Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Osteoarthritis (OA) is the most common form of joint disease, and its impact is set to grow as the prevalence of obesity rises and the elderly population increases. Many clinicians regard OA as simply a disease of ‘wear and tear’, and by implication one in which disease modification is not possible. Such prejudices previously led to significant academic apathy in this disease area, reflected not only in our poor understanding of disease pathogenesis, but also in the failure to classify the disease with greater precision and develop sensitive tools for diagnosis and prognostic assessment. The identification of key degradative enzymes in cartilage, the appreciation that damaged articular cartilage has repair capabilities and the recognition that ‘good’ and ‘bad’ mechanical stress triggers different molecular pathways have greatly changed the outlook in recent years. Evidence-based management of the condition is outlined in international guidelines: education, weight control/loss and exercise (general, joint specific) are core interventions. Analgesia and non-pharmacological and surgical approaches that favourably affect joint biomechanics are used for treating painful OA unresponsive to core interventions. The disease remains the most common reason for joint replacement surgery. There are no licensed disease-modifying OA drugs but recent clinical trials suggest that these may be within reach.

Original publication




Journal article


Medicine (United Kingdom)

Publication Date