Chondrocytes—the cells responsible for maintaining cartilage—undergo senescence in osteoarthritis, triggering a senescence-associated secretory phenotype (SASP) that amplifies inflammation and accelerates cartilage breakdown. This senescent state disrupts the delicate balance between cartilage formation and degradation while impairing cellular responses to mechanical stress. The review identifies four core mechanisms driving this process: extracellular inflammation, mechanical overload, intracellular metabolic dysfunction, and genetic alterations. This convergence on cellular senescence represents a paradigm shift in understanding osteoarthritis progression. Rather than viewing arthritis as simple wear-and-tear, researchers now recognize it as an active process driven by aged, dysfunctional cells secreting inflammatory molecules. The therapeutic implications are profound—senolytic drugs that eliminate senescent cells, or senomorphic agents that reduce their inflammatory output, could potentially halt or reverse arthritis progression. This approach moves beyond symptom management toward genuine disease modification. However, the challenge lies in targeting cartilage senescence specifically without affecting beneficial senescent cells elsewhere in the body, particularly given that controlled senescence plays important roles in wound healing and tumor suppression.