ABSTRACT
Particulate wear debris is generated continuously at bone-cement and boneimplant interfaces by the normal wear and corrosion of the prosthesis. These nonbiodegradable particles pose a serious problem for the longevity of orthopaedic implants. High levels of ultra high molecular weight polyethylene (UHMWPE), polymethylmethacrylate (PMMA; bone cement), titanium (Ti), titanium alloy (TiAlV), and cobalt-chromium alloy (Co-Cr) are present within the interfacial tissues retrieved from implant failures associated with osteolysis and aseptic loosening (1-3). The accumulation of ultra fine particulate wear debris results in a chronic inflammatory condition involving the persistent activation of proinflammatory cytokines and chemotactic cytokines as well as increased production of prostaglandin E2 (PE2) and matrix metalloproteinases (4-21). However, the intracellular events and signaling pathways by which particulate wear debris activates these proinflammatory mediators are largely unknown and only now beginning to be studied.
