Osteoarthritis (OA) is a chronic disease process affecting synovial joints, particularly large weight-bearing joints. OA is particularly common in older patients but can occur in younger patients either through a genetic mechanism or, more commonly, because of previous joint trauma.
Joints can be classified as synovial, fibrous, or combination joints, based on the presence or absence of a synovial membrane and the amount of motion that occurs in the joint. Normal synovial joints allow a significant amount of motion along their extremely smooth articular surface. These joints are comprised of a synovial membrane, articular or hyaline cartilage, subchondral bone, synovial fluid, and a joint capsule.
Although traditional teaching prescribes that OA affects primarily the articular cartilage of synovial joints, pathophysiologic changes also occur in the synovial fluid, as well as in the underlying (subchondral) bone and overlying joint capsule. The affected cartilage initially develops small tears, known as fibrillations, at the articular surface, followed by larger tears; the cartilage eventually fragments off into joints. The cartilage-forming cells (ie, chondrocytes) replicate in an attempt to keep up with the cartilage loss; however, they eventually are unable to do so, and the underlying bone becomes exposed because of gross areas of bone denuded of cartilage.
The osteoarthritic joint is characterized by decreased concentration of hyaluronic acid because of reduced production by synoviocytes and increased water content because of inflammation, particularly during later stages of the disease.
Pain is usually of insidious onset, is generally described as aching or throbbing, and may result from changes that have occurred over the last 15-20 years. Most often, the pain is worse with activity involving the affected joint and is initially relieved with rest; eventually pain occurs even at rest. Since cartilage itself is not innervated, the pain is presumed to be from a combination of mechanisms, including (1) osteophytic periosteal elevation, (2) vascular congestion of subchondral bone leading to increased intraosseous pressure, (3) synovitis with activation of synovial membrane nociceptors, (4) fatigue of muscles that cross the joint, and (5) overall joint contracture.
In addition to the underlying pathophysiologic changes described above, overall, the joint may undergo mechanical deformation with resultant malalignment and instability. Alternatively, the joint can ankylose.
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Osteoarthritis – – Mayo Clinic – http://www.mayoclinic.com/health/osteoarthritis/DS00019