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The cellular response to trauma and infection was studied in a murine model of posttraumatic osteomyelitis. Osteoclast response differed markedly depending on whether infection with Staphylococcus aureus accompanied the bone trauma. In animals recovering from sterile trauma, osteoclastic activity that was limited to the damaged or dead bone fragments caused rapid elimination of all recognizable dead bone within 1 week. New bone was laid down in an orderly fashion. Animals with superimposed infection had an intense polymorphonuclear leukocyte response develop. Additionally, osteoclasts behaved as acute inflammatory responders with substantial activity at the margins of the infected site and at previously uninjured tibial cortex adjacent to the infection. Despite the exuberant osteoclast response, bony fragments were not resorbed (for at least 4 weeks after the trauma), that is, sequestra developed, and new bone was laid down over morphologically dead bone and on 7 the cortex (involucrum). When the inhibitory cytokine, interleukin 4 was given in a single dose with the bacterial inoculum, the osteoclast response was moderated with almost complete elimination of osteoclast activity at normal tibial cortex adjacent to the infected site. The limitation of osteoclastic activity did not impair the host's containment of bacterial growth.