨损碎片越来越多地参与抑制先天性和适应性免疫反应以解决感染或防止血行传播。本综述研究了磨损颗粒和感染相关植入物松动机制的相互联系，以及基于生物材料的对抗感染相关骨溶解的策略。