254-259 Grenga

Osteoarthritis (OA), also erroneously called degenerative joint disease, represents failure of a diarthrodial joint. In idiopathic OA, the most common form of the disease, no predisposing factor is apparent. Secondary OA is pathologically indistinguishable from idiopathic OA, but is attributable to an underlying cause, such as trauma or metabolic and endocrine diseases.1 Major trauma and repetitive joint use are also important risk factors for OA. The most striking changes in OA are usually seen in loadbearing areas of the articular cartilage. In the early stages, the cartilage is thicker than normal, but with progression of OA, the joint surface thins, the cartilage softens, the integrity of the surface is breached, and vertical clefts develop. Remodeling and hypertrophy of bone are also major features of OA. Appositional bone growth occurs in the subchondral region, leading to the bony “sclerosis” seen radiographically. Growth of cartilage and bone at the joint margins leads to osteophytes, which alter the contour of the joint and may restrict movement. OA develops in one of two settings: (1) the biomaterial properties of the articular cartilage and subchondral bone are normal, but excessive loading of the joint causes the tissues to fail; or (2) the applied load is reasonable, but the material properties of the cartilage or bone are inferior. Although articular cartilage is highly resistant to wear under conditions of repeated oscillation, repetitive impact loading soon leads to joint failure. This fact accounts for the high prevalence of OA at specific sites related to vocational or avocational overloading. In general, the earliest changes occur at the sites in the joint that are subject to the greatest compressive loads. Synovial fluid effusions and/or arthritis may be found in patients with chronic lymphocytic thyroiditis (CLT). These arthropathies can be attributed to the Osteoarthritis of the Temporomandibular Joint in an Adult Patient with Hashimoto Thyroiditis: Case Report