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..