OSTEOIMMUNOLOGY AND PERIODONTAL BREAKDOWN IN OSTEOPOROSIS

Irina-Georgeta Sufaru, Liliana Pasarin, Maria-Alexandra Martu, Diana Tatarciuc, Sorina-Mihaela Solomon, Silvia Martu, Ioana Martu

Abstract

Background: Osteoporosis and periodontitis are prevalent chronic conditions in aging populations and are both characterized by bone loss in distinct anatomical compartments. Increasing attention has focused on inflammation as a potential biological link between systemic skeletal deterioration and periodontal breakdown. Objective: This narrative review summarizes inflammatory mechanisms that may link osteoporosis (or low bone mineral density) with periodontal status and critically appraises the clinical evidence supporting these associations. Summary of evidence: Osteoporosis, particularly in postmenopausal and older individuals, is increasingly understood within an osteoimmune framework in which low-grade systemic inflammation contributes to remodeling imbalance. Cytokine networks and immune cell–mediated signaling can promote osteoclastogenesis and weaken coupling between resorption and formation. Periodontitis is driven by a dysbiosis-associated, non-resolving host response that sustains local inflammation and favors connective tissue degradation and alveolar bone resorption. Convergent pathways include upregulation of osteoclastogenic signals (notably RANKL/OPG imbalance), cytokine amplification loops, and adaptive immune polarization that may lower the threshold for destructive inflammation. Clinically, observational studies frequently report worse periodontal parameters in individuals with osteoporosis or low bone mineral density, with signals often more apparent in postmenopausal cohorts. Nonetheless, heterogeneity in phenotype definitions, residual confounding, and the predominance of cross-sectional designs limit causal inference; genetic causal-inference studies generally argue against a strong direct causal effect of bone mineral density on periodontitis risk. Conclusions: The most defensible interpretation is a modifier model: systemic skeletal status and osteoporosis-related inflammatory tone may influence susceptibility to periodontal breakdown or its progression once local dysbiosis-driven inflammation is established. Future work should prioritize standardized periodontal phenotyping, progression-focused longitudinal designs, and the integration of inflammatory and bone-turnover biomarkers, while accounting for menopausal stage and medication exposure.

DOI : 10.62610/RJOR.2025.4.17.17