Molecules absorbed on the surface of particulate wear debris may contribute to inflammatory reactions that lead to aseptic loosening of implants. Lipopolysaccharide (LPS), a bacterial endotoxin, can attach to many biomaterials and stimulate macrophages to secrete osteoclast-activating cytokines. We tested the adsorption of LPS by polyethylene particles in vitro and examined the biological effects of LPS absorption on bone remodeling around implants in vivo. Polyethylene particles were incubated in radiolabeled LPS solutions, and adsorption of LPS by the particles was quantified by radioassay. Because polyethylene particles are hydrophobic and less dense than water, they floated and clumped when incubated in a water solution of LPS, resulting in low adsorption of LPS. However, when particles were incubated in an ethanol solution of LPS, most of the LPS was adsorbed by the particles, and was resistant to washing with water. Triton X-100 (10%), however, effectively washed the LPS off the particles. In a rat model, the presence of polyethylene particles around the implant in the femoral canal decreased bone attachment to the implant at 6 weeks. Incubating the particles with LPS before implantation, or intermittent administration of LPS systemically, further decreased bone-implant attachment to similar extents, but had no effect on the bone density of the control side femurs. Our data indicate that polyethylene particles have high affinity for LPS, depending on many factors, especially the solvents of the LPS. Intermittent systemic administration of LPS affects bone remodeling but only occurs in the area containing polyethylene particles and titanium implants, supporting the hypothesis that the presence of polyethylene particles around implants can result in accumulation of LPS from exogenous sources. This may cause local levels of LPS that are high enough to affect bone remodeling around implants.