Osteoarthritis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
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Pathophysiology
Osteoarthritis (OA) is a well-known degenerative joint disease influencing millions of peopleworldwide. Osteoarthritis count as a complex disease caused by changes in the tissue homeostasis of articular cartilages and subchondral bones. The cell/extra-cellular matrix (ECM) and their interactions play an important role in the pathophysiology of articular cartilage and then the occurrence of Osteoarthritis. Different pathogenic mechanisms have been proposed to be responsible for the occurrence of OA. Heredity, obesity, hypoxia, synovitis–capsulitissubchondral bone overload, joint instability (mechanical integrity disturbances) are the most imprtant underlyin causes in this regard. In the current pathogenesis of osteoarthritis (OA) all joint tissues including cartilage, bone, synovium, ligamentous capsular structures, and surrounding muscle are involved. OA characterized by structural changes such as: active bone remodeling, synovial inflammation, and articular cartilage degradation leading to theloss of joint function and angular deformity or malalignment.
Although a variety of synovial fluid markers provide insight into the biological response of joints to injury, no chemical or anatomic (imaging) biomarkers have been identified that monitor the development and progression of OA or the response to therapy. Certain factors increase the risk of developing OA, such as repetitive trauma/loading, joint injury, age, obesity, physical activity, bone mineral density (BMD), and in some subgroups, congenital anomalies. OA is thought to be highly cytokine-driven, and is associated with mechanical stress resulting from overloading of subchondral bone from dysplasias, malalignment, and trauma. Interest has been focused recently on small protein Pathogenesis and Epidemiology of Osteoarthritis ROY K. AARON, MD; JENNIFER RACINE, BA mediators (cytokines) that provide chemical signaling or “cross-talk” among involved tissues. These signaling molecules incite inflammation in the synovium, remodeling subchondral bone, and enzyme activation and extracellular matrix degradation in articular cartilage.
The key functional feature of OA is that the articular cartilage can no longer act as a shock absorber because the extracellular matrix has been destroyed. This does not mean that other joint tissues, such as the subchondral bone, the synovial capsule, and the membrane (Fig. 1.3), are not also involved in the disease process or in causing the pain associated with the disease. Nonetheless, it is the articular cartilage that is central for the initiation and progression of OA, inasmuch as resistance to loading is mostly due to the mechanical properties of the articular cartilage. These properties, in turn, are due to the composition of the extracellular matrix. Degradation of matrix components corresponds to failure of the cartilage to withstand cyclic loading, which, in turn, accelerates further degradation in the load-bearing regions.