69 Osteoarthritis

Overview/pathophysiology

Osteoarthritis (OA) is the most prevalent articular disease in adults 65 yr of age and older. OA has been known by many names, including degenerative joint disease (DJD), degenerative arthritis, or hypertrophic arthritis. It is no longer regarded as a wear-and-tear condition that occurs as a normal result of aging. In fact, joint changes that result from arthritis can be distinguished readily from age-related changes in articular cartilage of an asymptomatic older adult. In OA, chondrocytes within the joint fail to synthesize good-quality matrix in terms of both resistance and elasticity; this makes the cartilage more prone to deterioration. OA is recognized as a process in which all joint structures produce new tissue in response to joint injury or cartilage destruction. This chronic, progressive disease is characterized by gradual loss of articular cartilage combined with thickening of the subchondral bone and formation of bony outgrowths (osteophytes) at the joint margins. Affected individuals experience increasing pain, deformity, and loss of function. Prevalence of OA varies among different populations, but it is a universal human problem that actually may begin by 20-30 yr of age. The majority of people are affected by 40 yr of age, but few experience symptoms until after 50 or 60 yr of age. Before 50 yr of age, men are affected more often than women. After 50 yr of age, however, incidence of OA is twice as great in women as in men.

OA may be classified as either idiopathic or secondary. Idiopathic OA occurs in individuals with no history of joint injury or disease or of systemic illness that might contribute to the development of arthritis. Aging may be one influence on the deterioration of cartilage in arthritic joints, but additional evidence suggests existence of an autosomal recessive trait for gene defects that causes premature cartilage destruction. Prevalence of OA in postmenopausal women also suggests involvement of hormones in initiation of the disease. In contrast, secondary OA has an identifiable cause. Any condition or event that directly damages or overloads articular cartilage or causes joint instability can result in arthritic changes. Secondary OA typically occurs in younger individuals because of congenital processes (e.g., Legg-Calvé-Perthes disease), trauma, repetitive occupational stress, hemophilic joint hemorrhage, or infection.

OA is characterized by site specificity, with certain synovial joints showing higher disease prevalence. These include the weight-bearing joints (hips, knees); cervical and lumbar spine; distal interphalangeal (DIP), proximal interphalangeal (PIP), and metacarpophalangeal (MCP) joints in the hands; and metatarsophalangeal (MTP) joints in the feet (bunion deformity, or hallux valgus). The hips are most often affected in men and the hands in women, especially after menopause.

Health care setting

Primary care

Assessment

Signs and symptoms:

Joint pain and stiffness are the dominant symptoms and most common reason for seeking medical evaluation. However, because onset of pain is typically insidious, the patient may not be able to recall exactly when it began. The patient often describes an “aching” asymmetric pain that increases with joint use and is relieved by rest, especially in early stages of OA. Pain often is worse with using stairs, standing, and walking; less pain is experienced at night and when sitting. As the disease progresses, however, night pain or pain at rest is likely to occur. The patient also may state that pain increases with cool, damp, and rainy weather. This has been attributed to changes in intraarticular pressure associated with the fall in barometric pressure that precedes inclement weather. Joint stiffness ranges from slowness to pain with initial movement. Early morning stiffness is common but typically lasts less than 30 min. Stiffness after periods of rest or inactivity (articular gelling or gel phenomenon) is also characteristic of OA but resolves within several minutes. Patient may describe a squeaking, creaking, or grating with movement (crepitus) caused by loose cartilage particles in the joint capsule.

Physical assessment:

Pairs of joints should be compared for symmetry, size, shape, color, appearance, temperature, and pain. Bony enlargement is common, and affected joints are likely to be tender to palpation. Reduced range of motion (ROM) is extremely common in osteoarthritic joints and contributes greatly to disability. Generally it is related to osteophyte formation, joint surface incongruity from severe loss of cartilage, or spasm and contracture of surrounding muscle. Locking during movement may be accentuated by mild effusion and soft tissue swelling; large effusions are uncommon in OA and in fact would suggest other processes such as septic arthritis or gout. Crepitation during passive movement is present in more than 90% of patients with knee OA and indicates loss of cartilage integrity. Deformities may include Heberden’s nodes on DIP joints and Bouchard’s nodes on PIP joints of the hands. Almost 50% of patients with knee OA have a joint malalignment, typically a varus deformity due to cartilage loss in the medial compartment. Leg length discrepancy may be noted due to loss of joint space in advanced hip OA. In addition, muscular atrophy may be seen in advanced disease secondary to joint splinting for pain relief.

Diagnostic tests

OA almost always can be diagnosed by history and physical examination.

Laboratory tests:

To rule out other arthropathic conditions (e.g., rheumatoid arthritis, septic arthritis) and to establish baselines before starting therapy.

Complete blood count (CBC):

Suggested for patients who will be taking nonsteroidal antiinflammatory drugs (NSAIDs) for arthritis symptom management, with additional CBC prescribed periodically to screen for anemia caused by occult gastrointestinal (GI) bleeding.

Renal and liver function tests:

For patients starting aspirin or NSAID therapy, with further testing done every 6 mo to assess for side effects such as electrolyte imbalance, hepatitis, or renal insufficiency.

Rheumatoid factor (RF) and erythrocyte sedimentation rate (ESR):

Neither excludes a diagnosis of OA in the older patient. About 20% of healthy older adults have positive RF, and ESR tends to rise with age. ESR evaluation is useful to rule out chronic conditions such as polymyalgia rheumatica. Synovial fluid analysis is another reliable method for differentiating OA from other arthritic disorders.

X-ray examination:

Radiographic findings do not always correlate with severity of patient’s clinical symptoms. With disease progression, x-ray examination reveals joint space narrowing, osteophytes at joint margins, subchondral cysts, and altered shape of bone ends that suggests bone remodeling.

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