Definition

Osteoarthritis (OA) is a degenerative joint disease characterised by biochemical, cellular and structural changes to the articular cartilage, joint space and subchondral bone. The diarthrodial joints of the body, including the knees, hips and hands, are the most commonly affected. Depending on the aetiology of OA, the condition can be classified as either primary OA (idiopathic aetiology) or secondary OA. Secondary OA can be further defined as traumatic, metabolic, neuropathic, inflammatory or anatomic.¹

Epidemiology

The prevalence of OA increases with advancing age. The prevalence rate of symptomatic OA in people under the age of 45 years, for example, is five per cent. Between the ages of 45 and 64 years, the prevalence rate increases to more than ten per cent, and over 75 years of age, to more than thirty per cent.² In radiological prevalence surveys, the prevalence rate of OA is much higher (i.e. more than fifty per cent of people over 65 years of age),³ and in autopsy studies, even higher again (sixty to seventy per cent of people aged between 70 and 80 years).⁴ The disease is also more prevalent in women than men, particularly radiologically confirmed hand and knee OA, with the female:male ratio varying between 1.5 and 4.0 across studies.⁴

Aetiology and pathophysiology

Many risk factors are associated with the pathogenesis of OA. Increasing age, female sex, ethnicity, congenital joint abnormalities and family history are some of the major non-modifiable risk factors of OA. The modifiable risk factors include obesity, repetitive joint loading (e.g. repetitive squatting, kneeling, lifting), trauma (e.g. fractures, dislocations, joint surgery, meniscal or cruciate ligament tears), diet (e.g. low vitamin D, vitamin C and fruit intake, and elevated omega 6 fatty acid intake), and quadricep weakness.⁴ Several pathological conditions are also associated with the development of OA, including metabolic disease (e.g. haemochromatosis, hypothyroidism, Wilson’s disease), joint inflammation or infection, neuropathy (e.g. Charcot’s arthropathy) and cartilage disorders (e.g. rheumatoid arthritis, chondrocalcinosis).⁵ All of these factors impair the integrity of joint tissue, causing direct damage to joint tissues, impairing repair processes or increasing joint susceptibility to injury.⁴

An initial insult to the joint stimulates chondrocyte activity, but at the same time triggers the release of inflammatory mediators from the synovium into the cartilage.⁵ While the chondrocytes attempt to repair the tissue by increasing the production of proteoglycans and collagen, they do so in opposition to the actions of the inflammatory mediators and proteolytic enzymes, which cause cartilage degradation. When the equilibrium between proteoglycan synthesis and degradation shifts towards net degradation, damage to articular cartilage occurs. Over time, subchondral bone becomes exposed, eburnated, sclerotic and stiff, which results in osseous infarction and subchondral cyst formation. In an attempt to protect the subchondral bone and to stabilise the joint, the body produces osteophytes.⁶ But instead of protecting the tissue, these spurs cause joint immobility and pain, and in some cases, synovitis. Eventually, joint mobility diminishes to such an extent that menisci fissure, supportive muscles weaken and periarticular tendons and ligaments become stressed, resulting in tendinitis and contractures.⁵

Clinical manifestations

OA is a progressive disease and, as such, may not present with any clinical manifestations in the early stages of development. Eventually, the client may begin to experience deep, aching arthralgia in one or several joints, particularly the hips, knees and hands. This pain is often aggravated by exercise, weight-bearing activity and changing weather, and alleviated with rest.⁷ As the disease progresses, joint stiffness develops, which is generally worse in the morning and after prolonged periods of rest. Further loss of articular cartilage results in reduced joint mobility, joint tenderness and crepitus. In the later stages of the disease, the client may experience joint instability and/or locking, muscle contractures and spasms. The structural changes to articular tissue, synovial thickening and joint effusion may also lead to joint enlargement.⁵ The pain and functional impairment associated with this disease also contribute to significant disability and reduced quality of life.²