Infections following osteosynthesis or total joint replacement, also known as “implant-associated posttraumatic osteomyelitis”, represent a major complication in orthopedic and trauma surgery. While the formation of bacterial biofilms on the implanted osteosynthesis materials is generally accepted as cause of the persistent infection, the molecular mechanisms leading to the progressive and destructive local inflammatory process and eventually to bone degradation, the osteolysis, have not been delineated. Here we provide evidence supporting the hypothesis that it is not the infection per se that causes tissue degradation and osteolysis, but rather the cytotoxic, proteolytic, and proinflammatory effector functions of cells of the host defense, particularly of the infiltrating polymorphonuclear neutrophils.
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