Osteoporosis Drug Prompts Increase in Certain Bone Cells

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"This is accomplished by two kinds of cells: armies of osteoclasts that erode cavities in the bone, then teams of osteoblasts which replace old bone with new, strong bone," he continued.

Postmenopausal osteoporosis results from an imbalance in that remodeling process. Fosamax, part of a class of drugs known as bisphosphonates, is thought to prevent that imbalance by decreasing the number of bone-eroding cells.

But, after examining 51 bone biopsy specimens from healthy postmenopausal women (40 to 59 years of age) who had participated in a three-year trial and who took different doses of Fosamax versus a placebo, the study authors found the opposite was actually true.

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Women receiving the highest dose of the drug (10 milligrams) once a day had 2.6 times the number of osteoclasts, compared with women in the placebo group. The number of osteoclasts increased with the dose, the study found.

Twenty-seven percent of the osteoclasts were "mega-cells" that were still present one year after the women had stopped taking Fosamax. The study authors hypothesized that bone cells weren't dying, allowing them to fuse together in this way.

"It's like disarming the soldiers in the bone army [osteoclasts] but increasing the size of the army by more than 260 percent," Weinstein said.

"The drugs do work, no question," he said. But, he added, it's important to figure out just how they work (knowledge that often doesn't come until drugs have been in use for a while) to make sure the right people are getting them and to anticipate side effects.

Liu said: "They [the study authors] say that osteoclasts did not die at an increased rate like they did in some of the animal studies but, rather, [Fosamax] slowed down the rate of death but also reduced the functionality or efficiency at which osteoclasts worked."

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