Periodontal biomarkers in cardiovascular disease: mechanisms, diagnostics, and clinical implications

Periodontal disease is a chronic inflammatory condition increasingly associated with cardiovascular disease (CVD) beyond shared risk factors. This review evaluates evidence linking periodontal inflammation to cardiovascular outcomes and identifies periodontal biomarkers with potential relevance for cardiovascular risk assessment.

A narrative review was conducted using PubMed, Scopus, and Web of Science databases, including studies published between 1990 and 2025. Epidemiological, clinical, and mechanistic studies examining associations between periodontal disease, inflammatory and microbial biomarkers, and cardiovascular outcomes were included. Biomarkers were categorized as inflammatory cytokines, acute-phase proteins, oxidative stress markers, lipid mediators, and microbial indicators. Evidence regarding periodontal therapy and emerging point-of-care diagnostic technologies was also reviewed.

Epidemiological studies demonstrate increased risks of coronary heart disease, stroke, and atherosclerosis in individuals with periodontitis, independent of traditional cardiovascular risk factors. Mechanistic evidence indicates that periodontal pathogens and host immune responses promote systemic inflammation, endothelial dysfunction, and atherogenesis. Key biomarkers associated with cardiovascular outcomes include cytokines (IL-1β, IL-6, TNF-α, IL-17), acute-phase proteins (C-reactive protein, fibrinogen), matrix-degrading enzymes such as active matrix metalloproteinase-8, oxidative stress markers (myeloperoxidase, malondialdehyde), lipid mediators (lipoprotein-associated phospholipase A2), and microbial markers such as antibodies to Porphyromonas gingivalis. Periodontal therapy has been associated with reductions in systemic inflammatory markers and improvements in endothelial function, although large, randomized trials remain limited.

Periodontal biomarkers reflect biologically plausible mechanisms linking oral and cardiovascular inflammation and may enhance cardiovascular risk stratification. Further standardization, validation, and interdisciplinary collaboration are required for clinical translation.