Oral diseases · 2026
The Oral Microbiome-Inflammaging Axis in Elderly Periodontitis: Emerging Immunopathogenic and Systemic Mechanisms.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
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Feruza Jabborova, Otajon Masharipov, Shaxobiddin Mukimov, Mamura Afakova, Aziz Kubaev, Nargiza Khakimova, Alimova Zebiniso
Аннотация
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.
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.