Osteoarthritis (OA)

Osteoarthritis (OA), also erroneously called degenerative joint disease, represents failure of the diarthrodial (movable, synovial-lined) joint. In idiopathic (primary) OA, the most common form of the disease, no predisposing factor is apparent. Secondary OA is pathologically indistinguishable from idiopathic OA but is attributable to an underlying cause.

 

Treatment of OA is aimed at reducing pain, maintaining mobility, and minimizing disability. The vigor of the therapeutic intervention should be dictated by the severity of the condition in the individual patient. For those with only mild disease, reassurance, instruction in joint protection, and an occasional analgesic may be all that is required; for those with more severe OA, especially of the knee or hip, a comprehensive program comprising a spectrum of nonpharmacologic measures supplemented by an analgesic and/or NSAID is appropriate.

Nonpharmacologic Measures

Reduction of Joint Loading  OA may be caused or aggravated by poor body mechanics. Correction of poor posture and a support for excessive lumbar lordosis can be helpful. Excessive loading of the involved joint should be avoided. Patients with OA of the knee or hip should avoid prolonged standing, kneeling, and squatting. Obese patients should be counseled to lose weight. In patients with medial-compartment knee OA, a wedged insole may decrease joint pain.

Rest periods during the day may be of benefit, but complete immobilization of the painful joint is rarely indicated. In patients with unilateral OA of the hip or knee, a cane, held in the contralateral hand, may reduce joint pain by reducing the joint contact force. Bilateral disease may necessitate use of crutches or a walker.

Physical Therapy  Application of heat to the OA joint may reduce pain and stiffness. A variety of modalities are available; often, the least expensive and most convenient is a hot shower or bath. Occasionally, better analgesia may be obtained with ice than with heat.

It is important to note that patients with OA of weight-bearing joints are less active and tend to be less fit with regard to musculoskeletal and cardiovascular status than normal controls. An exercise program should be designed to maintain range of motion, strengthen periarticular muscles, and improve physical fitness. The benefits of aerobic exercise include increases in aerobic capacity, muscle strength, and endurance; less exertion with a given workload; and weight loss. Those who exercise regularly live longer and are healthier than those who are sedentary. Patients with hip or knee OA can participate safely in conditioning exercises to improve fitness and health without increasing their joint pain or need for analgesics or NSAIDs.

Disuse of the OA joint because of pain will lead to muscle atrophy. Because periarticular muscles play a major role in protecting the articular cartilage from stress, strengthening exercises are important. In individuals with knee OA, strengthening of the periarticular muscles may result, within weeks, in a decrease in joint pain as great as that seen with NSAIDs.

Drug Therapy of OA  Therapy for OA today is palliative; no pharmacologic agent has been shown to prevent, delay the progression of, or reverse the pathologic changes of OA in humans. Although claims have been made that some NSAIDs have a "chondroprotective effect," adequately controlled clinical trials in humans with OA to support this view are lacking. In management of OA pain, pharmacologic agents should be used as adjuncts to nonpharmacologic measures, such as those described above, which are the keystone of OA treatment.

Although NSAIDs often decrease joint pain and improve mobility in OA, the magnitude of this improvement is generally modest¾on average, about 30% reduction in pain and 15% improvement in function. In a double-blinded, controlled trial in patients with symptomatic knee OA, an anti-inflammatory dose of ibuprofen (2400 mg/d) was no more effective than a low (i.e., essentially analgesic) dose of ibuprofen (1200 mg/d) or than acetaminophen (4000 mg/d), a drug with essentially no anti-inflammatory effect. Other studies confirm that an analgesic dose of ibuprofen may be as effective as anti-inflammatory doses of other NSAIDs, including the potent agent, phenylbutazone (400 mg/d), in symptomatic treatment of OA. Even in the presence of clinical signs of inflammation (e.g., synovial effusion, tenderness), relief of joint pain by acetaminophen may be as effective as that achieved with an NSAID. Nonetheless, if simple analgesics are inadequate, it is reasonable to cautiously prescribe an NSAID for a patient with OA.

It should be recognized that concern over the use of NSAIDs in OA has grown in recent years because of side effects of these agents, especially those related to the gastrointestinal (GI) tract. Those at greatest risk for OA, i.e., the elderly, appear also to be at greater risk than younger individuals for GI symptoms, ulceration, hemorrhage, and death as a result of NSAID use. The annual rate of hospitalization for peptic ulcer disease among elderly current NSAID users was 16 per 1000¾four times greater than that for persons not taking an NSAID. Among those age 65 and older, as many as 30% of all hospitalizations and deaths related to peptic ulcer disease have been attributed to NSAID use. In addition to age, risk factors for hemorrhage and other ulcer complications associated with NSAID use include a history of peptic ulcer disease or of upper GI bleeding, concomitant use of glucocorticoids or anticoagulants, and, possibly, smoking and alcohol consumption (Table 321-4).

In patients who carry risk factors for an NSAID-associated GI catastrophe, a cyclooxygenase (Cox)-2-specific NSAID may be preferable to even a low dose of a nonselective Cox inhibitor. In contrast to the NSAIDs available to date¾all of which inhibit Cox-1 as well as Cox-2¾two Cox-2-specific inhibitors (CSIs), celecoxib and rofecoxib, are now available. Both appear to be comparable in efficacy to the nonselective NSAIDs. Endoscopic studies have shown that both agents are associated with an incidence of gastroduodenal ulcer lower than that of comparator NSAIDs and comparable to that of placebo. Of additional advantage with respect to the issue of upper GI bleeding, CSIs do not have a clinically significant effect on platelet aggregation or bleeding time, suggesting that CSIs may be especially advantageous in patients at high risk for incurring an NSAID-associated GI catastrophe. Long-term studies are now in progress that are designed to ascertain whether clinically important differences exist between CSIs and nonselective NSAIDs with respect to major GI clinical outcomes.

Systemic glucocorticoids have no place in the treatment of OA. However, intra- or periarticular injection of a depot glucocorticoid preparation may provide marked symptomatic relief for weeks to months. Because studies in animal models have suggested that glucocorticoids may produce cartilage damage, and frequent injections of large amounts of steroids have been associated with joint breakdown in humans, the injection should generally not be repeated in a given joint more often than every 4 to 6 months.

Intraarticular injection of hyaluronic acid has been approved recently for treatment of patients with knee OA who have failed a program of nonpharmacologic therapy and simple analgesics. Because the duration of benefit following treatment may exceed by months the synovial half-life of exogenous hyaluronic acid, the mechanism of action is unclear. The placebo response to intraarticular injection of hyaluronic acid is often large and sustained. Although relief of knee pain is achieved more slowly after hyaluronic acid injection than after intraarticular glucocorticoid injection, the effect may last much longer after hyaluronic acid injection than after glucocorticoid injection.

Capsaicin cream, which depletes local sensory nerve endings of substance P, a neuropeptide mediator of pain, may reduce joint pain and tenderness when applied topically by patients with hand or knee OA, even when used as monotherapy, i.e., without NSAIDs or systemic analgesics.