Abstract
Osteoarthritis (OA) represents a clinical collection of conditions involving a progressive pathological alteration of joint structure that involves the degeneration of articular cartilage, a remodeling of subchondral bone, and limited synovitis. OA may be described as a part of a process of age-related change or as a disease. It is twice as prevalent in women than men and increases in incidence with age, there being a major rise in incidence after 60 yr (1). Changes that lead to the development of OA are slow. In idiopathic OA, clinical presentation may result from change over a period of up to 30 yr. The disease can involve one or two large joints or may be generalized and involve multiple joints, as in postmenopausal OA. Following joint trauma, there is an increased incidence (1), which probably results from accelerated degeneration over a period of up to 15 yr. Degeneration may also be accelerated by synovitis. In contrast, familial OA presents very early, resulting from a genetic defect causing changes in cartilage matrix and physiology, leading to the manifestation of joint degeneration following natural cessation of growth. Such a condition is seen for example in patients with a mutation in the type II collagen gene and is usually accompanied by skeletal dysplasia.
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Poole, A.R., Webb, G. (2000). Osteoarthritis. In: Tsokos, G.C. (eds) Principles of Molecular Rheumatology. Current Molecular Medicine, vol 1. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-018-6_25
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DOI: https://doi.org/10.1007/978-1-59259-018-6_25
Publisher Name: Humana Press, Totowa, NJ
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