“颗粒病”中自稳机制的研究进展

Research progress of homeostatic mechanisms in the periprosthetic osteolysis after arthroplasty

目前诸多研究表明,与假体磨屑相关的炎症反应的触发和放大机制在假体周围多种来源的炎症细胞反应中发挥着重要作用,最终结局导致骨吸收超过骨生成过程.但实际上,炎症反应是一个高度自我调节的过程,为阻止假体周围骨组织的继发性损伤,炎症反应过程同时伴有组织保护反应和再生机制的启动.各种不同的细胞因子、趋化因子、激素和特定的细胞群(包括巨噬细胞、树突状细胞和干细胞等)都在试图平衡和保护组织结构并减少炎症反应.局部组织自稳机制的失平稳可能是假体磨屑导致假体周围骨溶解的理论基础.因此,为开辟新的研究方向和潜在的治疗策略,未来的研究方向应关注假体周围骨溶解过程中局部组织的自稳机制方面.

Numerous studies provide detailed insight into the triggering and amplification mechanisms of the inflammatory response associated with prosthetic wear particles,promoting final dominance of bone resorption over bone formation in multiple bone multicellular units around an implant. In fact,inflammation is a highly regulated process tightly linked to simultaneous stimulation of tissue protective and regenerative mechanisms in order to prevent collateral damage of periprosthetic tissues. A variety of cytokines,chemokines,hormones and specific cell populations,including macrophages,dendritic and stem cells,attempt to balance tissue architecture and minimize inflammation. In this line of thinking,periprosthetic osteolysis after arthroplasty can be resulted from,at least partially,the failure of local tissue homeostatic mechanisms. As a result,we envision focusing current research on homeostatic mechanisms in addition to traditional efforts to elucidate details of pro-inflammatory/pro-osteolytic pathways. We believe this approach could open newavenues for research and potential therapeutic strategies.