From senescence and inflammaging to systemic comorbidities: Drivers of aging-associated periodontitis.

James Cheng, Chew Tin Zar Aung, Samuel F Suslavich, Sinem Esra Sahingur, Yvonne L Hernandez-Kapila

Section of Periodontics, Division of Regenerative and Reconstructive Sciences, UCLA School of Dentistry, Los Angeles, California, USA.Section of Periodontics, Division of Regenerative and Reconstructive Sciences, UCLA School of Dentistry, Los Angeles, California, USA. · pubmed

Paper

Abstract

Aging is accompanied by a chronic low-grade inflammatory process, known as inflammaging, as well as immunosenescence, an age-related decline and dysregulation of immune function, and cellular senescence, a process in which cells enter a state of irreversible growth arrest while actively releasing pro-inflammatory factors. These processes alter the host immune regulation and tissue homeostasis. Aging-associated mechanisms are being explored for their role in periodontal and peri-implant diseases because of their promotion of dysregulated inflammation, impaired healing, and heightened susceptibility to tissue destruction. Rather than viewing periodontitis as a condition driven solely by microbial burden, it should be understood as a multifactorial disease shaped by complex host-microbe interactions, in which host-driven processes, particularly senescence and inflammaging, play a central role in amplifying bidirectional oral-systemic interactions.

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Research summary

The paper claims that aging-associated mechanisms, particularly senescence and inflammaging, significantly contribute to the pathogenesis of periodontitis through altered immune regulation and tissue homeostasis. This research is relevant as it explores the underlying biological processes of aging that may influence systemic health and disease, rather than merely addressing symptoms.

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