During joint inflammation, various reactive oxygen species (ROS) are present in the surrounding tissue and joint fluid. In the laboratory, hydrogen peroxide (H 2 O 2) is typically used to simulate inflammatory conditions, and media containing proteins and hyaluronic acid (HA) are employed to simulate joint synovial fluid. Electrochemical interactions between H 2 O 2 and HA in the presence of a CoCrMo surface are expected, since HA molecules contain redox-active moieties. We hypothesized that any redox reactions of these moieties with ROS will mitigate the oxidizing effect of H 2 O 2 on the CoCrMo surface, limiting the corrosion rate of the metal. Non-destructive electrochemical measurements (open circuit potential, linear polarization resistance and electrochemical impedance spectroscopy) were used to investigate the corrosion response of CoCrMo in synovial model fluid containing physiologically relevant concentrations of albumin proteins and hyaluronic acid, with and without H 2 O 2. Two different molarities of H 2 O 2 , 3 mM and 30 mM, were tested. While both molarities are within physiological limits, 3mM is well within the range HA could mitigate, whereas 30 mM is not. Contrary to our hypothesis, HA did not alleviate corrosion in 3 mM H 2 O 2 and even caused a corrosion increase in the case of 30 mM H 2 O 2. The decrease in corrosion resistance of the alloy may be attributed to the complexation of degenerated HA molecular chains with chromium ions released from the metallic surface, which are necessary to build a protective oxide film. This finding has clinical implications, suggesting that HA accelerates corrosion of CoCrMo implants in the presence of strong inflammation.