Tribochemical Degradation at the Implant-Abutment Interface and Its Implications for Marginal Bone Loss and Peri-Implant Mucositis: A Narrative Review.

The implant-abutment interface is the only non-osseointegrated junction of an implant-supported restoration and is continuously exposed to cyclic mechanical loading. Micromovement and fretting at this junction repeatedly disrupt the protective titanium dioxide film that confers corrosion resistance on titanium, so that mechanical wear and electrochemical corrosion act together in a process termed tribocorrosion. The resulting release of titanium ions and particulate debris into the peri-implant environment has been proposed as a contributor to peri-implant inflammation and marginal bone loss, yet its clinical significance remains uncertain. This narrative review synthesizes recent evidence on tribocorrosion at the implant-abutment interface, emphasizing repetitive passive-film disruption as the central mechanism of titanium degradation and the oral environment's modulating influence. The literature was retrieved from PubMed, prioritizing publications from the last five years and including narrative and systematic reviews, in vitro and finite element studies, and observational and clinical investigations addressing degradation mechanisms, biological consequences, peri-implant tissue changes, and preventive strategies. Experimental work consistently shows that connection geometry, preload maintenance, and material selection govern micromotion and microgap behavior, and that surface roughness influences bacterial adhesion and biofilm composition. Human studies confirm that titanium micro- and nanoparticles are commonly present in peri-implant soft tissues, including sites without a foreign-body reaction and without peri-implantitis, while particle uptake by macrophages is associated with oxidative stress, pro-inflammatory cytokine release, and increased receptor activator of nuclear factor kappa-B ligand signaling. Taken together, the available data support a bidirectional model in which tribocorrosion amplifies an existing inflammatory process rather than initiating it, and in which inflammation and instrumentation may in turn accelerate degradation. Tribochemical degradation may therefore contribute to peri-implant inflammation and marginal bone loss through mechanical instability, surface deterioration, and metallic debris release, but current evidence does not establish direct causality. Standardized tribocorrosion testing and longitudinal clinical studies are needed to clarify its clinical relevance and to guide preventive strategies.