Circadian disruption and cellular senescence: emerging perspectives in periodontitis.

Periodontitis is a chronic inflammatory disease characterized by progressive destruction of periodontal tissues and alveolar bone, traditionally attributed to microbial dysbiosis. Emerging evidence suggests that host-intrinsic factors, including circadian rhythm disruption (CRD) and cellular senescence(definition), may critically influence disease susceptibility and progression. CRD, resulting from misalignment between central and peripheral clocks, is known to impair stem cell function, alter telomere(definition) maintenance, and disrupt oxidative stress and metabolic homeostasis across multiple tissues. In parallel, cellular senescence exacerbates tissue damage through the senescence-associated secretory phenotype (SASP), which promotes inflammation and extracellular matrix degradation. Although direct evidence linking CRD and cellular senescence to periodontitis remains limited, mechanistic studies in related models suggest that these processes may converge to dysregulate immune responses, metabolic activity, and bone remodeling in the periodontium. Circadian disruption may impair stem cell regenerative capacity, alter immune cell rhythmicity, and enhance osteoclastogenesis, whereas senescent cells may further aggravate chronic inflammation and tissue destruction. This conceptual framework integrates circadian biology with aging-related mechanisms, highlighting potential pathways through which CRD and cellular senescence may modulate periodontitis. Understanding these interactions may inform novel preventive and therapeutic strategies, including circadian alignment, senolytic approaches, and metabolic modulation, for the early and precise management of periodontal disease.