Ageing is closely linked to the development of osteoarthritis (OA), but they are independent processes. Several mechanisms by which ageing contributes to OA have been identified, including age-related inflammation (inflammaging), cellular senescence, mitochondrial dysfunction, oxidative stress, and changes in energy metabolism. These processes promote a proinflammatory, catabolic state that leads to joint tissue destruction and defective repair. Studies have focused on articular cartilage, but similar mechanisms may occur in other joint tissues. Understanding these mechanisms could lead to new therapies for OA. Risk factors for OA include prior joint injury, obesity, genetics, sex, and joint anatomy. Age is the most significant risk factor. A Spanish study found that incident hand OA in women peaks between 60-64 years, while hip and knee OA increases with age. A US study reported that symptomatic knee OA peaks between 55-64 years, with higher prevalence in obese women. OA is a major cause of disability worldwide and contributes significantly to healthcare costs. Advanced OA often requires joint replacement, and the number of knee replacements has increased over the past 20 years. The ageing population will increase the number of people disabled by OA. OA in young adults is often caused by joint injury, while in older adults, age-related factors contribute to OA. These factors likely work with other risk factors. Differences between joint ageing and OA indicate they are distinct processes. Research has mainly focused on articular cartilage, but studies on the meniscus, anterior cruciate ligament, and bone have shown similar age-related changes. Nine cellular and molecular hallmarks of ageing have been proposed, including genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, dysregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. These hallmarks are relevant to OA. Ageing is associated with low-grade systemic and local inflammation, which may promote OA. Inflammaging, caused by increased visceral fat, is a key factor. Obesity is a well-known risk factor for OA. Inflammation and metabolic changes (meta-inflammation) contribute to OA by increasing cytokines, adipokines, free fatty acids, and oxidative stress. Sarcopenic obesity is associated with knee OA and increases joint instability and fall risk in older adults. Local fat depots, such as the infrapatellar fat pad, increase with age. This fat pad produces adipokines that may contribute to OA. However, studies on fat pad conditioned media found a protective effect on cartilage. Cellular senescence is a hallmark of ageing and is associated with OA. Senescent cells produce proinflammatory cytokines and matrix-degrading enzymes, contributing to OA. Senescence is characterized by stress-induced proliferation arrest and resistance to mitogenic and oncogenic stimuli. Chondrocytes exhibit low proliferation rates, makingAgeing is closely linked to the development of osteoarthritis (OA), but they are independent processes. Several mechanisms by which ageing contributes to OA have been identified, including age-related inflammation (inflammaging), cellular senescence, mitochondrial dysfunction, oxidative stress, and changes in energy metabolism. These processes promote a proinflammatory, catabolic state that leads to joint tissue destruction and defective repair. Studies have focused on articular cartilage, but similar mechanisms may occur in other joint tissues. Understanding these mechanisms could lead to new therapies for OA. Risk factors for OA include prior joint injury, obesity, genetics, sex, and joint anatomy. Age is the most significant risk factor. A Spanish study found that incident hand OA in women peaks between 60-64 years, while hip and knee OA increases with age. A US study reported that symptomatic knee OA peaks between 55-64 years, with higher prevalence in obese women. OA is a major cause of disability worldwide and contributes significantly to healthcare costs. Advanced OA often requires joint replacement, and the number of knee replacements has increased over the past 20 years. The ageing population will increase the number of people disabled by OA. OA in young adults is often caused by joint injury, while in older adults, age-related factors contribute to OA. These factors likely work with other risk factors. Differences between joint ageing and OA indicate they are distinct processes. Research has mainly focused on articular cartilage, but studies on the meniscus, anterior cruciate ligament, and bone have shown similar age-related changes. Nine cellular and molecular hallmarks of ageing have been proposed, including genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, dysregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. These hallmarks are relevant to OA. Ageing is associated with low-grade systemic and local inflammation, which may promote OA. Inflammaging, caused by increased visceral fat, is a key factor. Obesity is a well-known risk factor for OA. Inflammation and metabolic changes (meta-inflammation) contribute to OA by increasing cytokines, adipokines, free fatty acids, and oxidative stress. Sarcopenic obesity is associated with knee OA and increases joint instability and fall risk in older adults. Local fat depots, such as the infrapatellar fat pad, increase with age. This fat pad produces adipokines that may contribute to OA. However, studies on fat pad conditioned media found a protective effect on cartilage. Cellular senescence is a hallmark of ageing and is associated with OA. Senescent cells produce proinflammatory cytokines and matrix-degrading enzymes, contributing to OA. Senescence is characterized by stress-induced proliferation arrest and resistance to mitogenic and oncogenic stimuli. Chondrocytes exhibit low proliferation rates, making