Several medical therapies and life-style activities changes now exist for the treatment of osteoarthritis. However, at this point, their use is based solely on treating the symptoms of osteoarthritis, including pain, swelling from inflammation and reduced joint movement. Among the medicines employed, corticosteroids can be administered directly into the affected joint. Corticosteroids remain the most potent anti-inflammatory drugs employed in the therapy of osteoarthritis. There are reasons to minimize the use of injectable corticosteroids or oral formulations as these drugs have significant side-effects when employed for long periods of time. Aspirin and aspirin-like drugs were developed to reduce inflammation and so they are very useful in the medical therapy of osteoarthritis. This class of drugs, the non-steroidal anti-inflammatory drugs (NSAIDs) target a class of molecules called prostaglandins which are very much involved in the inflammatory processes accompanying osteoarthritis. NSAIDs inhibit an enzyme, called cyclooxygenase, which is required for the production of prostaglandins. However, the same enzyme is also required for normal function of the gastrointestinal mucosa, which lines the stomach and for normal kidney function. Long-term use of NSAIDs can result in gastrointestinal bleeding. It was for this reason that a new class of NSAIDs were developed, which reduce cyclooxygenase only at sites of inflammation and spare the normal cyclooxygenase. These so-called COX-II inhibitors are now widely employed for the medical therapy of osteoarthritis.

Naturally occurring substances such as glucosamine, chondroitin sulfate and hyaluronic acid has been used for treating patients with osteoarthritis with varying results. Nutritional supplements such as glucosamine and chondroitin sulfate may be more efficacious in maintaining cartilage health in symptom-free individuals than in restoring function in patients with osteoarthritis.

The development and continuous refinement of prostheses for joint replacement surgery for osteoarthritis of the knee and other joints has been instrumental in improving the quality of life for individuals for whom medical therapy is no longer feasible. While it has been argued that knee replacement surgery is underutilized, it is an intervention that is not without problems. It is a significant cost to health insurers and in many cases, the original replacement must be revised over time adding additional costs to our health delivery system.

People should be aware of how life-style modifications affect their chance of developing osteoarthritis. Physical exercise may be a risk factor for developing osteoarthritis, but in and of itself does not appear to accelerate minor damage to the cartilage. Thus, a well-designed and carefully monitored physical exercise program should be maintained to provide muscle tone support and to promote cardiovascular fitness. Prior participation and regular participation in sports resulting in the potential for repetitive trauma may play more of a role than the proposal to maintain a moderate physical exercise program. Normal symptom-free individuals should not avoid physical exercise in an attempt to forestall the development of osteoarthritis. In certain families, however, where individuals have the potential to develop precocious forms of osteoarthritis as a result of a genetic disorder in the joint cartilage, physical exercise may play a greater role in the progression of disease activity. In these individuals, a diagnosis of increased risk for developing osteoarthritis based on the results of genetic testing could provide needed information allowing for a more prudent physical exercise plan to be developed for these individuals.

We are certainly aware of the fact that individuals sustaining major injury to the knee such as rupture of the meniscus or anterior cruciate ligament may proceed to develop osteoarthritis in the absence of any other risk factors. Surgical repair of the knee damage and physical rehabilitation is commonly employed to prevent such an outcome.

What about weight reduction? While obesity has clearly been determined to be a risk factor for developing knee osteoarthritis, unlike the other risk factors previously mentioned (physical exercise and/or trauma), recent studies by Cooper and colleagues now suggest that only obesity defined a body mass index (BMI) of 22.7-25.4 or greater was associated with progression of osteoarthritis of the knee as measured by x-ray analysis. A weight-reduction plan should be designed for individuals who have an x-ray diagnosis of knee osteoarthritis in its early stages. This life-style change becomes important as attempts are made to medically regulate the progression of osteoarthritis over time.

The importance of developing strategies for preventing osteoarthritis cannot be underestimated. A recent paper in the science journal, Arthritis and Rheumatism by Cyrus Cooper and colleagues indicated that the World Health Organization considers knee osteoarthritis to be a global burden as knee osteoarthritis is the fourth most important cause of disability in women and the eighth most important in men. The pain and stiffness in the knee joint developing as a consequence of changes in the articular cartilage which covers the skeletal joints is undoubtedly a cause of the significant morbidity associated with the condition.

What happens in the knee and other peripheral joints such as the hip and shoulder to cause osteoarthritis? In the general population on a background of risk factors such as over-weight, trauma or significant damage as a result of repetitive physical activity, the joint undergoes changes in the metabolism of the cartilage, which sits on top of the skeletal long bones. This articular cartilage is responsible for ensuring that the joint can withstand significant levels of compressive loading over many years of use.

Changes in the metabolism of the cartilage alters the way in which joint loads are transmitted to the underlying bone. Eventually, the cartilage fragments and breaks down. At that point, the underlying bone fails to properly function as a “shock absorber.” That is why osteoarthritis has been called a “wear and tear” disease. In reality, the fraying of cartilage is accompanied by attempts to repair the damage by cartilage cells, but the inbalance caused by inflammation in the joint that accompanies the breakdown of cartilage prevents repair from occurring properly. Eventually, the cartilage is no longer functional and the joint must be replaced by a prosthesis.

Experimental therapies designed to be eventually employed for the treatment of osteoarthritis in man are targeted at restoring normal joint function. Some experimental therapies being tested in animal models of osteoarthritis are designed to inhibit the chemical mediators, called cytokines, that stimulate inflammation, while other experimental strategies are focusing on the enzymes that destroy the cartilage itself. Still another tactic is related to stimulating cartilage repair by employing principles of gene therapy. In that strategy, the genes responsible for stimulating cartilage growth and/or repair are transferred to the affected joint where the proteins encoded by these genes are produced at a stable rate. Cartilage cell transplantation has also been experimentally tested in animals and current trials in man are currently underway. Many of these experimental studies appear to reduce the progression of osteoarthritis experimentally induced in animals. Hopefully, in the not to distant future, some of these experimental therapies will reach the marketplace and join the already established armamentarium of medical therapies now employed for treating osteoarthritis.

to be continued..