Research frontiers: What’s ahead for arthritis
February/March 2007 Vol. 14, No. 1
Each treatment, diagnostic test, and new insight into the cause of arthritis is an outgrowth of hundreds of hours of research. As a result of this effort, many people with arthritis are able to lead active, productive lives. But challenges remain, and scientists continue to research the disease in hopes of conquering arthritis—or at least furthering our ability to slow its progress.
Early detection
Scientists searching for ways to identify people with an aggressive form of rheumatoid arthritis (RA) in the earliest stages have zeroed in on antibodies found primarily in people with the disease. A blood test that detects these antibodies gives a strong indication that the individual has RA. While the person may not need treatment yet, doctors are alerted to keep a close watch on the patient’s condition.
Some people develop osteoarthritis (OA) early in adulthood, and by middle age damage has occurred to cartilage—the protective tissue covering the ends of bones in a joint. X-rays, however, may not reveal cartilage damage until it becomes severe. Researchers are now studying whether chemicals released by the breakdown of cartilage can serve as early markers of OA. If so, people found to have high levels of the substances in their blood or joint fluid can be advised to make some lifestyle changes, including reducing stress on their joints through exercise and, if necessary, weight loss.
Novel treatments
Antibiotics have recently shown promise as a means of slowing OA progression. In a preliminary study, a group of overweight women with moderate knee OA were treated for 2 1/2 years with the antibiotic doxycycline. At the end of the study, they reported less pain and showed less cartilage loss than did members of a control group who did not take the antibiotic.
In another approach to slowing cartilage loss, researchers are studying enzymes involved in the natural breakdown and repair of cartilage. One version of the enzyme aggrecanase appears to be particularly destructive. In studies with mice predisposed to developing OA, eliminating the gene for this enzyme caused a reduction in cartilage damage. Similar results were found with mice predisposed to RA. Scientists hope to develop a drug that will help to control this enzyme.
From The Cleveland Clinic’s Arthritis Advisor
Arthritis Health monitor



