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Osteoarthritis (OA) is the most common form of arthritis. Also known as degenerative joint disease, OA is characterized by loss of articular cartilage within a joint resulting in chronic pain, stiffness, deformity, and subsequent functional disability. Osteoarthritis may be classified as primary/idiopathic, for which the cause is unknown, or secondary osteoarthritis, which occurs as a result of trauma, infection, neuropathy, bone ischemia, congenital abnormality, chronic inflammatory arthropathy, or other cause.


It is estimated that, in the United States, symptomatic osteoarthritis afflicts 13.9% of adults age 25 and older and 33.6% of those above the age of 65. The prevalence of the disease has been increasing in recent years: an estimated 21 million suffered from the disease in 1990 compared with 26.9 million in 2005.1 The incidence of osteoarthritis increases with age; however, there has been a recent increase in patients presenting with symptoms earlier in adulthood, prior to the age of 65. The precise etiology of osteoarthritis is unknown. A number of biomechanical and biochemical causes have been implicated to suggest that the etiology is multifactorial. The risk factors for OA can be classified into modifiable and nonmodifiable. Modifiable risk factors include obesity, joint trauma, occupations that involve repetitive loading of the joint, and muscle weakness. Nonmodifiable risk factors include older age, gender (women are at higher risk in most joints), race (possible lower risk in some Asian populations), and congenital deformity or ligamentous laxity. A genetic predisposition to OA is speculated; however, this has not yet been well defined.2


Although older age is associated with OA, the changes in osteoarthritic cartilage are pathologic and distinct from those of normal senescence.3-5 In healthy cartilage, the chondrocytes maintain a balance between synthesis and regeneration of hyaline cartilage by producing the proteoglycans and collagen that form the matrix. In OA, this balance is interrupted and chondrocytes do not synthesize a sufficient matrix. As a result, clefts and fissures occur in the hyaline cartilage. In the early stages of OA, the cartilage softens, and, with more advanced disease, portions of full thickness cartilage are lost. Some of these cartilage fragments may become free within the joint space as loose bodies. Loose bodies within a joint can cause pain and mechanical symptoms such as locking of the joint. Once the matrix fails mechanically, the underlying bone is exposed. New bone forms in the subchondral region, resulting in sclerosis. This sclerotic subchondral bone is more apt to fissure, allowing synovial fluid to extrude into the bone, creating subchondral cysts. As the bone attempts to repair itself, bone spurs—or osteophytes—occur inside and at the margins of the joint. These changes within the articular cartilage surface and surrounding bone then manifest as pain and deformity of the joint.




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