Stage-Gated Biomaterial Strategies for Peri-Implantitis Management

Peri-implant biomaterials are commonly compared as isolated antimicrobial technologies, although their clinical relevance depends on linked requirements spanning prevention and treatment. Preventive approaches must preserve tissue integration and future cleanability; once disease develops, treatment must provide access to and disruption of mature biofilm, preserve or recover implant-surface competence, control destructive inflammation, support defect-specific regeneration, and enable durable maintenance. This structured critical review proposes a six-gate framework that evaluates preventive surfaces, decontamination methods, local delivery systems, host-directed materials, and regenerative adjuncts against those downstream requirements. Human peri-implant evidence was prioritized for treatment claims. Animal studies, clinically representative in vitro models, simplified implant models, and indirect oral-biofilm or general materials evidence were considered separately. The synthesis shows that mechanical and surgical strategies have the most direct clinical evidence, but no decontamination protocol has shown consistent, durable superiority across clinical settings. Reconstructive biomaterials can improve radiographic defect fill in selected defects, but their additional benefit for composite disease resolution remains uncertain. Meanwhile, antimicrobial coatings, plasma electrolytic oxidation platforms, smart hydrogels, and immunomodulatory materials remain supported mainly by preclinical models. Across different technologies, the same bottlenecks recur restricted access to threaded and protein-conditioned surfaces, reliance on immature or simplified biofilms, unmeasured surface damage or chemical residues, incomplete host-cell assessment, short follow-up, and little evidence on recurrence. Mechanics are considered separately as device biomechanics, interfacial transport, microbial contact cues, and host mechanobiology, which function through different mechanisms and levels of evidence, rather than as a unified cause of disease. The proposed framework links antimicrobial findings with surface integrity, host compatibility, regeneration and maintenance to identify gaps in translational evidence. Its generalizability and ability to predict clinical outcomes remain untested.