Osteoarthritis (OA), also referred to as degenerative joint disease, is characterized by a generally progressive loss of articular cartilage accompanied by attempted repair of articular cartilage, remodeling, and sclerosis of subchondral bone, and in many instances, the formation of subchondral bone cysts and osteophytes19-24 (Fig. 7).

Figure 7 A, Histologic section of osteoarthritic cartilage from a humeral head removed at surgery for total shoulder arthroplasty. Note the significant fibrillation, vertical cleft formation, the tidemark, and the subchondral bony end plate. B, Another viewof surface fibrillation showing vertical cleft formation and widespread large necrotic regions of the tissue devoid of cells. Clusters of cells, common in osteoarthritic tissues, are also seen. (Reproduced from Mankin HJ, Mow VC, Buckwalter JA: Articular cartilage repair and osteoarthritis, in Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2000, pp 471-488.)

 

In addition to the histopathologic changes in the synovial joint, diagnosis of OA requires the presence of symptoms and signs that may include joint pain, restricted motion, crepitus with motion, joint effusions, and deformity. The structural changes characteristic of OA include fissuring and focal erosive cartilage lesions, cartilage loss and destruction, subchondral bone sclerosis, and cyst and large osteophyte formation at the joint margins. Unlike the destruction seen in joint diseases with a major inflammatory component, OA consists of a sequence of cell and matrix changes that result in loss of articular cartilage structure and function, accompanied by cartilage repair and bone remodeling reactions. Because of the repair and remodeling reactions, the degeneration of the articular surface in OA is not uniformly progressive,24 and the rate of joint degeneration varies among individuals and among joints. Occasionally, it occurs rapidly, but in most joints it progresses slowly over many years. OA may stabilize or even improve spontaneously with at least partial restoration of the articular surface and a decrease in symptoms. OA has no single cause, but by a variety of means reaches a common end stage. Despite many years of research, considerable speculation still exists concerning various factors that may contribute to the initiation and perpetuation of the disorder. OA develops most commonly in the absence of a specific known cause, a condition referred to as primary or idiopathic OA.19 Less frequently, it develops as a result of joint injuries, infections, or a variety of hereditary, developmental, metabolic, and neurologic disorders, a group of conditions referred to as secondary OA.19 The age of onset of secondary OA depends on the underlying cause; thus, it may develop in young adults and even children as well as the elderly. In contrast, a strong association exists between primaryOAand age. Despite this strong association and the widespread view that OA results from wear-andtear processes, the relationships among joint use, aging, and joint degeneration remain uncertain. Furthermore, the changes observed in articular cartilage from the normal joints of older individuals differ from those observed in OA, and normal lifelong joint use has not been shown to cause degeneration.14 Thus, OA is not simply the result of mechanical wear from joint use; the biologic processes of tissue maintenance and remodeling certainly play important roles in the continued normal function of articular cartilage with age.