Osteoarthritis (OA) is a common joint disorder characterized primarily by cartilage degeneration and osteophyte formation, leading to a substantial decline in patients’ quality of life. Temporomandibular joint OA (TMJOA) is a degenerative lesion within temporomandibular joint disorders, accounting for approximately 8%–16% of diagnosed cases. Its clinical manifestations include joint pain, limited mouth opening, joint noises, and related symptoms. Cellular senescence plays a pivotal role in OA pathogenesis. Senescent processes contribute to functional impairment of chondrocytes, synovial cells, and osteocytes through multiple signaling pathways. DNA damage, telomere attrition, oxidative stress, and the release of inflammatory mediators are major drivers of cellular senescence. However, current literature lacks a systematic integration of senescence-related mechanisms in OA and TMJOA. Furthermore, anti-aging therapeutic strategies for these conditions lack targeted approaches that account for interactions among distinct senescence mechanisms. This review elucidates the various characteristic types of cellular senescence, their interactions, and the senescence-induced pathogenesis of OA and TMJOA. A comprehensive investigation into the mechanisms of cellular senescence may yield novel insights and inform the development of therapeutic strategies for managing OA.