Implant-associated orthopedic infections remain difficult to eradicate because biofilm persistence is coupled to progressive changes in bone and local immunity. This narrative review presents the Bone-biofilm Interface (BBI) as an integrative framework linking microbial biofilms, implant properties, bone cells, immune cells, and the mineralized matrix. Its contribution is primarily organizational: it consolidates evidence on intracellular bacterial reservoirs, inflammatory osteolysis, immune dysfunction, and biofilm adaptation within a single spatial and functional unit. The framework also advances testable, but not yet clinically established, hypotheses concerning ion-mediated matrix remodeling, the dual role of osteoclasts as resorptive cells and potential bacterial reservoirs, and niche-dependent transitions between dormancy and resuscitation. We further consider how polymicrobial communities, temporal evolution, and implant material properties may modify these interactions. The available evidence is weighted according to source, with human observations distinguished from animal and in vitro studies. Established clinical management, including surgical source control and guideline-based antimicrobial therapy, remains central; proposed approaches involving microenvironment modulation, metabolic interference, immune reprogramming, anti-resorptive agents, and responsive biomaterials should be viewed as investigational adjuncts. By clarifying evidence boundaries and translational readiness, the BBI framework provides a structured research agenda for testing how disruption of host-microbe crosstalk might complement current treatment of chronic implant-associated infection.
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Zhu et al. (2026) studied this question.
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