This paper summarizes the results of our studies of the pathogenesis and prevention of osteolysis around total joint arthroplasties. We focused on the polyethylene wear particles which are considered to be responsible for osteolysis. First, polyethylene particles were extracted with tissue digestion method and characterized using scanning electron microscopy. Second, interface tissues with adjacent bone were retrieved and histopathologically investigated with reference to cells on the bone surface. Finally, an animal model for osteolysis was created and possible prevention of osteolysis by improving the interface condition was evaluated.
A quantitative extraction of polyethylene particles demonstrated a significant difference in the number of particles between osteolysis positive and negative cases, whereas the size of particles was similar between these two groups. The critical number of particles for osteolysis was around 1×1010 particles/g tissue, and cellular reaction against phagocytosable particles which accumulated over this concentration could be the prerequisite for progression of osteolysis.
Histopathological examinations demonstrated that active bone formation, regarded as a repair process, was the most common 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 bone loss in osteolytic lesions.
The animal model for osteolysis indicated that progression of osteolysis depended on the integrity of the bone-implant interface. It was proposed that solid fixation of the prosthesis performed using a contemporary technique (e.g. improved cementing technique, hydroxyapatite coating) was beneficial to prevent particle migration and subsequent osteolysis.
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