Ironically, while more effective disease-modifying therapies have been developed for rheumatoid arthritis, particularly within the last 10-15 years, rheumatologists still treat osteoarthritis with symptomatic and supportive therapies.

As a result, the inexorable progression of this disease results in the performance of more than half a million joint replacements annually in the United States. While joint replacement surgery has made gigantic strides, it is still a major surgical procedure.

Risk factors for the development of OA include: genetic factors, obesity, joint injury, surgery, and the presence of associated metabolic disease.

It is clear from the research that OA is a disease that involves not only the cartilage- the gristle that caps the end of long bones and cushions the joint, but also the synovium- the tissue lining the joint- as well as the bone that underlies cartilage.

While genetic factors play a significant role in the incidence of osteoarthritis, the damage that occurs is a result of a complex interaction of inflammatory messengers. Among these are cytokines, prostaglandins, nitric oxide, growth factors, and proteases.

These substances, which are produced by chondrocytes (cartilage cells) that are subjected to abnormal forces lead to a situation where there is premature aging and destruction of cartilage substance.

The production of these inflammatory proteins also contributes to inflammation of the synovium and excessive amounts of bone growth.

Present therapies, as issued by guidelines proposed by the Osteoarthritis Research Society International (OARSI), are clearly aimed at symptom relief. These treatments include: analgesics, non-steroidal-anti-inflammatory drugs (NSAIDS), topical agents (“rubs”), and joint injections with either glucocorticoids (“cortisone”), or hylauronic acid lubricants.

Current research has been aimed at finding the triggers that cause inflammation to start and also to identify specific markers that might identify those patients who are at greatest risk for rapid progression of disease. These markers would also be useful in measuring improvement once newer drugs that can slow down disease progression in OA can be discovered.

However, all of these investigations are futile unless and until specific disease-modifying osteoarthritis drugs (DMOADS) – drugs that slow down the rate of cartilage loss- can be developed.

Drugs aimed at inhibiting cytokine and protease function show some promise but it is still too early to tell whether they will have the desired effect. Examples of these drugs include: matrix metalloproteinase inhibitors, drugs that block interleukin 1, bisphosphonates, calcitonin, as well as nutritional supplements such as glucosamine and chondroitin.

And it may not be enough to find drugs that simply slow disease progression.

The “holy grail” is still the treatment(s) that will rebuild cartilage. The type of therapy that shows the greatest promise to date is the use of autologous stem cells. These are stem cells harvested from the patient and reintroduced into the affected joint along with a specific matrix to which the stem cells can adhere and grow.

Early results look promising. For more information about stem cell treatment for osteoarthritis of the knee, contact the Arthritis and Osteoporosis Center of Maryland at (301) 694-5800.