Microenvironmental Succession and Host Immune Responses in Peri-Implantitis

Peri-implantitis (PI) is a prevalent complication following dental implant therapy, characterized by progressive bone resorption, peri-implant tissue destruction, and potential implant failure. Its management poses substantial challenges for long-term oral health. Current diagnostic and therapeutic approaches mainly depend on clinical examination and imaging techniques, which often detect the disease only after progression. Moreover, treatment methods frequently lack long-term stability, highlighting the need for early biomarkers and mechanistic insights. Recent studies demonstrate that plaque biofilms undergo a microbial succession, shifting from early facultative anaerobes to late strict anaerobes, while extracellular polysaccharides and proteases contribute to the stability of the pathogenic community. In parallel, dysregulation of the IL-23/Th17 axis and macrophage M1/M2 polarization amplify local immune imbalance and chronic inflammation. Bone resorption is further accelerated by disruption of the RANKL/OPG pathway and matrix metalloproteinase-mediated extracellular matrix degradation. Emerging biomarkers in peri-implant crevicular fluid, such as IL-17, RANKL/OPG, and MMP-8, together with imaging modalities including CBCT, hold promise for early diagnosis and risk prediction. This review aims to elucidate the interplay between biofilm succession, host immunity, and bone metabolism in PI, while evaluating potential biomarkers and diagnostic strategies for clinical application.