The shape of the hip and knee joint predispose to OA. The most obvious example in is someone with developmental abnormalities, e.g. Perthes’ disease, slipped femoral epiphysis or joint dysplasia (e.g. acetabular) predisposing to hip OA. It is probable that some normal variants of joint development contribute to the risk of OA. Premature hip OA in runners may be associated with the so called ‘bullet’ shaped appearance of the femoral head.

Strong heritability has been demonstrated for OA of the hand, knee, hip, and spine. This susceptibility probably results from multiple unidentified genes, but individual genetic abnormalities may cause OA, e.g. abnormalities of the Col2A1 gene predispose to premature widespread OA.

Stating the obvious, but age is clearly an important risk factor for OA—the older you are the more likely you are to have OA joints.

Obesity is associated with knee OA, there is still debate about its association with hip and hand OA. There appears to be a linear relationship between BMI and the risk of knee OA. Furthermore, the prognosis of knee OA, once developed, is worse in patients with a higher BMI.

OA affecting the hand and knee is more prevalent in females, although the exact explanation for this has yet to be confirmed. It has been suggested that female sex hormones modify chondrocyte function.

Repetitive activity in work has been shown to increase the risk of OA. Examples of this are:

Joint movement is essential for normal joint health. There is no evidence that exercise is damaging to a healthy joint. However, significant injury to a joint, e.g. meniscal tear, which may have been sustained through exercise, does predispose that joint to premature OA. Exercise, in particular excessive loading of a damaged joint, almost certainly further increases the risk of OA, although what constitutes excessive loading is unknown. Debate also exists as to whether subtle alterations to biomechanics when exposed to excessive loading, as might be seen in endurance runners, predisposes to OA. Even if a certain form of exercise does predispose a susceptible individual to OA, the well documented benefits of exercise would have to be considered against any perceived risk.

Hypermobility is found in normal healthy populations, as well as being a feature of certain inherited conditions, e.g. Ehlers-Danlos. It is uncertain to what effect joint mobility has on the risk of OA.

High bone density, while helpful in reducing fracture risk, is associated with OA at the hip and knee.

Smoking seems to have a protective effect, not that anyone would advocate this as a preventative strategy.

In addition to the above factors, a number of systemic conditions are associated with OA, e.g.:

Patient education is essential. Confirm diagnosis:

Irrespective of how ‘badly’ you think your patient will respond to a discussion on weight management, you are doing them a disservice by not drawing their attention to the need to lose weight. You must be supportive and empathetic, it is difficult to break out of the overweight— joints hurt, don’t exercise, comfort eat, gain weight vicious circle. Exercise physicians have a considerable role to play in advising on the role of exercise to help manage a weight problem, and there is no better place to start than with your overweight OA sufferer.

The OA joint should be viewed as a dysfunctional unit in which one or more of the components has failed. In simple terms, you have a two-pronged approach, reduce the stress on the joint, e.g. weight management, footwear modification, or increase the capacity of the joint to withstand that stress. Joint rehabilitation to try and restore more normal joint function, or to ensure that other structures, e.g. muscles are more able to compensate for OA changes, is central to OA management. Basic rehabilitation principles should be followed with, if possible, an achievable functional outcome that is patient-centered.