[The role of aging in degenerative temporomandibular joint diseases: from cellular senescence to systemic imbalance].

Abstract

Degenerative temporomandibular joint disease (TMJ-DJD), a common condition in middle-aged and elderly populations, has seen a continuous rise in incidence with global population aging. Aging synergistically promotes TMJ degeneration through multilevel mechanisms. At the cellular level, aging manifests as epigenetic alterations, formation of the senescence-associated secretory phenotype, mitochondrial dysfunction, exacerbated oxidative stress, and declined stem cell repair capacity, collectively accelerating degradation of the chondrocyte extracellular matrix and apoptosis. At the systemic level, immunosenescence leads to a chronic low-grade inflammatory state; various endocrine changes (e.g. in sex hormones, the growth hormone/insulin-like growth factor-1 axis, and thyroid hormones) impair tissue anabolic and repair capacity. Meanwhile, declined tissue mechanosensation and hardening of the extracellular matrix further reduce the joint's adaptability to external load. Additionally, aging acts as an endogenous factor that disrupts central and peripheral circadian rhythms, indirectly promoting TMJ degeneration by impairing cartilage metabolism and inflammatory responses. In summary, aging drives the pathogenesis and progression of TMJ-DJD via multiple pathways, including cellular dysfunction, systemic homeostasis imbalance, and disruption of biological rhythms. Targeting the above mechanisms may provide novel therapeutic strategies for future clinical interventions in TMJ degenerative joint diseases.