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Nearly 100 million of the 170 million composite and amalgam restorations placed annually in the United States are replacements for failed restorations. The primary reason both composite and amalgam restorations fail is recurrent decay, for which composite restorations experience a 2.0–3.5-fold increase compared to amalgam. Recurrent decay is a pernicious problem—the standard treatment is replacement of defective composites with larger restorations that will also fail, initiating a cycle of ever-larger restorations that can lead to root canals, and eventually, to tooth loss. Unlike amalgam, composite lacks the inherent capability to seal discrepancies at the restorative material/tooth interface. The low-viscosity adhesive that bonds the composite to the tooth is intended to seal the interface, but the adhesive degrades, which can breach the composite/tooth margin. Bacteria and bacterial by-products such as acids and enzymes infiltrate the marginal gaps and the composite's inability to increase the interfacial pH facilitates cariogenic and aciduric bacterial outgrowth. Together, these characteristics encourage recurrent decay, pulpal damage, and composite failure. This review article examines key biological and physicochemical interactions involved in the failure of composite restorations and discusses innovative strategies to mitigate the negative effects of pathogens at the adhesive/dentin interface.