The replacement of cement with biological ingrowth systems for fixation has not resolved the problem of aseptic loosening nor that of osteolysis in association with metal and polyethylene wear debris. In order to investigate the role of wear debris in the failure of surface replacements, a histopathological study of ten titanium alloy porous-coated (PSR) and ten cobalt-chrome (Co-Cr) alloy cemented components was conducted. Wear-debris-laden histiocytes (metal and polyethylene) were associated with massive osteolysis in several of the PSR components, but bone loss in the cemented Co-Cr components was confined to localized areas adjacent to the cement membrane. The results of this study suggest that histiocytes activated by the ingestion of fine wear debris are responsible for bone loss. The mechanism of bone loss shown by this “model” is applicable to all joint replacement implant systems where wear debris is generated.