BackgroundCobalt-chromium-molybdenum (CoCrMo) and titanium alloys have been used for orthopaedic implants for decades. However, recent evidence has shown that inflammatory cell-induced corrosion (ICIC) can damage these metal alloys. This study aimed to investigate the mechanisms of ICIC by coculturing macrophages with lymphocytes. We hypothesized that macrophages would be able to alter the surface oxide layer of CoCrMo and titanium alloy (Ti6Al4V) disks, with greater oxide layer damage occurring in groups with a coculture compared to a macrophage monoculture and in groups with inflammatory activators compared to nonactivated groups. MethodsMurine macrophages were cultured on American Society for Testing and Materials F1537 CoCrMo and F136 Ti6Al4V disks for 30 days and activated with interferon gamma and lipopolysaccharide. Interferon gamma and lipopolysaccharide were added to the culture medium to simulate local inflammation. Macrophages were either cultured alone or in a coculture with T helper lymphocytes. After the 30-day experiment, scanning electron microscopy was used to examine the disk surfaces, and oxide levels were found using energy dispersive x-ray spectroscopy. ResultsPitting features consistent with previous reports of ICIC were found on disks cultured with cells. Both CoCrMo and Ti6Al4V disks had significantly lower oxide levels in all groups with cells compared to control groups with no cells (P < .01). Additionally, CoCrMo disks had significantly lower oxide levels when cultured with activated macrophages and lymphocytes compared to nonactivated macrophages alone (P < .001), activated macrophages alone (P < .01), and nonactivated macrophages and lymphocytes (P < .05). No differences in the oxide levels were found among the Ti6Al4V groups. ConclusionsThis study demonstrates the ability of macrophages to alter the surface chemistry of commonly used orthopaedic alloys. We found that the addition of lymphocytes and a simulated local inflammatory response may contribute to the ICIC of CoCrMo implants.