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The joint lubrication was not what it was when I was competing, and I decided that not having arthritis or rheumatism for the rest of my life was a lot more important to me than returning to the track.

Edwin Moses, former world and Olympic 400-metre hurdles champion, on his decision to retire

Osteoarthritis (OA) is increasingly recognised to be a heterogeneous disorder that can present with pain and functional limitations and affects the entire joint, including cartilage, synovial membrane, subchondral bone, ligaments and periarticular musculature.1 It has traditionally been seen as a condition of the elderly but is increasingly presenting at a younger age.2 Osteoarthritis has affected some of the most famous athletes of all time, from golfers Tiger Woods and Jack Nicklaus to NBA stars Shaquille O’Neal and Kobe Bryant. The previous edition of Clinical Sports Medicine quoted comedian Jack Benny as saying ‘I don’t deserve this award, but then I have arthritis and I don’t deserve that either’. The question is: to what extent is OA preventable? Many sports carry a higher risk of joint injury and therefore supporting the older athlete to remain actively involved in sports and their activities of daily living is key to their long-term health.

The most recent definition of OA proposed by the Osteoarthritis Research Society International (OARSI) is:

… a disorder involving movable joints characterised by cell stress and extracellular matrix degradation initiated by micro- and macro-injury that activates maladaptive repair responses including pro-inflammatory pathways of innate immunity. The disease manifests first as a molecular derangement (abnormal joint tissue metabolism) followed by anatomic, and/or physiologic derangements (characterised by cartilage degradation, bone remodelling, osteophyte formation, joint inflammation and loss of normal joint function), that can culminate in illness.3

It is anticipated that this definition will continue to be subject to regular refinement with advances in scientific evidence.3, 4

Recent studies have attempted to classify OA into different phenotypes5, 6 and subpopulations,7 as a means of categorising clinical presentations, including aetiological factors, risk factors, mechanisms of disease and treatment effects. The most recent systematic review of knee OA phenotypes discusses the clinical relevance in each subgroup, with the subgroups being clinical phenotypes, imaging phenotypes and laboratory phenotypes.6 The extension of these definitions to other joints affected by OA is yet to be determined.


The total burden of disease for OA increased substantially between 1990 and 2015, with disability-adjusted life years (DALYs) increasing by 35%.8 Osteoarthritis also has the highest prevalence among all joint diseases, and with increasing trends in obesity and joint injury—which are the two most important risk factors for OA—these figures will increase further. A systematic review concluded that individuals with obesity and previous knee trauma had a 2.6-fold and 3.9-fold risk of developing knee OA, ...

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