Osteoarthritis (OA) represents a large burden on healthcare resources worldwide with continually increasing prevalence. This has led to renewed interest in the causes and pathogenesis of the condition. In recent years, there has been a move away from a simple ‘wear and tear’ model of cartilage to one of a complex inflammatory process involving cellular and extracellular derangements that allow a catabolic state to dominate. Ultimately, OA is now seen as pan-joint disease involving synovium, menisci, ligaments and muscle, in addition to cartilage. There are several classification systems including radiographic, MRI-based, clinical and combined classification systems. As radiographs only detect OA in latter stages, there has been a focus on early diagnosis using MRI and serum biomarkers. New physiological MRI sequences can now measure the proteoglycan content in cartilage and new semiquantitative analyses have been developed to score total knee joint involvement in the disease process. Serum biomarkers can be divided into those that are collagen breakdown products and those that are inflammatory cytokines; these can be used in early detection of OA before radiographic appearances arise. The risk factors for OA include ageing, knee injury, obesity, altered limb alignment, impaired muscle strength, female gender, heavy physical work and genetic susceptibility. Research continues to identify the mechanisms involved that lead to OA development, with possibly unique processes underpinning each risk factor. Our understanding of the pathophysiology of OA will continue to improve in the next few years which should lead to new intervention strategies that target different processes. More informative MRI sequences will continue to be developed and the optimum combination of biomarkers to detect early OA will need to be identified. Genetic studies will continue to identify new susceptibility loci that could be targeted in future therapies.
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