Fukunishi S
Hyogo College of Medicine, Department of Orthopedic Surgery, Japan.
Nihon Seikeigeka Gakkai Zasshi. 1995 Jan;69(1):53-63.
Aseptic loosening of a prosthesis is a hazardous problem after total joint replacement. In revision surgery, fibrous granulation tissue is always seen between the prosthesis and the bone or between the bone cement and the bone. We refer to this granulation tissue as the "bone-implant-interface" and it invades into the bone, resulting in osteolysis around the prosthesis. In order to investigate the histology of this granulation tissue and the mechanism of bone resorption, we produced an experimental model of the loosening of implants (alumina ceramic, PMMA, HDP) in the distal femoral condyles of rabbit. Each implant was inserted into the distal femoral condyle and connected with a Kirschner wire which was wired down to the tibia and fixed tightly to the tibial cortex. The implants could then be mobilized when the rabbits moved their knees. We called this a "micro-motion model". Besides doing this, we also developed a similar model in rabbit with ferritin-induced arthritis to investigate whether or not arthritis exacerbated the loosening of a prosthesis. The histological examinations of the bone-implant-interface in the micro-motion model in normal rabbit revealed three layers: a surface layer containing small round cells such as synovial lining cells, a middle layer containing many fibroblasts, macrophages and giant cells which phagocytize wear debris, and a deep layer adjacent to the bone containing many osteoclasts. In the models with ferritin-induced arthritis, more synovial lining cells were seen in the surface layer and more osteoclasts were seen in the deep layer. Also more osteolysis occurred around the implant in the arthritis model. In summary, the results suggested that the mechanical stress of motion stimulated the growth of synovial lining cells and macrophages in the bone-implant-interface, resulting in increased numbers of osteoclasts and in subsequent osteolysis.
人工关节置换术后,假体无菌性松动是一个棘手的问题。在翻修手术中,总是能在假体与骨之间或骨水泥与骨之间见到纤维肉芽组织。我们将这种肉芽组织称为“骨-植入物界面”,它侵入骨内,导致假体周围骨质溶解。为了研究这种肉芽组织的组织学及骨吸收机制,我们制作了兔股骨远端髁部植入物(氧化铝陶瓷、聚甲基丙烯酸甲酯、高密度聚乙烯)松动的实验模型。将每个植入物插入股骨远端髁部,并用克氏针连接至胫骨,紧紧固定于胫骨皮质。这样,当兔子活动膝关节时,植入物便可产生微动。我们称其为“微动模型”。除此之外,我们还在兔身上建立了铁蛋白诱导性关节炎的类似模型,以研究关节炎是否会加剧假体松动。对正常兔微动模型中骨-植入物界面的组织学检查显示有三层:表层含有小圆细胞,如滑膜衬里细胞;中层含有许多成纤维细胞、巨噬细胞和吞噬磨损碎屑的巨细胞;深层靠近骨,含有许多破骨细胞。在铁蛋白诱导性关节炎模型中,表层可见更多滑膜衬里细胞,深层可见更多破骨细胞。关节炎模型中植入物周围也出现了更多骨质溶解。总之,结果表明运动产生的机械应力刺激了骨-植入物界面滑膜衬里细胞和巨噬细胞的生长,导致破骨细胞数量增加,进而引起骨质溶解。