Riboflavin-mediated extracellular electron transfer enhances microbiologically influenced corrosion of 316L stainless steel by Enterococcus faecalis

316L stainless steel (SS) is widely used in medical implants due to its excellent mechanical properties. However, the increasing use of metallic implants has made microbiologically influenced corrosion (MIC) a significant safety concern, as it can release harmful metal ions in the body. Despite this risk, research on MIC behavior and mechanisms of 316L SS in the intestinal environment is limited. This study provides novel evidence that Enterococcus faecalis, an intestinal electroactive microorganism, contributes to MIC of 316L SS. MIC occurrence by E. faecalis was confirmed in nutrient-rich media and simulated intestinal fluid, with increased MIC rates under carbon starvation, suggesting an extracellular electron transfer (EET) mechanism. Electrochemical tests and material analyses supported a riboflavin-mediated EET mechanism, indicating that E. faecalis biofilms deteriorate the protective oxide layer on 316L SS through EET, with riboflavin accelerating corrosion. These findings identify EET as the primary mechanism by which E. faecalis enhances MIC in the gut, providing insights into intestinal corrosion risks and guiding the development of corrosion-resistant biomaterials.