Department of Orthopedics, The Affiliated Lianyungang Hospital of Xuzhou Medical University (The First People's Hospital of Lianyungang), Lianyungang, China.
Department of Geriatrics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Front Immunol. 2023 Oct 4;14:1274679. doi: 10.3389/fimmu.2023.1274679. eCollection 2023.
Joint replacement surgery is the most effective treatment for end-stage arthritis. Aseptic loosening caused by periprosthetic osteolysis is a common complication after joint replacement. Inflammation induced by wear particles derived from prosthetic biomaterials is a major cause of osteolysis. We emphasize that bone marrow-derived macrophages and their fusion-derived osteoclasts play a key role in this pathological process. Researchers have developed multiple intervention approaches to regulate macrophage/osteoclast activation. Aiming at wear particle-induced periprosthetic aseptic osteolysis, this review separately discusses the molecular mechanism of regulation of ROS formation and inflammatory response through intervention of macrophage/osteoclast RANKL-MAPKs-NF-κB pathway. These molecular mechanisms regulate osteoclast activation in different ways, but they are not isolated from each other. There is also a lot of crosstalk among the different mechanisms. In addition, other bone and joint diseases related to osteoclast activation are also briefly introduced. Therefore, we discuss these new findings in the context of existing work with a view to developing new strategies for wear particle-associated osteolysis based on the regulation of macrophages/osteoclasts.
关节置换手术是治疗终末期关节炎最有效的方法。假体周围骨溶解引起的无菌性松动是关节置换后的常见并发症。由假体生物材料衍生的磨损颗粒引起的炎症是骨溶解的主要原因。我们强调骨髓来源的巨噬细胞及其融合衍生的破骨细胞在这个病理过程中起着关键作用。研究人员已经开发了多种干预方法来调节巨噬细胞/破骨细胞的激活。针对磨损颗粒诱导的假体周围无菌性骨溶解，本综述分别讨论了通过干预巨噬细胞/破骨细胞 RANKL-MAPKs-NF-κB 通路调节 ROS 形成和炎症反应的分子机制。这些分子机制通过不同的方式调节破骨细胞的激活，但它们不是相互孤立的。不同机制之间也存在大量的串扰。此外，还简要介绍了与破骨细胞激活相关的其他骨骼和关节疾病。因此，我们在现有工作的背景下讨论这些新发现，以期基于巨噬细胞/破骨细胞的调节，为与磨损颗粒相关的骨溶解开发新的策略。
