"New Compound Prevents Osteoporosis"

May 12, 1997
NEW YORK (Reuters) - Though bone may appear to be as solid as a rock, it is in fact a dynamic living tissue that is constantly being created by one type of cell and then destroyed by another type, called osteoclasts. When that process is skewed towards destruction, the result is osteoporosis, the bone-thinning disease responsible for the broken hips and wrists so common in old age.

Now, a new study in rats suggests that a compound that blocks a receptor used by osteoclasts can prevent the cells from attaching to and destroying bone. In rats that had their ovaries removed - a process that causes rapid bone-thinning similar to that seen in women after menopause - the compound prevented bone loss, according to a report in the Journal of Clinical Investigation. Normally, the rats would have lost 30% to 50% of their bone density during the six-week study.

In fact, the compound was as effective as giving rats estrogen, “the most effective antiosteoporotic agent known,” according to the report. The compound, called SC56631, is a short protein that blocks the integrin alpha-V beta-3, a molecule used by osteoclasts to attach to the bony matrix. Unable to attach to the bone, the osteoclasts cannot release the acid they use to break down the substance, according to lead study author Dr. Steven Teitelbaum, a professor of pathology at Washington University in St. Louis, Missouri. “We proved that we could block osteoporosis,” said Teitelbaum in a release from the University. “That is a very exciting prospect, but we still have a lot of work to do.” Much more study is needed to determine if such a compound would be safe and effective in humans. The rats were given a constant intravenous infusion of SC56631 during the study, a drug-delivery method that is clearly impractical for humans. And it is not yet clear what side effects the drug may have. SC56631 also blocks integrin receptors on the surface of platelets, key cells in the formation of blood clots. The platelet receptor normally interacts with fibrinogen, a crucial blood-clotting protein, though in the rats, this did not cause any noticeable side effects, the authors noted.