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Titanium is a commonly utilized metal in joint arthroplasty and titanium debris induces the production of the pro\u2010inflammatory cytokine IL\u20101. To further elucidate the role of IL\u20101, this study examined the response of murine femora to the presence of titanium particles following implantation of an intramedullary rod in mice lacking the receptor for IL\u20101. We hypothesized that the inflammatory effects of wear debris on bone would be mitigated in IL\u20101R1 deficient mice with a resultant decrease in resorption. Femora receiving titanium particles demonstrated a marked inflammatory response in wild\u2010type mice with increased endocortical resorption, periprosthetic membrane formation, and significant histomorphometric changes. Femora exposed to titanium particles in the knockout mice also demonstrated osteolysis with irregular deposition of trabecular bone and increased cortical porosity. The persistence of inflammation and osteolysis, despite the lack of functional IL\u20101R1, suggests a multi\u2010factorial role for IL\u20101 in the proinflammatory cascade resulting from wear debris. This intramedullary murine model provides the ability to evaluate and quantify the proinflammatory cascade in an <jats:italic>in vivo<\/jats:italic> model approximating prosthesis failure. \u00a9 2007 Wiley Periodicals, Inc. 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