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Arthritis - Osteoarthritis

age genetic clinical joints disease usually cartilage

Osteoarthritis is common and, at older ages, becomes virtually universal. It is an active process, not just wearing out of joints or "degenerative joint disease" (Joint Working Group of the British Society for Rheumalology and, Research Unit of the Royal College of Physicians).

Causes and disease mechanisms. There are progressive changes in osteoarthritic cartilage. Initially the collagen (the material that provides important lining of bones) framework is damaged by changes in structural complex sugars (proteoglycans), in the cartilage matrix, and in water content. Attempted repair increases the number and activity of cartilage cells (chondrocytes). This leads to the production of degradative enzymes. Subsequent fissuring, cartilage ulceration and matrix loss makes damage irreversible. There is variable accompanying inflammation of the synovium that lines the joints, as well as changes in adjacent bone. Predisposing factors for osteoarthritis include age, female sex, family history (indicating genetic predisposition), obesity, previous trauma, repetitive occupational stress, and previous inflammation, such as rheumatoid arthritis. Osteoarthritis increases with age. By sixty-five years most people have X-ray evidence of osteoarthritis, though under 30 percent have symptoms.

Clinical features. Pain is the dominant symptom. It is usually activity related, varies in severity, and has periods of remission. Associated symptoms include morning stiffness (usually under thirty minutes), postexercise gelling, bony swelling, limited movement, and muscle weakness. Examination shows bony swelling, tenderness, and crepitus. Effusions, usually in the knees, are common.

Osteoarthritis can involve one or many joints. Generalized osteoarthritis involves the small joints of the fingers, especially those at the knuckles closest to the ends, as well as the wrists, knees, and hips.

Investigations. Blood tests are usually normal, although some elevation of tests for inflammation can be seen. Tests for the protein known as rheumatoid factor are negative. X-rays show joint space loss, and increased bone underneath and at the edges of joints, called subchondral sclerosis and marginal bony outcroppings (osteophytes), respectively. In late disease, joints can be totally destroyed. Isotope bone scanning (scintigraphy) shows increased activity of the joints in early disease.

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