Definition

Osteoarthritis (OA) is generally considered a family of degenerative joint disorders characterized by specific clinical and radiographic findings. OA is the most prevalent chronic joint disease and has become the most common cause of walking disability in older adults in the United States [1–3]. It is estimated that 26.9 million adults have clinical OA, and the total cost for all arthritis, including OA, is more than 2% of the United States gross domestic product [4,5]. The disease burden of OA is likely to continue to increase with the aging population and higher incidence of obesity [2,5].

OA has traditionally been thought of as just a condition of cartilage degeneration [6]. It is actually a complex combination of genetic, metabolic, biomechanical, and biochemical joint changes that lead to failure of the normal cartilage remodeling process (Fig. 139.1). The joint then accumulates increasing cartilage degeneration changes in response to stress or injury [2,6]. More recent evidence implicates bone changes and synovial inflammation also as integral to the pathologic process of OA [2]. As a whole, OA is characterized by degradation and loss of articular cartilage, hypertrophic bone changes with osteophyte formation, subchondral bone remodeling appearing as sclerosis or cysts, and chronic synovitis or inflammation of the synovial membrane [1,6].

Joint involvement in OA is usually asymmetric, with a predilection for weight-bearing joints. Common sites of involvement are the hips, knees, hands, feet, and spine. Less common sites of involvement are the ankles, wrists, shoulders, and sacroiliac joints. Secondary arthritis may be manifested with an atypical pattern of joint involvement.

OA is classified into two groups: primary and secondary. Primary or idiopathic OA can be localized or generalized. Localized OA usually refers to a single joint; generalized OA describes involvement of three or more joints. Secondary OA is due to a specific condition known to cause or to worsen development of OA (Table 139.1).

Multiple risk factors have been linked to the development of OA (Table 139.2). Systemic factors include age, gender, genetics, bone mineral density, and body weight. Age is consistently one of the strongest if not the strongest risk factor for OA [3,5]. Female gender is associated with higher prevalence of symptomatic knee, hip, and hand OA [3,5]. Heritable genetic traits may play a role in OA, but identification of such traits has been challenging. Some genetic markers strongly implicated in OA include GDF5, MCF2L, and the genomic region 7q22 [7,8]. There is an inverse relationship between bone mineral density and OA [3,9]. Both overweight and obese people are shown to be at a greater risk for OA, especially in weight-bearing joints like the knee [3,10,11]. Low levels of factors like vitamin C, vitamin D, vitamin E, and vitamin K may have an effect on OA, but there is no consensus recommendation currently [3].

Local biomechanical factors implicated in OA include previous joint injury, joint malalignment, bone anatomic variation or abnormality, and muscle weakness. Those with previous injury have a 15% greater lifetime risk of symptomatic knee OA [11]. Lower extremity malalignment may be associated with greater radiographic knee OA. Bone abnormality like acetabular dysplasia is associated with greater incidence of hip OA [12]. Muscle weakness, specifically of the knee extensor muscles, predicts knee OA in most cohorts of women [3,13].

In terms of physical loading, some suggest that there is greater risk of knee OA with work activities such as squatting, lifting, prolonged standing, or climbing stairs, but this is not seen consistently [11]. Currently, there is no strong evidence to show that sports or physical activity itself leads to an increased risk of symptomatic OA [3]. Historical data have correlated certain sports with OA of specific joints, but there are many confounders in these studies that make interpretation inconclusive [3].

Symptoms

Patients usually complain of pain, stiffness, reduced movement, and swelling in the affected joints that is exacerbated with activity and relieved by rest. Pain at rest or at night suggests severe disease or another diagnosis. Early morning stiffness, if it is present, is typically less than 30 minutes. Joint tenderness and crepitus on movement may also be present. Swelling may be due to bone deformity, such as osteophyte formation, or an effusion caused by synovial fluid accumulation. Systemic symptoms are absent.

In early disease, pain is usually gradual in onset and mild in intensity. Pain is typically self-limited or intermittent. Patients with advanced disease may describe a sense of grinding or locking with joint motion and buckling or instability of joints during demanding tasks. Periarticular muscle pain may be prominent. Patients may complain of fatigue if biomechanical changes lead to increased energy requirements for activities of daily living. Overuse of alternative muscle groups can lead to development of pain syndromes in other parts of the musculoskeletal system.

Diagnosis of OA involves assessment of the affected joints for common clinical features (Table 139.3). These usually include tenderness, bone enlargement, and malalignment. Osteophytes, joint surface irregularity, or chronic disuse may also result in decreased range of motion, pain, effusion, and crepitus. Locking during range of motion may suggest loose bodies or floating cartilage fragments in the joint. Joint contracture can result from holding a joint in slight flexion, which is less painful for inflamed or swollen joints. There may be secondary abnormalities in joints above or below the primarily involved joint. Remember to assess joints bilaterally because asymptomatic joints may also have abnormal findings.

Neuromuscular and General Examination

A thorough musculoskeletal examination should include inspection, palpation of soft tissues surrounding the joint of interest, assessment of muscle strength and flexibility, and joint-specific provocative maneuvers. First, gait should be observed. There may be an antalgic gait or a slow gait pattern because of pain in a specific joint. If the patient uses a cane, appropriate use of the cane should be assessed during gait.

Both functional strength and manual muscle testing should be performed. Periarticular muscle atrophy and weakness may be present in chronic OA. However, manual muscle testing is typically unreliable in the lower extremities because of the high baseline strength of these muscle groups. Function tests like sit-to-stand testing may be more informative. Palpation and dynamic testing of soft tissues may differentiate pain from tendinopathy or bursitis from OA. Joint-specific provocative maneuvers may help isolate the source in symptomatic patients with poorly localized pain. A careful neurologic examination should be performed to ensure that pain is not the result of nerve impingement or a neuropathic process.

Clinicians may also consider performing a general examination. Evaluation of other systems may also help differentiate primary OA from secondary OA due to a systemic process. Because obesity has been identified as a risk factor for OA, assessment of the patient’s body mass index may also be useful.

Functional Limitations

Functional limitations will depend on the joints affected by OA. Patients with disease in the hips and knees will have impairments in mobility, locomotion, and activities of daily living involving the lower body. Patients may complain of increasing difficulty with climbing up and down stairs, walking, making chair or toileting transfers, and lower body dressing and grooming. Degeneration in the shoulders or hands limits vocational and recreational activities, self-care, and upper body activities of daily living. Patients may initially have trouble with using the computer or lifting boxes, which then progresses to difficulties with activities of daily living like feeding, grooming, bathing, and dressing. Spine OA can result in limitations with all mobility.

Diagnostic Studies

Although imaging studies are not needed to confirm the diagnosis, plain radiographs may help elucidate the severity of joint damage and progression of OA. The classic findings include asymmetric joint space narrowing, osteophytes at joint margins, subchondral sclerosis, and subchondral cyst formation. There is a well-demonstrated discordance between x-ray findings and symptoms in OA. Asymptomatic individuals may have significant radiographic disease, and severe pain and dysfunction can occur in the setting of limited radiologic changes. Computed tomography scans, ultrasonography, and magnetic resonance imaging are typically not needed for evaluation of OA but can be helpful in providing better visualization not only for OA severity evaluation but also for identification of other tissue pathologic processes and diagnosis [1].

Routine laboratory test results should be normal, and laboratory testing is usually not needed in uncomplicated cases of OA. If laboratory tests are available, clinicians should take care in interpreting the results. There is a high prevalence of laboratory abnormalities in elderly people, such as a raised erythrocyte sedimentation rate or anemia, because of comorbid conditions. Autoimmune markers may be useful to differentiate OA from other musculoskeletal disorders like inflammatory arthritides.

Joint aspiration should be pursued in patients with significant joint effusion or inflammation. Joint fluid analysis can be helpful in ruling out crystal deposition disease like gout or pseudogout, inflammatory arthritis, or infectious arthritis. In contrast to other arthritides, synovial fluid in OA is usually clear with normal viscosity and leukocyte counts typically less than 1500 to 2000 cells/mm³.