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Key Points Ageing-associated changes promote the development of osteoarthritis (OA), but ageing and OA are independent processes Several hallmarks of ageing could contribute to OA: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, dysregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication The increase in fat mass and related metabolic changes that occur with ageing can result in ageing-related inflammation (referred to as 'inflammaging'), a chronic low-grade systemic proinflammatory state Elevated levels of reactive oxygen species can contribute to OA by causing oxidative damage and disrupting normal cell signalling, leading to imbalanced anabolic and catabolic activity and ultimately cell death Chondrocytes can undergo cellular senescence with age and OA in response to growth signals released as a result of underlying cellular damage The non-enzymatic crosslinking of collagen that occurs with ageing alters the mechanical properties of cartilage, and the resulting changes to mechanotransduction pathways reduce extracellular matrix synthesis by chondrocytes Abstract Ageing-associated changes that affect articular tissues promote the development of osteoarthritis (OA)