Many factors influence its onset and the speed of joint deterioration, including aging, gender, obesity, heredity, trauma (related to sports or occupation), joint overuse, joint instability, and malalignment. Involved basic mechanisms of pathophysiology include “normal” loading on abnormal cartilage versus “abnormal” loading on normal cartilage. Secondary osteoarthritis, the term used to designate osteoarthritis appearing as a sequel to other forms of arthritis, injury, internal derangement, or dysplasia of the joint, is not uncommonly seen in younger persons..
Evidence of osteoarthritis has been found in the skeletal remains of prehistoric animals and humans. The true prevalence is difficult to determine because mild or early osteoarthritis may be asymptomatic and is demonstrated primarily radiographically. In asymptomatic persons, osteoarthritis is often discovered accidentally on radiographs performed for other diagnostic purposes.
Unlike rheumatoid arthritis, osteoarthritis is not a systemic disease; instead, it is a process that is localized in joint structures, with involvement primarily of cartilage, bone, and synovial tissues (see Plate 5-22). Bone marrow lesions and synovitis add significantly to clinical symptoms.
Changes in Articular Cartilage. Pathologic changes in cartilage are characterized by alterations in proteoglycan and collagen. This leads to a softening of the cartilage followed by fraying and fibrillation; cracks develop extending more deeply into the cartilage. Clusters of chondrocytes proliferate in efforts at repair. As degeneration progresses, the entire cartilage becomes thinner and the surface becomes rough from the focal ulcerations. Eventually, the articular surface is denuded of cartilage. Because cartilage has no blood supply, regeneration is limited.
Changes in Bone. New bone forms at two sites: in subchondral bone and at joint margins. In subchondral tissue, the new bone grows chiefly beneath the eroded cartilage surface, thus eventually becoming the articular surface. The new bone becomes smooth, glistening, and sclerotic, or eburnated.
The most characteristic pathologic feature is the growth of osteophytes at the margins of affected joints (spur formation). The osteophyte, which consists of bone growing from the joint margin, usually follows the contour of the articular surface within the capsule and ligamentous attachments.
Changes in Soft Tissue. The synovial and capsular tissues may show mild-to-moderate inflammation and fibrous thickening in joints severely deranged by extensive damage to cartilage and bone. These soft tissue changes are associated with the stress, strain, and mechanical irritation that are secondary to the degenerative changes.
The pathogenesis of osteoarthritis involves a number of factors, any one or a number of which might be operative in a given patient. As noted, many tissues are involved in the process, including subchondral bone, synovium, cartilage, and bone at the joint periphery, as well as ligaments and muscles. Not well recognized is the presence of synovial inflammation as the disease progresses, related to inflammatory mediators such as IL-1, TNF-α, and prostaglandins. Proteases targeted to proteoglycans and collagen play an important role in joint breakdown. Obesity has a strong relationship to osteoarthritis, especially in the presence of additional factors such as joint instability and malalignment. Genetic predisposition to osteoarthritis has been well defined, especially in women with the development of Heberden’s nodes, the nodular swellings at the terminal joints (distal interphalangeal joints) of the fingers. There is a suggestion that aging per se may play an etiologic role in the form of advanced glycation endproducts that lead to formation of cross-links between sugars and proteins, making the cartilage more susceptible to injury from other risk factors.
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