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Development of osteoarthritis

Osteoarthritis symptoms develop slowly and are therefore difficult to detect. 

The onset of symptoms

Many joints with signs of OA on examination or on xrays show no symptoms as far as the person is concerned. Onset of symptoms is usually insidious (medic speak for slow and sneaky) and people can seldom indicate exactly when they felt the trouble started.

The typical onset of OA in a joint is variable but people often notice changes in a joint related to, or immediately after, some activity with that joint. This can be a vague and occasional ache or pain in the joint, sometimes with mild joint stiffness and aching in the muscles near the joint.

Range of motion of the joint may also be affected, either slowly by gradually becoming aware of a restriction in doing a normal activity or quickly by having a minor injury. A small injury can set off a process where all the symptoms of OA will develop over a few days, in some cases rather severely. OA changes were almost certainly present in the joint prior to the injury, which converts a previously trouble-free joint into a painful and stiff one.

Aches and pains in our joints and muscles is a normal part of human life, and people with OA may just notice an increase in the severity and frequency of these normal symptoms. This is usually taken as nothing to worry about and part of the ageing process until the severity of the symptoms drives the person to consult a doctor.

A disease of articular cartilage?

OA is thought primarily to be a disease of the articular cartilage, the smooth lining of the joints. Changes also occur in the bone beneath the cartilage and it is not known where the first areas of abnormality are.

Articular cartilage has two main functions:

  1. To absorb stress by compressing under mechanical load
  2. To provide smooth, friction-free joint movement

The cartilage matrix (the chemical and biological constituents) is in a state of constant change in life, which in healthy people is a balance between the processes of building up and breaking down. OA is seen by some people as a failure to maintain this balance, due either to a reduction in formation or an increase in breakdown.

Patients with well-defined OA often show changes in the bone underlying the cartilage on their x-rays. These changes are increasingly thought to be a cause of OA rather than a consequence. The cartilage relies on the mechanical health of the underlying bone to maintain its own normal function.

Underlying bone the culprit?

In one model (view) of OA the idea is that a stiffening of the underlying bone results in bone which is no longer a good shock absorber for the cartilage. This may result from repetitive micro fractures in the bone.

There are various lines of evidence which support this view, as well as the inverse association between OA and diseases of low bone density such as osteoporosis. This means that when the bone density is low the occurrence of OA is much less common, indicating bone density is important.

In people with hip OA, bone density is higher on x-ray than the density of people with normal x-rays, and not just at the hip but also in other areas away from the hips.


The presence or absence of inflammation as an important factor appears unclear. There may be some inflammatory process some of the time. Inflammatory processes are usually concerned with healing but in OA seem to be harmful and lead to increased cartilage loss.

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