The Oral Microbiome-Inflammaging Axis in Elderly Periodontitis: Emerging Immunopathogenic and Systemic Mechanisms.

BACKGROUND

Periodontitis prevalence increases with age, yet "elderly periodontitis" is not merely cumulative plaque exposure. Aging remodels mucosal immunity, elevates chronic inflammation, and promotes senescent cell accumulation with pro-inflammatory secretory phenotypes.

OBJECTIVE

To critically evaluate the self-reinforcing oral microbiome-inflammaging axis in elderly periodontitis.

METHODS

Narrative synthesis of mechanistic studies, human cohorts, and preclinical models investigating interactions between oral microbial ecology, immunosenescence, cellular senescence, and inflammaging.

RESULTS

Dysbiotic biofilms deliver persistent pressure interpreted by aged immune-stromal networks with heightened inflammatory gain. Mechanistic studies implicate aging-sensitive TLR9 sensing, age-amplified inflammasome-linked macrophage responses to P. gingivalis, and senescent niches that potentiate inflammation. Microbes directly induce senescence programs, including epithelial senescence and exosome-mediated paracrine immune senescence. Systemically, periodontitis induces multi-organ frailty-like phenotypes, neuroinflammatory changes, persistent gut dysbiosis, and altered metabolomes despite local therapy.

CONCLUSION

Elderly periodontitis represents a geroscience-relevant disorder where dysbiosis and biological aging jointly establish a self-sustaining inflammatory ecosystem. Priority gaps include longitudinal elderly cohorts integrating microbiome function with senescence markers and stratified trials combining biofilm control with host modulation.