Wear and osteolysis in total joint replacements.
This presentation summarizes the results of our recent studies on the pathogenesis of osteolysis around total joint arthroplasties. First, interface tissues with adjacent bone were retrieved and histopathologically investigated with reference to the cells on the bone surface. Secondly, polyethylene particles were extracted with the tissue digestion method and characterized with scanning electron microscopy. Finally, an animal model for osteolysis was created and various interface conditions were compared concerning their resistance to particle migration. Histopathological examinations demonstrated that active bone formation, regarded as a repair process, was the commonest feature, even in revised cases. They also highlighted the role played by macrophages, not as cells producing inflammatory mediators which could activate osteoclasts, but as cells primarily responsible for the bone loss in osteolytic lesions. Among the particle species present, only polyethylene particles were shown to play a significant role in macrophage recruitment and subsequent osteolysis. A quantitative extraction of polyethylene particles showed a significant difference in the "number" of particles between osteolysis positive and negative cases whereas the "sizes" of particles were similar in these two groups. The critical number of particles for osteolysis was around 1 x 10(10) particles/g tissue and the cellular reaction against phagocytosable particles accumulated over this concentration may be the prerequisite for progression of osteolysis. The animal model for osteolysis indicated that the progression of osteolysis depends on the integrity of the bone-implant interface. We suggest that the solid fixation of the prosthesis performed by current techniques (e.g., improved cementing technique, hydroxyapatite coating) is beneficial for preventing particle migration and subsequent osteolysis.


CONCLUSIONS
Osteolysis induced by particulate wear debris from implant materials has been recognized as the major cause of long-term failure in total joint replacements. However, the development of preventive measures for this phenomenon has not been successful because the mechanism in which wear particles cause osteolysis is not quite clear. On the basis of results obtained in this study, we believe that the basic strategy for addressing the problem of osteolysis is to reduce the "number" of accumulated wear particles in the interface tissues. This could be achieved either by improving the materials or the geometry of the articulating counterface. Another possibility is to increase the integrity of the bone-implant interface to prevent particle migration. It is important to note that pre-clinical testing of materials and prosthetic designs should include an analysis of the characteristics of the particle generated (e.g., size and number). The widespread bone formation, even in revised cases, is encouraging in view of "conservative treatment" of aseptic loosening. Assuming that bone loss in aseptic loosening is not a remorseless process, some form of intervention, whether mechanical or pharmacological, might be possible to tip the balance more in favour of bone formation than resorption. A comprehensive understanding of the bone reactions in osteolysis, including the basic mechanisms of bone loss, shown in this study, are decisive for the development of preventive measures that may minimize the clinical impact of this phenomenon.
Kadoya
Y
Y
Department of Orthopedics, Osaka City University Medical School, Japan.
Kobayashi
A
A
Ohashi
H
H
D000818:Animals; D019644:Arthroplasty, Replacement, Hip / Q000009:adverse effects*; D019645:Arthroplasty, Replacement, Knee / Q000009:adverse effects*; D003343:Corrosion; D005260:Female; D006622:Hip Prosthesis / Q000009:adverse effects*; D006652:Histological Techniques; D006801:Humans; D007720:Knee Prosthesis / Q000009:adverse effects*; D008264:Macrophages / Q000648:ultrastructure; D008854:Microscopy, Electron; D010006:Osteoblasts / Q000648:ultrastructure; D010010:Osteoclasts / Q000648:ultrastructure; D010014:Osteolysis / Q000000981:diagnostic imaging / Q000209:etiology* / Q000473:pathology; D010316:Particle Size; D011817:Rabbits; D011859:Radiography