Over 50% of those 65 years of age and about 80% of those over age 75 have radiographic evidence of the disease.1 The Centers for Disease Control and Prevention (CDC) estimates that the prevalence of all forms of arthritis will increase from 47 million people to 60 million by 2020. This increase is likely due to several factors: advancing age of the population, increases in injuries, and rapidly advancing rates of obesity.
 

Of the known causes, serious joint injuries are most highly associated with future development of OA.

How can you enjoy your activity and not get injured? The best way is to make sure your muscles are in good shape and that your technique is proper. Muscle weakness, especially in the quadriceps, is associated with an increased risk of knee OA. Taking skiing lessons will reduce your chance of an injury, and tennis lessons, for instance, can help prevent shoulder, back, and elbow injuries.

There is some preliminary evidence that using the supplements glucosamine and chondroitin and, perhaps, hyaluronic acid injections (like sodium hyaluronate and perhaps hylan G-F 20) can help prevent further cartilage damage.

The other thing people can do to help prevent and treat osteoarthritis is to lose weight. Two recent studies2,3 have shown that being overweight antedates the development of OA. In overweight people, weight loss can reduce the risk for OA. In the Framingham Study, four women who lost an average of 5 kg decreased their risk for knee osteoarthritis by 50%.

The current American College of Rheumatology guidelines27 for treatment of OA of the hip and knee recommend acetaminophen as the first-line pharmacologic intervention for treating OA pain. This guideline has been challenged by several studies showing that patients prefer nonsteroidal anti-inflammatory drugs (NSAIDs).

In perhaps the landmark study4 comparing acetaminophen with an NSAID (diclofenac plus misoprostol), some staggering, but not unexpected news was reported. Only 42% of patients taking 4 g of acetaminophen per day reported their OA pain symptoms to be better (by 20% or more), and about 30% actually reported their symptoms to be worse (by 20% or more).

Acetaminophen, partly because it is used so frequently, is the number one cause of accidental drug poisoning. Regular use, however, is not commonly associated with problems, unless one has liver disease or drinks excessive amounts of alcohol. Despite this, and the relatively low effectiveness of acetaminophen compared to NSAIDs, acetaminophen is slightly safer.

According to a 1999 review in the New England Journal of Medicine,6 an estimated 16,500 deaths and 107,000 hospitalizations each year in the United States are directly related to the bleeding ulcers, medication interactions, kidney damage, high blood pressure, and other adverse effects of NSAIDs. As a result of the serious risk, the risk to benefit ratio, according to most experts, still favors acetaminophen, despite its diminished effectiveness in relieving pain.

In two very large studies (each with more than 8,000 subjects), the CLASS study7 for celecoxib and the VIGOR trial8 for rofecoxib, each drug was able to reduce the number of bleeding ulcers by about half or more. The FDA became concerned for other reasons, however. It appears that the benefit from using celecoxib was lost when the subjects were taking small doses of aspirin for preventing cardiovascular problems. The problem is that celecoxib tends to be prescribed to seniors, many of whom require aspirin as a cardiovascular preventive agent. Furthermore, in the VIGOR trial, the incidence of serious cardiovascular events (such as clots, strokes, and heart attacks), was about four times higher in the subjects taking rofecoxib than in those taking a regular NSAID (naproxen, in this instance). It appears that blocking the COX-2 enzyme reduces the body’s production of certain compounds called prostacyclins. Prostacyclins are important in preventing abnormal blood clotting so blocking them can lead to adverse effects.

Perhaps of even greater concern, certainly a concern that will affect more people, is exemplified by a study9 funded by the maker of rofecoxib. In a 1-year, prospective, randomized study, rofecoxib users lost significant amounts of cartilage in their knees (as evaluated by pre and post x-ray evaluation). The average rofecoxib user taking 12.5 mg per day lost 0.14 mm cartilage and those taking 25 mg per day lost a whopping 0.27 mm. The 50-mg dose was not evaluated.

Osteoarthritis directly does not cause death. Some might argue that the inactivity from the disease, however, might contribute to death indirectly by causing weight gain, diabetes, cardiovascular problems, and depression.

In any event, the fact is that we are currently using these drugs to treat the pain of arthritis, not the actual disease process. Pain relief, however, comes at a high price if you consider the deaths and adverse effects, not the least of which could be a worsening of the damage to the cartilage. In essence, the current pharmacologic treatment may be worse than the disease itself.