Osteoarthritis is a disease of joints, particularly the cartilage of the joints. The main load on articular cartilage, the major target tissue in OA is produce by contraction of the muscles that stabilize or move the joint.
Although cartilage is an excellent shock absorbers, at most sites it is only 1 to 2 mm thick too thin to serve as the sole shock absorbing structure in the joint. However, additional protective mechanisms are provided by subchondral bone and muscles around the joint.
Articular cartilage serves two essential function in the joint
- It provides a remarkably smooth bearing surface, so that, with joint movement, the bones glide effortlessly over each other. With synovial fluid as lubricant, the coefficient of friction for cartilage rubbed against cartilage, even under physiologic loading, is 15 times lower than that of two ice cubes passed across each other!
- Articular cartilage prevents concentration of stresses, so the bones do not shatter when the joint is loaded.
When does Osteoarthritis develop?
- The biomaterial properties of the articular cartilage and subchondral bone are normal, but excessive loading of the joint causes the tissues to fail,
or
- The applied load is reasonable, but the material properties of the cartilage or bone are inferior.
Repetitive impact loading soon leads to joint failure.
This fact accounts for the high prevalence of OA at specific sites related to vocational or avocational overloading. In general, the earliest changes occur at the sites in the joint that are subject to the greatest compressive loads.
More than 80 percent of all cases of idiopathic OA of the hip may be due to subtle congenital or development defects, such as
- Congenital subluxation or dislocation
- Acetabular dysplasia,
- Legg-Calve-Perthes disease
- Slipped capital femoral epiphysis
There has been a marked decrease in the prevalence of hip OA in adults in Brittany after institution in the 1940s of screening of newborns and infants for congenital hip disease.
Clinical conditions that reduce the ability of the cartilage or subchondral bone to deform may result in osteoarthritis.
For example, in ochronosis, accumulation of homogentisic acid polymers lads to stiffening of the cartilage and in osteopetrosis, stiffness of the subchondral trabeculae occurs.
In both conditions, severe generalized OA results usually by the age of 40.
The most striking changes in OA are usually seen in load-bearing areas of the articular cartilage. In the early stages the cartilage is thicker than normal, but with progression of OA, the joint surface thins, the cartilage softens, the integrity of the surface is breached, and vertical cleft or fibrillations develop folowed by deep cartilage ulcers.
In an usual attempt of repairing the defect by body, damage might be filled by fibrocartilage. But the repairing tissue is inferior to hyaline articular cartilage and is inferior in withstandin its iability to withstand mechanical stress.
Remodeling and hypertrophy of bone are also major features of OA. Appositional bone growth occurs in the subchondral region, leading to the bony sclerosis.
Growth of cartilage and bone at the joint margins leads to osteophytes or bone spurs, which alter the contour of the joint and may restrict movement. A patchy chronic synovitis and thickening of the joint capsule may further restrict movement. Periarticular muscle wasting is common.
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