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Osteoarthritis (OA), the most common form of joint disease, affects nearly 50 percent of the population older than the age of 65 and virtually everyone over the age of 75.(1) OA affects primarily the weight-bearing joints of the peripheral and axial skeleton, causing pain, limitation of motion, deformity, and progressive disability. Osteoarthritis may be described as degenerative joint disease (DJD) or hypertrophic arthritis, however these terms may not reflect that OA is not a single disorder, but a pattern of reactions or sequence of events that lead to joint injury.
It is often best described as a disorder of both mechanical and biologic events that alter the normal synthesis and degradation of articular cartilage.(2) Recent advances and knowledge concerning articular cartilage function and physiology have dispelled the traditional wear-and-tear theory as the cause of OA, focusing on biomechanical forces, as well as inflammatory, biochemical, and immunologic factors.
Generally, OA can be classified into two major categories. Primary (idiopathic) OA occurs without any previous triggering event or known cause and reflects the majority of cases. This category can be further classified into localized OA and generalized OA. Localized OA usually reflects involvement of one joint, while generalized OA indicates involvement of three or more joints. Erosive OA, yet a third category, reflects changes in the underlying bone. The secondary classification of OA is based on other known abnormalities or trauma. Metabolic or endocrine disorders and congenital factors would be included in this category. To assist in uniform reporting of rheumatic diseases, a classification scheme and criteria for OA of the hip, knee, and hand have been reported by the American College of Rheumatology.(3) These criteria include objective and subjective factors such as pain, sedimentation rate, bony changes on examination, and radiographic features consistent with osteoarthritis.
Cartilage is a metabolically active tissue that undergoes a continual internal remodeling of its extracellular matrix (ECM). Histologically, articular cartilage is 75-80 percent water by weight. The ECM is comprised of a small number of chondrocytes (less than 5 percent) and the remainder (20-25 percent) consists of three classes of molecules: collagens, large aggregates of proteoglycans or aggrecans, and noncollagenous proteins.
The chondrocytes control the synthesis and degradation of the ECM by affecting the production of collagen and proteoglycans. The collagens provide tensile strength and maintenance of tissue volume and shape. The proteoglycans (PGs) provide the "stuffing material" for the matrix. The PGs consist of a protein core and at least one or more glycosaminoglycan chains (chondroitin sulfate, keratan sulfate, and dermatan sulfate). These aggregates retain and maintain the water content of the cartilage because of their highly hydrophilic and anionic properties. This is what gives cartilage its resilience and load bearing properties.
The slow, progressive changes seen in osteoarthritis consist of an increase in water content, loss of proteoglycans, and reduction of PG aggregates in cartilage. The net result is failure of the cartilage to repair itself.(4)
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