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ARTHROSCOPIC DEBRIDEMENT AND LAVAGE* Arthroscopic surgery can be helpful in alleviating knee pain and improving function in the subgroup of patients with knee OA1 in whom loose bodies, flaps of cartilage, or disruption of the meniscus (e.g., a bucket handle tear) cause mechanical symptoms, such as locking, giving way of the limb, or catching. Although arthroscopic debridement, e.g., smoothing of the surface of fibrillated articular cartilage or meniscus, trimming of osteophytes, and removal of inflamed synovium, is employed widely in patients with symptomatic knee OA who do not have mechanical symptoms, but who have not benefited from pharmacologic therapy, this therapeutic modality appears to be of no greater symptomatic benefit than placebo in such patients.

Pharmacologic Therapy* •* NSAIDS22 AND ACETAMINOPHEN (N-ACETYL-P-AMINOPHENOL, APAP)* Drug therapy for OA1 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 NSAID23s slow the rate of cartilage damage, adequately controlled clinical trials in humans with OA to support this view are lacking.

In management of OA1 pain, pharmacologic agents should be used as adjuncts to nonpharmacologic measures, such as those described above. The latter are the keystone of OA treatment. Although NSAIDs24 often decrease joint pain and improve mobility in OA, the magnitude of improvement is generally modest — on average, about 30% reduction in pain and 15% improvement in function. Many patients taking a full therapeutic dose of NSAIDs continue to experience a significant level of residual joint pain. On the other hand, low (i.e., analgesic) doses of NSAIDs may be as effective as anti-inflammatory doses; 30 to 40% of patients with OA may find APAP25 — an analgesic recommended for treatment of mild-moderate pain — as effective as an NSAID. Even in patients with clinical signs of joint inflammation (synovial effusion, tenderness), relief of joint pain by APAP may be as effective as that achieved with an NSAID. Nonetheless, if simple analgesics are inadequate, it is reasonable to prescribe an NSAID for the patient with OA.

However, concern over the use of NSAIDs26 in OA1 has grown in recent years because of the adverse effects of these agents, especially those related to the gastrointestinal tract. Those at greatest risk for OA, i.e., the elderly, appear to be at greater risk than younger individuals for gastrointestinal 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 1000, i.e., four times greater than that for persons not taking an NSAID. Among people age =65, as many as 30% of all hospitalizations and deaths related to peptic ulcer disease have been attributed to NSAID use. Risk factors for hemorrhage and other ulcer complications associated with NSAID use include, in addition to age, a history of peptic ulcer disease or of upper gastrointestinal bleeding, concomitant use of glucocorticoids or anticoagulants, and, possibly, smoking and alcohol consumption (Table 312-4).

SELECTIVE COX-2 INHIBITORS* In patients who carry risk factors for an NSAID27-associated gastrointestinal catastrophe, a cyclooxygenase (COX)-2 selective NSAID may be preferable to even a low dose of a nonselective COX inhibitor. In contrast to the nonselective NSAIDs, all of which inhibit COX-1 as well as COX-2, selective COX-2 inhibitors, e.g., celecoxib, rofecoxib, valdecoxib, are now available. These exhibit no greater efficacy than nonselective NSAIDs, but endoscopic studies show that they are associated with a lower incidence of gastroduodenal ulcer than nonselective NSAIDs. Of additional advantage with respect to the issue of upper gastrointestinal bleeding, selective COX-2 inhibitors do not have a clinically significant effect on platelet aggregation or bleeding time.

Results of two large-size gastrointestinal safety studies, the CLASS trial and VIGOR study, have been published (Table 312-5). Both were designed to ascertain whether treatment with celecoxib or rofecoxib, respectively, resulted in a lower incidence of clinically important NSAID28-associated ulcers and ulcer complications than that seen with nonselective NSAIDs. In the VIGOR trial, a clear reduction in the incidence of upper gastrointestinal events was apparent in the rofecoxib treatment arm, in comparison with the naproxen arm. The risk of all clinical upper gastrointestinal events was reduced by some 54% (p<. 01), of complicated upper gastrointestinal events by 57% (p =. 005), and of any gastrointestinal bleeding by 62% (p<. 01). In the CLASS study, the annualized incidence rates of ulcer complications (the primary outcome measure) with celecoxib was not significantly different from that and with the comparator nonselective NSAIDs after 6 months of treatment, although the difference for ulcer complications combined with symptomatic ulcers was significant (2.08% vs 3.54%, respectively, p =. 02). Although a significant reduction in ulcer complications was seen with celecoxib, use of low-dose aspirin for cardiovascular prophylaxis appeared to mitigate the gastroprotective effect of celecoxib. (Although only 22% of subjects in the CLASS study were taking low-dose aspirin, as many as 60% of patients with OA1 >60 years old may do so in clinical practice.) Furthermore, the superiority of celecoxib observed among nonaspirin users during the first 6 months was not sustained in patients treated for 12 months.

Unexpectedly, the incidence of myocardial infarction (MI) in the VIGOR study was fourfold greater among patients treated with rofecoxib than with naproxen. Although (1) the absolute number of MIs was small; (2) the study was not powered to compare the effects of the two treatments on MI; (3) the comparability of the treatment groups with respect to the prevalence of risk factors for MI (e.g., obesity, smoking, hypercholesterolemia, diabetes mellitus) was unknown; (4) the dose of rofecoxib was two to four times greater than that used for treatment of OA; and (5) the trial was conducted in patients with rheumatoid arthritis, in which the incidence of MI is about twice as great as that in OA1. The rofecoxib label contains a caveat about use of this drug in patients predisposed to ischemic heart disease.

GLUCOCORTICOID INJECTION* Systemic glucocorticoids have no place in the treatment of OA1. 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 HYALURONAN* Intraarticular injection of hyaluronan has been approved for treatment of patients with knee OA1 who have failed a program of nonpharmacologic therapy and simple analgesics. Because the duration of benefit following treatment may exceed by many months the synovial half-life of exogenous hyaluronan, the mechanism of action is unclear. However, the placebo response to intraarticular injection of hyaluronan is often large and sustained. For example, the pivotal clinical trial of Hyalgan failed to demonstrate superiority of oral naproxen, 500 mg bid, over intraarticular injections of saline. Furthermore, intraarticular injection of a preparation of the high-molecular-weight hylan (Synvisc) which had been denatured to eliminate its viscoelasticity, was no less efficacious than injection of the intact hylan or non-cross-linked lower molecular weight hyaluronan. Consistent with this observation, no difference in efficacy was observed in a randomized placebo-controlled trial of Synvisc, a lower molecular weight hyaluronan formulation, and placebo.

OPIOIDS* Health professionals and patients hold concerns about tolerance and physical and psychological dependence, and many physicians hesitate to prescribe opioids for patients with nonmalignant chronic pain because of concerns about legal action by governmental regulatory authorities. However, the prevalence of narcotic abuse among older people is low: <1% of patients attending methadone maintenance programs are =60 years.

For acute flares of OA1 pain, when APAP29 or an NSAID30 does not provide adequate pain relief or is not well tolerated, a weak opioid, e.g., oral codeine, deserves consideration. Because codeine, when taken alone in a dose of 60 mg, is no more effective than 650 mg of aspirin or APAP, it is used in combination with these drugs to treat moderate or moderately severe OA pain.

Opioids may also be useful for chronic OA1 pain. The major problem associated with the use of chronic opioid therapy for OA pain is the side effects of these agents, e.g., nausea, vomiting, constipation, urinary retention, mental confusion, drowsiness, and respiratory depression. In the elderly, the central nervous system effects of opioids (e.g., dizziness) may have particularly serious consequences. Prescription of either codeine or propoxyphene may increase the risk of hip fracture by 60%. Concurrent use of these opioids and a psychotropic drug (e.g., sedative, antidepressant, antipsychotic) carries a fracture risk 2.6 times as high as that in nonusers of either drug class.