ABSTRACT
New England Baptist Bone and Joint Institute, Rheumatology and Metabolic Bone Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston,
Massachusetts, U.S.A.
INTRODUCTION
Aseptic loosening is the major cause of long-term failure of orthopaedic implants. Particulate wear debris released from the implants contributes to the loosening process by activating macrophages, inducing peri-implant granulomatous inflammation, and subsequently leading to osteolysis. Numerous in vitro models have demonstrated the capacity of wear particles to stimulate the release of soluble proinflammatory cytokines with the ability to induce local osteoclastic bone resorption. Recent observations have demonstrated that the binding of bacterial endotoxins, or lipopolysaccharides (LPS) to particulate wear debris, can significantly modulate the pattern of cell responses in in vitro models (1-4). These findings might suggest a potential role of LPS in the pathogenesis of aseptic loosening after total joint replacements.
