Osteoarthritis

The pathogenesis of osteoarthritis (OA) appears to be the result of a complex interplay between mechanical, cellular and biochemical forces. Obesity is the strongest risk factor for disease onset in the knee, and mechanical factors dominate the risk for disease progression. OA is a highly prevalent and disabling disease. The current pre-eminent focus in OA research and clinical practice is on persons with established radiographic symptomatic disease. This is the very end-stage of disease genesis, and modern therapies hence are largely palliative. In an effort to mitigate the rising tide of increasing OA prevalence and disease impact, we need to focus more on preventing the onset of disease and modifying the structural progression of OA. Greater therapeutic attention to the important role of mechanical factors, joint injury and obesity in OA etiopathogenesis, is required if we are to find ways of reducing the public health impact of this condition.

Osteoarthritis (OA) is a highly prevalent and disabling disease that consequently has a formidable individual and societal impact. Approximately 10–12% of the adult population has symptomatic OA . The risk of mobility disability (defined as needing help walking or climbing stairs) attributable to knee OA alone is greater than that due to any other medical condition in people aged 65 and over .

OA reduces both quality and quantity of life. In the estimates for the Global Burden of Disease 2000 study , OA is the fourth leading cause of total years lost due to disease at the global level. On average, a 50–84-year-old non-obese person with knee OA will lose 1.9 quality-adjusted life years due to OA . If obese with knee OA, this increases loss to 3.5 quality-adjusted life years and the estimated remaining quality-adjusted life expectancy is decreased by 21–25%. This effect of symptomatic knee OA on quality of life is similar to that of metastatic breast cancer. A recent study also found that persons with OA are at higher risk of death compared with the general population (standardised mortality ratio 1.55, 95% confidence interval 1.41–1.70) .

If you consider OA to be a common disease now, by the year 2020, the number of people with OA will have doubled, due in large part to the exploding prevalence of obesity and the greying of the ‘baby boomer’ generation . This will have a tremendous impact on already strained health-care resources with most western countries spending 1–2% of their gross domestic product on care for persons with arthritis . A large component of the direct health-care costs for managing persons with OA is the cost of total joint replacements, for which OA accounts for about 95% of surgical volume.

The aetiology of OA

OA is a heterogeneous disease characterised by failure of the synovial joint organ . The disease occurs when the dynamic equilibrium between the breakdown and repair of joint tissues becomes unbalanced, often in a situation where the mechanical loads applied exceed those that can be tolerated by the joint tissues . OA is characterised by progressive cartilage loss, subchondral bone remodelling, osteophyte formation and synovial inflammation, with resultant joint pain and increasing disability (see Fig. 1 ). Whilst the progressive joint failure may cause pain and disability , many persons with structural changes consistent with OA are asymptomatic .

The aetiology of OA is perhaps best understood as resulting from excessive mechanical stress applied in the context of systemic susceptibility. Susceptibility to OA may be increased in part by genetic inheritance (a positive family history increases risk), age, ethnicity, nutritional factors and female gender . In persons vulnerable to the development of knee OA, local mechanical factors such as abnormal joint congruity, joint malalignment, muscle weakness or alterations in the structural integrity of the joint environment such as meniscal damage, bone-marrow lesions or ligament rupture can facilitate susceptibility to, and progression of, OA. Loading can also be affected by obesity and joint injury (either acutely as in a sporting injury or after repetitive overuse such as occupational exposure), both of which can increase the likelihood of development or progression of OA.

In epidemiological investigation, OA is typically defined using conventional radiographs, and less frequently self-report. The reported prevalence of OA varies according to the method used to define the disease. The characteristic radiographic features used to define and classify OA severity are osteophytes (osteocartilaginous growths) ( Fig. 2 ), subchondral sclerosis and joint space narrowing. By contrast, symptomatic OA is defined as the concomitant presence of pain (usually defined as pain on most days of the last month) and radiographic features. It is the presence of symptomatic OA that is important clinically, not simply the radiographic identification of an osteophyte or self reported OA (where misclassification is even more problematic than the commonly used radiographic OA definition).