Joint replacement surgery is the gold-standard therapeutic approach to treat patients with end-stage hip and knee arthritis, providing pain relief and joint function recovery. Despite the improvements in implant design and surgical techniques, revisions after total joint replacement are expected to grow. The periprosthetic inflammation, featured by the sustained inflammatory response to the implant debris, elicits the activation of osteoclasts and consequent periprosthetic osteolysis (PPOL), ultimately leading to implant aseptic loosening, which is the most common cause of long-term implant failure. There are currently no effective strategies to control periprosthetic inflammation, and long-term implant survival remains a major challenge in orthopedics. A broad knowledge of the mechanisms underlying the biological response to implant debris would support the development of novel and effective pharmacological strategies to manage PPOL and promote implant lifespan. In this review, a detailed description of the cellular and the molecular mechanisms underlying the biological response to implant debris is provided, highlighting the most recent findings. Furthermore, we reviewed novel therapeutic strategies that are being investigated to prevent inflammatory periprosthetic osteolysis.

关节置换手术是治疗晚期髋部和膝部关节炎患者的金标准治疗方法，可减轻疼痛并恢复关节功能。尽管植入物设计和手术技术有所改进，但全关节置换后的修订预计会增加。假体周围的炎症以对植入物碎片的持续炎症反应为特征，引起破骨细胞的活化和随后的假体周围溶骨（PPOL），最终导致植入物无菌性松动，这是长期植入物失败的最常见原因。当前没有有效的策略来控制假体周围的炎症，并且假体的长期存活仍然是整形外科的主要挑战。对植入物碎片的生物反应的潜在机制的广泛了解将支持开发新颖有效的药理策略，以管理PPOL和延长植入物的寿命。在这篇综述中，提供了对植入物碎片的生物学反应基础的细胞和分子机制的详细描述，突出了最新发现。此外，我们审查了正在研究的预防炎症性假体周围骨溶解的新型治疗策略。