Osteoarthritis Pathophysiology
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    Osteoarthritis Pathophysiology

Despite much research and testing, we still do not know what actually causes osteoarthritis. It was long thought that osteoarthritis was simply a natural consequence of aging. However, experts have abandoned that long-held belief. The American Journal of Medicine states: “There is no evidence that a normal joint, subject to common stresses, will break down over the life of a person.” Then what causes osteoarthritis? Efforts to understand its exact cause are “plagued by controversy,” according to the British magazine The Lancet. Some investigators propose that damage to a bone, such as microfractures, may occur first. This, in turn, may trigger bony outgrowths and cartilage deterioration. Others think that OA starts in the cartilage itself. As it degenerates and frays, they reason, stress increases on the underlying bone. Pathological changes occur as the body attempts to repair the damaged cartilage. Despite the controversy, it appears that osteoarthritis is the result of a complex interplay of environmental, genetic, metabolic and biochemical factors.

Osteoarthritis is predominantly a process of articular cartilage disorder that results from an imbalance between the destructive and reparative processes of the cartilage. The cells in articular cartilage are called chondrocytes. Osteoarthritis appears to trigger the multiplication and division of chondrocytes. This is thought to result from excessive force being applied to the joint. The Chondrocytes now try to produce increased quantities of proteoglycans and collagen. This may result in an initial thickening of the articluar cartilage. However the excess proteoglycans and collagen are not mature and, in fact, resemble immature fetal forms. This results in impairment of the cartilage’s normal physiological function. Over time, the normal smooth surface of the cartilage becomes rough and / or cracked.

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