Pizzoferrato A, Stea S, Ciapetti G, Cenni E, Tarabusi C, Toni A
Laboratorio di Biocompatibilità dei Materiali da Impianto, Istituti Ortopedici Rizzoli, Bologna.
Chir Organi Mov. 1992 Oct-Dec;77(4):337-48.
Based on the results obtained in histological examinations carried out on periprosthetic tissues in a large series of cases of prosthetic hip joint explants, the authors analyze the cellular events that may occur in loosening phenomena as compared to what occurs in the paraphysiological repair process that is observed in the stable prosthesis. Like other authors, they believe that the principal role in the mechanism of loosening is played by macrophages which are recalled in a large number, at times together with multinucleate giant cells, at the bone-implant interface, after micromovements of the prosthesis and the formation of wear particles have occurred. The macrophages would be capable of favoring resorption of the periprosthetic bone tissue, producing areas of osteolysis in which the transmission of the mechanical stress of loading is modified. The ensuing prosthetic instability increases wear phenomena, causes a greater amount of osteolysis, and, in a vicious cycle, loss of the relationship between bone and implant, and, thus, prosthetic loosening. Finally, the authors report a hypothesis on the pathogenesis of the phenomenon, based on which non-physiological stress, associated with wear and eventually infection, leads to loosening.
基于对大量人工髋关节翻修病例的假体周围组织进行组织学检查所获得的结果,作者分析了与稳定假体中观察到的生理性修复过程相比,松动现象中可能发生的细胞事件。与其他作者一样,他们认为,在松动机制中起主要作用的是巨噬细胞,在假体发生微动并形成磨损颗粒后,大量巨噬细胞有时还会与多核巨细胞一起被募集到骨-植入物界面。巨噬细胞能够促进假体周围骨组织的吸收,产生骨溶解区域,其中负荷的机械应力传递会发生改变。随之而来的假体不稳定会增加磨损现象,导致更多的骨溶解,并在恶性循环中导致骨与植入物之间的关系丧失,进而导致假体松动。最后,作者报告了一种关于该现象发病机制的假说,在此基础上,与磨损并最终与感染相关的非生理性应力会导致松动。