surrounding the joint, with loss of cartilage and irregular, abnormal bone formation at the edges of the joint (osteophytes; fig 1) and narrowing of the joint space. Microscopically, there is flaking and fibrillation of the articular cartilage surface and destruction of the cartilage microarchitecture with formation of holes within it, as well as bony cysts.6 Variations in the cellularity and vascularity of subchondral bone leads to sclerosis in some areas and new bone and callous formation where the synovium is continuous with the periosteum. The cartilage itself has three discrete zones within it: a surface layer adjacent to the synovium consisting of collagen aligned parallel to the surface, a middle zone consisting of thicker, wider spaced collagen molecules arranged randomly, and an inner zone adjacent to bone, consisting of collagen arranged perpendicular to the surface.6 RISK FACTORS Age The normal ageing process is thought to cause increased laxity around joints, reduced joint proprioception, cartilage calcification, and reduced chondrocyte function, all leading to a propensity for osteoarthritis. The Framingham Study found that 27% of those aged 63 to 70 had radiographic evidence of knee osteoarthritis, increasing to 44% in the over 80 age group.7 Other studies have found that 80% of people over the age of 65 have some radiographic evidence of osteoarthritis (although this may be asymptomatic), but that incidence and prevalence of symptomatic osteoarthritis levelled off or declined in men and women at around 80 years of age.8 Studies of proprioception in osteoarthritis have found that it is reduced in an elderly patient group with knee osteoarthritis.9 Trauma Cruciate, collateral ligament and meniscal tears as well as joint fracture lead to increased risk of osteoarthritis. The Framingham Study found men with a history of knee injury were at a 5–6-fold increased risk of developing osteoarthritis.7 This usually occurs in a younger age group and can lead to prolonged disability and unemployment. Meniscectomy after a knee injury resulted in an increased risk of developing tibiofemoral osteoarthritis.10 Occupation Osteoarthritis is commoner in those performing heavy physical work, especially if this involves knee bending, squatting, or kneeling. Dockers and miners have been found to have a higher prevalence of knee osteoarthritis than those in sedentary jobs.11 There is a significant relationship between occupational kneeling12 or repetitive use of joints during work and osteoarthritis. Exercise Elite athletes who take part in high impact sports do have an increased risk of knee osteoarthritis.8 Primary quadriceps weakness is a risk factor for its development by decreasing the stability of the joint and reducing the shock absorbing properties of the muscle.11 Gender and ethnicity Under the age of 50, men have a higher prevalence and incidence than women. However, once over 50, women have a higher overall prevalence and incidence than men. This difference tends to become less marked after the age of 80. A withdrawal from oestrogen at menopause may be a trigger.13 Although ubiquitous, osteoarthritis is generally commoner in Europeans than in Asians. Osteoarthritis of the hip is more common in Europeans (7%–25%) than in Chinese, Africans from Nigeria and Liberia, and Jamaicans (1%–4%). Osteoarthritis of the hand is more common in European women than in women of Afro-Caribbean descent.13 There is conflicting evidence as to whether oestrogen based hormone replacement therapy protects against large joint osteoarthritis.14,15 Genetics There is increased concordance for osteoarthritis in monozygotic twins compared with dizygotic twins, indicating there is a genetic susceptibility to the disease.16 Many genes have been linked to osteoarthritis. There is most concordance with chromosomes 2q, 4, and 16. Families have been found with rare autosomal dominant patterns of inheritance of osteoarthritis. The defective genes are often coding for structural proteins of