Department of Orthopedic Surgery, Montefiore Medical Center, 1250 Waters Place, New York, NY 10461, USA.
Nat Rev Rheumatol. 2011 Sep 6;7(10):600-8. doi: 10.1038/nrrheum.2011.128.
Joint replacement surgery is one of the success stories of modern medicine, restoring mobility, diminishing pain and improving the overall quality of life for millions of people. Unfortunately, wear of these prostheses over time generates debris, which activates an innate immune response that can ultimately lead to periprosthetic resorption of bone (osteolysis) and failure of the implant. Over the past decade, the biological interactions between the particulate debris from various implant materials and the immune system have begun to be better understood. The wear debris induces a multifaceted immune response encompassing the generation of reactive oxygen species and damage-associated molecular patterns, Toll-like receptor signaling and NALP3 inflammasome activation. Acting alone or in concert, these events generate chronic inflammation, periprosthetic bone loss and decreased osteointegration that ultimately leads to implant failure.
关节置换手术是现代医学的成功案例之一，为数百万患者恢复了活动能力，减轻了疼痛，提高了整体生活质量。不幸的是，这些假体随着时间的推移会产生磨损碎片，从而激活先天免疫反应，最终导致假体周围骨吸收（骨溶解）和植入物失效。在过去的十年中，人们开始更好地理解各种植入材料的颗粒磨损碎片与免疫系统之间的生物学相互作用。磨损碎片会引发多方面的免疫反应，包括活性氧和损伤相关分子模式的产生、Toll 样受体信号转导和 NALP3 炎性小体的激活。这些事件单独或协同作用，会引发慢性炎症、假体周围骨丢失和骨整合减少，最终导致植入物失效。
