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 composed of a synovial membrane, articular or hyaline cartilage, subchondral bone, synovial fluid, and a joint capsule.
Although traditional teaching prescribes that osteoarthritis (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 the 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 as gross areas of the bone become denuded of cartilage.
In the early degenerative process, increased expression and content of various metalloproteinases occur. These proteinases are very much involved in the excessive matrix degradation that characterizes cartilage degeneration in OA.1 Bone along the periphery of the joint replicates to form osteophytes, while the subchondral bone along the midportion of the joint becomes sclerotic, and areas within it may eventually undergo cystic degeneration because of focal resorption. Synovial fluid is formed through an ultrafiltration process of serum by cells that form the synovial membrane (synoviocytes). Synovial cells also manufacture the major protein component of synovial fluid, hyaluronic acid (also known as hyaluronate). Synovial fluid supplies nutrients to the avascular articular cartilage; it also provides the viscosity needed to absorb shock from slow movements, as well as the elasticity required to absorb shock from rapid movements.
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.
The onset of pain is usually insidious, is generally described as aching or throbbing, and may be the result of changes that have occurred over the previous 15-20 years of the patient’s life. Most often, the pain worsens with activity involving the affected joint and is initially relieved with rest; eventually, however, pain occurs even at rest. Since cartilage itself is not innervated, the pain is presumed to arise from a combination of mechanisms, including the following:
Osteophytic periosteal elevation
Vascular congestion of subchondral bone, leading to increased intraosseous pressure
Synovitis with activation of synovial membrane nociceptors
Fatigue in muscles that cross the joint
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 (OA) is the most prevalent musculoskeletal condition that causes joint pain. The incidence of OA increases with age, with estimates based on radiologic evidence indicating the following incidence patterns:
At age 18-24 years, 7% of men and 2% of women show signs of OA in the hands.
At age 55-64 years, 28% of men and women show signs of OA in the knee, and 23% show signs of OA in the hip.
At age 65-74 years, 39% of men and women show signs of OA in the knee and 23% show signs of OA in the hip.
At age 75-79 years, approximately 100% of men and women show some signs of OA.
Mortality does not occur directly from osteoarthritis (OA), but it can result indirectly from complications associated with immobility and deconditioning, medications used to relieve pain associated with OA, or from joint-related surgery.
Morbidity can take the form of pain or loss of function.
No significant correlation exists between the incidence of osteoarthritis (OA) and race, with the exception of the Chinese population, which demonstrates a decreased incidence of OA. Different prevalences are cited for different ethnic groups.
Osteoarthritis (OA) is equally prevalent in men and women aged 45-55 years. After age 55 years, the prevalence of OA increases in women in comparison with men. The primary differences in incidence between males and females are related to the sites affected by OA. The most common sites affected in females are distal interphalangeal joints, proximal interphalangeal joints, first carpometacarpal joints, metatarsophalangeal joints, hips (in those aged 55-64 y), and knees (in those aged 65-74 y). In males aged 65-74 years, the hips and knees are affected more frequently than they are in females.
Most adults older than 55 years show radiographic evidence of osteoarthritis (OA).2 Males develop OA before age 45 years, possibly because of a higher incidence of posttraumatic OA. After age 55 years, women are affected more frequently by OA and tend to have more severe disease than do men.
Patients with osteoarthritis (OA) generally complain of insidious throbbing arthralgias with activity. Although initially, resting relieves the pain, the patient eventually begins to suffer pain even when he/she is at rest. Morning stiffness, which usually lasts less than 30 minutes, may also be experienced in the joint. Intermittent joint swelling and give-way weakness in the knees (ie, quadriceps pain inhibition) are noted.
Early in the disease process of osteoarthritis, physical examination findings include the following:
Joints may appear normal.
Gait may be antalgic if weight-bearing joints are involved.
Later in the disease process, physical examination findings include the following:
Visible osteophytes may be noted.
Joints may be warm to palpation.
Palpable osteophytes frequently are noted.
Joint effusion frequently is evidenced in superficial joints.
Range-of-motion limitations, because of bony restrictions and/or soft tissue contractures, are characteristic.
Crepitus with range of motion is not uncommon.
Primary osteoarthritis (OA), which can be either localized or generalized, is most often idiopathic, except in rare cases in which a defective gene has been found to cause a familial form of OA.
Secondary OA can be caused by the following:
Obesity (increases mechanical stress)3, 4
Repetitive use (ie, jobs requiring heavy labor and bending)5
Previous trauma (ie, posttraumatic OA)
Previous rheumatoid arthritis (ie, burnt-out rheumatoid arthritis)
Heritable metabolic causes (eg, alkaptonuria, hemochromatosis, Wilson disease)
Hemoglobinopathies (eg, sickle cell disease, thalassemia)
Neuropathic disorder leading to a Charcot joint (eg, syringomyelia, tabes dorsalis, diabetes)
Underlying orthopedic disorders (eg, congenital hip dislocation, slipped femoral capital epiphysis)
Disorders of bone (eg, Paget disease, avascular necrosis)