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Osteoarthritis (OA) is a ubiquitous degenerative disease that generates signi"cant global disability and socio-economic burden, forcing more than 8.75 million people aged 45 or over to seek treatment in the UK/annum. (1) OA predominantly a!ects the lower limbs, however prevalence in the knee is 10-fold higher than in the ankle, with notably di!ering aetiology between the joints. Knee OA is characteristically a ‘wear-and-tear’ primary arthritis; in contrast, 90% of ankle OA cases are preceded by trauma-induced joint instability. (2) Hence, ankle cartilage is thought to be relatively protected from the catabolic phenotype that constitutes primary OA pathogenesis. Such protection is likely mediated through biochemical and biomechanical variations including lower concentrations of matrix metalloproteinases (MMPs) cartilage degrading enzymes, and a reduced sensitivity to pro-in#ammatory cytokines. These include Interleukin 1ß (IL-1ß) and Tumour Necrosis Factor(TNF ), which potentiate an OA phenotype in cartilage. (3, 4)

Effects of Superoxide Dismutase 1 on cartilage chondrocyte metabolism: a protective mechanism against ankle osteoarthritis?