western world.1 In England and Wales, between 1.3 and 1.75 million people have symptomatic osteoarthritis.2 Data from the Arthritis Research Campaign show that up to 550 000 people in the UK have severe knee osteoarthritis and two million people visited their general practitioner in the past year because of osteoarthritis. More than 80 000 hip or knee replacements were performed in 2000 in the UK with a cost of £405 million.3 As a cause of disability (such as walking and stair climbing) in the elderly in the west, osteoarthritis is second only to cardiovascular disease. Altogether 10%–15% of adults over 60 have some degree of osteoarthritis, and with an ageing population it is becoming an increasingly important disease. Osteoarthritis is classified into two groups. Primary osteoarthritis can be localised or generalised, the latter more commonly found in postmenopausal women, with development of Heberden’s nodes. Secondary osteoarthritis has an underlying cause, such as trauma, obesity, Paget’s disease, or inflammatory arthritis. CLINICAL FEATURES Patients are usually over the age of 50 and complain of pain and stiffness in the affected joint(s), which is exacerbated with activity and relieved by rest. Early morning stiffness, if present, is typically less than 30 minutes. Joint tenderness and crepitus on movement may also be present. Swelling may be due to bony deformity such as osteophyte formation, or due to an effusion caused by synovial fluid accumulation. Systemic symptoms are absent, with a normal erythrocyte sedimentation rate. The presence of fever, weight loss, anorexia, or abnormal blood tests should alert the physician to other disease processes such as infection or malignancy. The American College of Rheumatology have produced criteria for the diagnosis of osteoarthritis.4 They were developed for epidemiological purposes and are not recommended for use in routine clinical practice. PATHOGENESIS Traditionally, osteoarthritis was viewed as an inevitably progressive, degenerative disease process. New work suggests that it is a dynamic process that may progress episodically. It is a heterogeneous group of diseases characterised by an adaptive response of synovial joints to a variety of environmental, genetic, and biomechanical stresses. Cartilage is made of water (70%) and a type II collagen framework with proteoglycans and glycosaminoglycans (consisting mainly of aggrecan and also chondroitin), produced by chondrocytes. Proteoglycans in turn bind to hyaluronate which stabilises the macromolecule. Chondrocytes receive nutrition from the synovium by diffusion and the synovial fluid is circulated by joint movement. It has been postulated that if the joint stops moving (as a result of a fracture or immobility) and chondrocytes lose their source of nutrition, they go into shock and cartilage repair ceases. Metalloproteinases are produced, which catalyse collagen and proteoglycan degradation. The synovium has been shown to be variably inflamed in osteoarthritis producing increased levels of interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-α), cytokines that induce nitric oxide and metalloproteinase production. Interleukin-6 (IL-6) and mechanical loading of the joint also induce catabolic cytokine receptors. These bind IL-1 and TNF-α within cartilage causing more destruction. It is thought that the osteophytes and subchondral sclerosis seen in osteoarthritis may be the body’s way of trying to compensate for lack of cartilage, although some researchers have found bony changes before cartilage changes in animal models.5 This sort of abnormal bone is also thought to lead to further degradation of the cartilage surrounding it. Poor synthesis of cartilage building blocks may be caused by dysfunctional forms of insulin-like growth factor-1 and transforming growth factor-beta, agents which normally promote new cartilage formation.5 PATHOLOGICAL FINDINGS Macroscopically, the osteoarthritic process results in cystic degeneration of the bone