Abstract

In vivo retrievals of metallic orthopedic implants have shown selective dissolution of Ti-6Al-4V, where the vanadium-rich β phase preferentially corrodes from the surface. This damage, typically observed in crevices, is not directly caused by wear mechanics and the underlying electrochemical mechanism remains poorly understood. Previous studies show that fretting corrosion can cause negative potential drops, resulting in a decrease in surface oxide passivation resistance and the electrochemical generation of reactive oxygen species (ROS) at metallic surfaces. In this study, we combine cathodic activation and hydrogen peroxide to induce selective dissolution in vitro. After a 600 s -1 V hold and 4 h recovery in 20 °C 1 M H2O2 solution, the Ti-6Al-4V β phase was preferentially dissolved. An initial activation threshold of -0.5 V induced a significant increase in β dissolution (p = 0.000). Above this threshold, little selective dissolution occurred. In an Arrhenius-like fashion, decreasing solution concentration to 0.1 M required 72 h to generate β dissolution instead of 4 h at 1 M. Heating 0.1 M solution to body temperature (37 °C) resulted in a decrease in the time needed to replicate a similar level of β dissolution (>90%). Electrochemical impedance shows that both cathodic activation and inflammatory species are necessary to induce selective dissolution, where the combinatorial effect causes a significant drop in oxide passivation resistance from 106 to 102 (p = 0.000). Statement of significanceThough hip arthroplasties are considered a successful procedure, revision rates of 2–4% result in tens of thousands of additional surgeries within the United States, subjecting patients to increased risk of complications. Corrosion is associated with implant failure and retrieval studies show that titanium and its alloys can severely corrode in vivo in ways not yet duplicated in vitro. Here, we reproduce selective dissolution of Ti-6Al-4V β phase simulating key characteristics of in vivo degradation observed in orthopedic retrievals. We establish both cathodically activated corrosion, a relatively unexplored concept, and the presence of inflammatory species as prerequisites, furthering our understanding of this clinically relevant damage mode. We introduce an Arrhenius-based approach to assess the concentration-temperature-time interactions present.

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