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Ultra high molecular weight polyethylene (UHMWPE) particles were introduced into established air pouches on BALB\/c mice, followed by implantation of calvaria bone from syngeneic littermates. Macrophages were depleted by the intraperitoneal injection of clodronate liposome (2 mg) 2 days before bone implantation and re\u2010injection every 3 days (1 mg) until the sacrifice of the mice. Mice without clodronate liposome therapy or treated with empty liposome as well as mice injected with saline alone were included in this study as controls. Pouch tissues were collected 14 days after bone implantation for molecular and histology analysis. Our findings indicated that (1) macrophage depletion in clodronate\u2010liposome\u2010treated mice was achieved, as illustrated by F4\/80 immunostaining in both pouch and spleen tissues; (2) clodronate\u2010liposome treatment significantly reduced UHMWPE\u2010induced tissue inflammation, with diminished pouch membrane thickness, reduced inflammatory cellular infiltration, and lowered interleukin 1\u03b2 (IL\u20101\u03b2) and tumor necrosis factor \u03b1 (TNF\u03b1) expression; (3) clodronate\u2010liposome treatment markedly reduced the number of TRAP<jats:sup>+<\/jats:sup>cells in pouch tissues and protected against bone collagen depletion. In conclusion, this study demonstrates that macrophage depletion using clodronate\u2010liposome reduces UHMWPE particle\u2010induced inflammatory osteolysis. This observation supports the hypothesis that macrophages contribute to the severity of UHMWPE particles induced inflammatory osteolysis, and suggest that macrophage depletion represents a viable therapeutic approach to the prevention and treatment of patients with aseptic loosening. \u00a9 2007 Wiley Periodicals, Inc. 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