Intended for healthcare professionals


Osteoarthritis: time to shift the paradigm

BMJ 1999; 318 doi: (Published 15 May 1999) Cite this as: BMJ 1999;318:1299

This includes distinguishing between severe disease and common minor disability

  1. Paul Dieppe, Director
  1. MRC Health Services Collaboration, University of Bristol, Bristol BS8 2PR

The name “osteoarthritis” arose from observation of the striking overgrowth of marginal and subchondral bone by the pathologists and radiologists who classified the different forms of joint disease at the turn of the century.1 For many years it was regarded as a simple, age related, degenerative, “wear and tear” phenomenon, a view that led to negative approaches to both research and treatment. Over recent years this has changed: there is now plenty of interest in osteoarthritis, and the research effort has led to several new treatments, such as lubricating injections into joints2 and cartilage transplants.3 But this trend has inherent dangers. Not only do we not yet know whether these new treatments really help patients in the long term; the introduction of complex, expensive treatments for a disorder that may affect a quarter of the world's older people is unlikely to be of much use to most doctors or patients. We need to take stock and ask ourselves if current approaches are appropriate.

Osteoarthritis is obviously important: it is the main cause of joint replacement surgery and is so common that in the developed world it is set to become the fourth highest impact condition in women and the 8th most important in men.4 However, most people with osteoarthritis are not seriously affected, and community based studies have shown that joint pain and disability in older people depend as much on factors such as depression and isolation as they do on the severity of joint damage.5 Most mild osteoarthritis does not progress to severe joint damage, and recent research indicates that the risk factors for progression are different from those for the initiation of osteoarthritis,6 suggesting that severe joint damage depends on different processes from those that lead to the very high prevalence of early osteoarthritis.

Perhaps we should ask ourselves whether it is appropriate to regard all the discomfort, stiffness, and musculoskeletal disability that we attribute to osteoarthritis in older people as a medical problem, amenable to solutions through basic medical sciences and pharmacology. I would argue that medical science should concentrate on progressive joint damage and the need for joint replacement alone—that would still give us plenty to do.

A dominant pathological feature of the osteoarthritic joint is focal areas of damaged articular cartilage. Articular cartilage is a fascinating tissue: it survives in the absence of any vascular supply or innervation and with precious few cells in its highly organised matrix. A large international research effort, in both universities and industry, has aimed at understanding the normal control of cartilage integrity in the belief that we will be able to find pharmacological ways of preventing breakdown of the tissue, or stimulating repair, with a resulting “cure” for osteoarthritis. However, it is quite clear that osteoarthritis is a disorder of the whole synovial joint organ, not just the cartilage. Indeed, the articular cartilage may be the innocent bystander of a disease process that is centred more in bone than in cartilage—a large body of evidence on the importance of bone turnover in progressive osteoarthritis is accumulating. 7 8 So another paradigm shift that is needed is to change the emphasis from the cartilage to the joint as a whole, and perhaps to the subchondral bone in particular. Thus osteoarthritis might become “osteo”arthritis again.

Several investigators with an interest in this condition, including myself, have long railed against the “wear and tear” concept, pointing out that osteoarthritis involves active disease processes and that the tissue destruction and aberrant repair that are at the heart of the joint changes are mediated by alterations in cellular function. However, mechanical factors are also important in initiating joint damage—for example, there is strong evidence that certain occupational factors predispose to osteoarthritis9—and that the disease process must be driven by mechanical forces, even if it is mediated by biochemical processes. A recent and fascinating contribution to the evidence for a mechanical aetiology has come from an epidemiological study which indicates that quadriceps muscle weakness may precede the development of knee osteoarthritis.10 This suggests that any definitive answers to osteoarthritis will require us to understand biomechanics and the physiology of muscles and joints as much as biochemistry. So a further paradigm shift that we may need to make is to go back to concentrating on the mechanical aetiology of the disease.

Thus I am suggesting three major changes in our approach to osteoarthritis: that medical science should concentrate on progressive severe disease and the problem of joint replacement rather than attributing all pain and disability in elderly people to a condition that they believe can be cured by magic bullets aimed at joints; that we should shift the emphasis from cartilage to other tissues, including bones and muscles; and that basic science should explore the biomechanics of the joint as much as its cell biology. Is any of this relevant to doctors and patients today? I think so. We can be confident that most older people with minor degrees of joint damage will not become seriously disabled, and we should clearly look for psychosocial issues and other comorbidities that might explain their pain and disability, rather than concentrating on the joints alone.

Furthermore, some of this thinking has immediate relevance to management: no conservative measures are very effective in osteoarthritis,11 and the strength of the evidence is distressingly weak, but some physical and educational approaches—including simple aerobic exercises, specific muscle strengthening and range of motion exercises, and empowerment towards self management, appear to have a similar effect size to drug treatments,1214 and they are generally safer. An optimistic attitude, reassurance, simple advice about exercise, the use of measures such as sticks or shock absorbing shoes, attention to psychosocial problems, and “demedicalising” of minor joint problems may be all that many of our patients with osteoarthritis need.15