Bone resorption cells offer drug targets for osteoporosis, rheumatoid arthritis...( r. Teitelbaum. The popular anti-osteop...),Health

r. Teitelbaum. The popular anti-osteoporosis drug Fosamax works and quite effectively by inhibiting the osteoclasts. But the drug is stored in the skeleton for long periods of time and adverse effects in chronic users now are being encountered. Phase 2 clinical trials in humans are now underway for drugs that target the integrins, and Dr. Teitelbaum is hopeful these new drugs will bypass such problems.

In addition to the osteoporosis that often occurs in the aging process, Dr. Teitelbaum's group has made great advances in understanding bone loss in three other diseases.

Rheumatoid arthritis. The crippling bone loss that occurs around joints in people with rheumatoid arthritis is caused by the interaction of osteoclasts and the inflammatory cytokines produced by the immune system. Dr. Teitelbaum's group has identified many of the indirect and direct means by which these cytokines cause joint destruction and are pinpointing targets for drugs to prevent this loss.

HIV/AIDS. In recent years, scientists have documented that some of the protease inhibitor drugs that have had such a dramatic effect lowering the viral load in patients with HIV/AIDS have also had an effect on the osteoclast, causing changes in bone mass in patients taking these drugs. Dr. Teitelbaum's laboratory has documented specific proteases that have different effects on the osteoclasts, suggesting that changing the protease inhibitor being given might diminish bone loss, or that patients on protease inhibitor drugs may need to take antiosteoporosis drugs as well.

Cortisone-induced osteoporosis in transplant recipients, asthma, lupus, inflammatory diseases and other diseases requiring use of cortisone for therapy. Taking cortisone can lead to bone loss, with as much as 12 percent skeleton loss the first year and continuing loss of approximately 3 percent per year, says Dr. Teitelbaum. His laboratory has discovered novel mechanisms of how cortisone supp
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Contact: Sarah Goodwin
ebpress@bellsouth.net
770-270-0989
Federation of American Societies for Experimental Biology
3-Apr-2006

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