Abstract
Purpose: Osteoarthritis (OA) is a debilitating joint disease affecting around 80% of individuals aged over 65. A multitude of aberrant processes have been described to affect the aetiology of OA including cartilage thinning, osteophyte formation, subchondral osteosclerosis and synovial hypertrophy. Investigations into the cellular and molecular mechanisms responsible for these abnormal features have highlighted the role of chondrocyte hypertrophy and dysfunction in OA pathogenesis. Recently, chondrocyte senescence has been identified as yet an additional mechanism by which chondrocytes see their functionality perturbed.
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