Peri-implantitis is an immune-mediated biological complication that is attributed to bacterial biofilms on the implant surface. As both periodontitis and peri-implantitis have similar inflammatory phenotypes when assessed cross-sectionally, treatment protocols for peri-implantitis were modeled according to those used for periodontitis. However, lack of efficacy of antimicrobial treatments targeting periodontal pathogens coupled with recent discoveries from open-ended microbial investigation studies create a heightened need to revisit the pathogenesis of peri-implantitis compared with that of periodontitis. The tale of biofilm formation on intraoral solid surfaces begins with pellicle formation, which supports initial bacterial adhesion. The differences between implant- and tooth-bound biofilms appear as early as bacterial adhesion commences. The electrostatic forces and ionic bonding that drive initial bacterial adhesion are fundamentally different in the presence of titanium dioxide or other implant alloys vs mineralized organic hydroxyapatite, respectively. Moreover, the interaction between metal surfaces and the oral environment leads to the release of implant degradation products into the peri-implant sulcus, which exposes the microbiota to increased environmental stress and may alter immune responses to bacteria. Clinically, biofilms found in peri-implantitis are resistant to beta-lactam antibiotics, which are effective against periodontal communities even as monotherapies and demonstrate a composition different from that of biofilms found in periodontitis; these facts strongly suggest that a new model of peri-implant infection is required.
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