Wear and osteolysis in total joint replacements

Abstract

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 1010 particles/g tissue and the cellular reaction against phagocytosable panicles 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.