Causes: OA has long been referred to as a disease of wear and tear - with cartilage destruction a consequence of any process leading to increased pressure on one particular joint, or fragility of the cartilage structure. Whilst OA does often follow a joint injury, it is now clear that ‘wear-and -tear’ is an over-simplification, it is a much more complex disease, with several different subtypes.

Disease process: New research shows many factors are involved in causing the disease and its progression, including cartilage, the underlying bone, the synovial membrane, and chemicals involved in the inflammatory process produced by these tissues. It is secondary inflammation in the joint synovium which causes the painful symptoms of OA, and the formation of characteristic bony lumps (osteophytes).

Incidence: OA is the most common form of arthritis (and the most common cause of musculoskeletal disability and pain) - about 8.75 million people in the UK have the condition, representing a third of people over 45, and about half of people over 75.

Which joints? OA can affect any joint but the knee is the most commonly affected joint (an estimated 4.7 million people), followed by the hip (2.46 million people). It’s common for more than one joint to be affected.

Obesity is a major risk factor for OA, and has traditionally been thought to contribute by increasing the load on the joints. However it is also linked to OA in hand and finger joints. Recent research has indicated that chemicals produced in obese patients are linked to the production of inflammatory chemicals in the cells which produce cartilage.  There may also be genetic factors involved in OA susceptibility.

This research offers the hope of  disease modifying drugs for OA  (DMOAD), which could help retard or prevent cartilage destruction, and  supplement existing pain relieving  and anti-inflammatory treatments.