Posted on March 31, 2010.
Current Concepts in Osteoarthritis Research: Then, why my knees hurt and can make you better? Osteoarthritis (OA) is one of the most common disorders leading to disability and impaired quality of life in the Western world.
Paradoxically, while more effective disease-modifying therapies have been developed for rheumatoid arthritis, especially during the last 10-15 years, rheumatologists still treat osteoarthritis with symptomatic and supportive.
Accordingly, the relentless progression of this disease is caused in the performance of over half a million joint replacements each year in the United States. While joint replacement surgery has made tremendous progress, there remains a major surgical procedure.
Risk factors for developing osteoarthritis include: genetic factors, obesity, joint injury, surgery, and the presence of diseases associated with metabolism.
It is clear from research that osteoarthritis is a disease that involves not only the cartilage cartilage that caps the ends of long bones and cushions the joint, but also the synovium, the tissue lining the common good, as in the bone underlying cartilage.
Although genetic factors play an important role in the incidence of osteoarthritis, the damage that occurs is the result of a complex interaction of inflammatory messengers. Among these are cytokines, prostaglandins, nitric oxide, growth factors and proteases.
These substances are produced by chondrocytes (cartilage cells) are subjected to abnormal forces lead to a situation where there is premature aging and destruction of cartilage.
The production of these inflammatory proteins also contributes to inflammation of the synovial membrane and excessive amounts of bone growth.
Current therapies, such as published by the guidelines proposed by the Osteoarthritis Research Society International (OARSI) clearly aim to relieve symptoms. These treatments include: analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), topical agents ("rubbing"), and intra-articular injections of corticosteroids or ("cortisone"), or lubricants hylauronic acid.
The current research was designed to find the triggers that cause inflammation to start and also to identify specific markers that could identify patients who are most at risk of rapid progression of the disease. These markers are also useful in measuring improvement in both new drugs that can slow disease progression in osteoarthritis can be discovered.
However, these surveys are useless unless and until specific drugs disease-modifying osteoarthritis (DMOAD) - drugs that slow the rate of cartilage loss, can be developed.
Drugs to inhibit cytokine and protease function of promises, but it is still too early to say whether they will have the desired effect. Examples of these drugs include: matrix metalloproteinase inhibitors, drugs that block interleukin 1, bisphosphonates, calcitonin, and nutritional supplements such as glucosamine and chondroitin.
And it may not be sufficient to find drugs that disease progression is simply slow.
The "Grail" is still the treatment (s) will be the reconstruction of cartilage. The type of therapy that shows the most promise to date is the use of autologous stem cells. The stem cells are reintroduced into the patient and the affected joint with a specific matrix to which cells can adhere and grow.
The initial results seem promising. For more information about stem cell treatment of osteoarthritis of the knee, contact the Center for arthritis and osteoporosis of Maryland, at (301) 694-5800.
