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Pathogenesis of Osteoarthritis in General

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Cartilage

Abstract

Osteoarthritis (OA) is the most common joint disorder and is a leading cause of disability in the adult population. It is now appreciated that all components of the joint, including the cartilage, calcified cartilage, synovial joint lining, and periarticular bone, undergo pathological changes during the initiation and progression of OA. Some of these alterations can be attributed to direct injury and mechanical disruption of the tissues, but in general the mechanisms are dependent on active cell-mediated processes that occur during the long time course of the disease. Based on clinical observations and experimental studies, it is now recognized that it is possible for individual patients to exhibit common sets of symptoms and structural abnormalities due to distinct pathophysiological pathways that act independently or in combination. Recent research focusing on the underlying pathological mechanisms has identified complex signaling networks involving biochemical cross talk among the cartilage, synovium, bone, and other joint tissues. These complex networks involve interplay among anabolic, catabolic, and inflammatory signals within a background of poorly characterized genetic factors. A deeper understanding of the specific and unique roles of these mediators and their downstream targets will provide mechanistic insights into the pathologic processes that affect the cartilage and other joint tissues in OA but also may identify potential therapeutic targets for treatment of this debilitating disease.

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Goldring, M.B., Culley, K.L., Otero, M. (2017). Pathogenesis of Osteoarthritis in General. In: Grässel, S., Aszódi, A. (eds) Cartilage. Springer, Cham. https://doi.org/10.1007/978-3-319-45803-8_1

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