Peri-Implantitis and Periodontitis: Biological Convergence, Contextual Divergence.

Periodontitis and peri-implantitis are chronic inflammatory conditions of microbial origin that affect the supporting tissues of teeth and dental implants, respectively. Although they share comparable clinical features and several histopathological characteristics, they have traditionally been classified as distinct diseases, largely because they arise in different anatomical and clinical contexts. This narrative, question-driven review evaluates clinical, microbiological, histological, and molecular evidence to address whether observed similarities and differences between the two conditions reflect truly distinct diseases, context-dependent variations of a shared inflammatory spectrum, or artifacts of study design and nomenclature. While peri-implantitis is often described as progressing more rapidly or exhibiting more pronounced inflammatory infiltrates, the underlying reasons for these patterns remain under investigation. To date, no microbial species or host-response pathway has been conclusively identified as exclusive to either disease, although most available data derive from heterogeneous, often underpowered studies with limited head-to-head comparisons. Structural and anatomical distinctions, such as the absence of a periodontal ligament around implants and differences in connective tissue organization, may influence disease behavior, yet their precise role in determining divergent outcomes is still debated. Microbial variability also appears to reflect host-specific and site-specific factors more than strict disease categorization, and molecular and transcriptomic studies generally reveal overlapping patterns of immune activation and gene expression, although some analyses suggest potential quantitative or contextual differences, whose interpretation is constrained by small sample sizes and indirect comparisons. Overall, current evidence supports a substantial convergence in pathogenic pathways, superimposed on site-specific and host-specific modulators, rather than clearly segregated disease-specific mechanisms. Given the limited and inconsistent literature, particularly for advanced omics and tissue-based studies, any categorical distinction between periodontitis and peri-implantitis as separate entities remains premature. Future research should prioritize adequately powered, longitudinal, within-subject comparisons and high-resolution approaches, including spatial transcriptomics and integrated immune-molecular profiling, to refine diagnostic concepts and inform individualized therapeutic strategies.