Osteoarthritis (OA)

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Osteoarthritis (OA)

Osteoarthritis/arthrosis is a disease mainly characterized by degenerative

processes of the articular cartilage, but changes also involve the synovial

membrane and the bone next to the cartilage. It is a gradual decay that most

often affects the weight- bearing joints (knees, hips, and spinal joints) and

the joints of the hand. A breakdown of the cartilage matrix leads to cracks and

ulcers and a thinning of the cartilage with a loss of shock absorption. The

underlying bone starts to thicken as a response to the increasing stress, and

bone spurs are formed. In the advanced phases of osteoarthritis, an inflammatory

reaction in the synovial membrane can be seen. This severe degeneration causes

pain, swelling, deformation, and reduced range of motion.

Traditionally, osteoarthritis has been connected to aging, obesity, and repeated

mechanical joint stress. Predisposing factors such as trauma or inherited

abnormalities are also known to trigger degenerative changes and cause secondary

osteoarthritis at even younger ages. New research is beginning to shed light on

how osteoarthritis develops at the cellular and molecular levels.

Evidence is accumulating that the culprits may be factors called cytokines

together with enzymes that break down the collagen matrix. Cytokines are

proteins that carry messages between cells and regulate immunity and

inflammation. Two cytokines, tumor necrosis factor alpha (TNF-a) and interleukin

one beta (IL-1B), play an essential role in the cartilage destruction and

inflammation process (Feldman et al., 1996). They have been found in elevated

levels in the synovial membrane, the synovial fluid, and the cartilage of

osteoarthritis patients. In animal models it was shown that inhibition of TNF-a

results in decreased inflammation, while inhibition of IL-1B effectively

prevents cartilage destruction (Plows et al., 1995).

TNF-a has proven to be an even more important factor in rheumatoid arthritis

(RA), where it is a key factor in promoting inflammation and damage to cartilage

and bone (Bertolini et al., 1986; Saklatvala, J., 1986).

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