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[The bone-implant-interface: an experimental study on the effects of micro-motion].

作者信息

Fukunishi S

机构信息

Hyogo College of Medicine, Department of Orthopedic Surgery, Japan.

出版信息

Nihon Seikeigeka Gakkai Zasshi. 1995 Jan;69(1):53-63.

PMID:7699298
Abstract

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.

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