Bone Can Form in Arteries, Scientists Say : Health: UCLA research team links calcification to atherosclerosis. The discovery may open the way for new therapies. It also casts doubt on osteoporosis treatment.

In a surprising discovery, UCLA researchers have found that atherosclerosis, better known as hardening of the arteries, may arise in part through the formation of bone in the arteries.

The finding, reported today in the Journal of Clinical Investigation, could open the door to new therapies to prevent atherosclerosis, which is treated by controlling intake of cholesterol and fats, said Dr. Linda Demer, associate chief of cardiology at the UCLA School of Medicine.

Atherosclerosis contributes to two-thirds of the nearly 650,000 annual deaths from heart attacks and strokes in the United States, according to the American Heart Assn.

Atherosclerotic lesions contain bone-like calcium crystals and fatty deposits. Most researchers had previously thought that the calcium crystals formed passively from calcium in the blood. Demer’s results suggest that it is an active process--like the formation of bone--under the control of hormones and proteins released by the body.

“This research shows that in the future we may be able to look at calcification . . . as a process that can be slowed and controlled through diet, medication or other methods,” she said.

The study also suggests that current treatments to prevent bone loss (osteoporosis) in post-menopausal women by stimulating bone formation may have the inadvertent side effect of contributing to atherosclerosis. Treatments that stimulate bone formation could also stimulate deposition of bone minerals in arteries, she said.

Studies to examine such a link should be undertaken immediately, Demer said. “I don’t want to be an alarmist,” she said, “but we want to make sure we are doing the right thing (in treating osteoporosis) and not worsening the situation.”

Demer said she became interested in the subject when a pathologist showed her an atherosclerotic lesion from a cadaver that apparently contained bone tissue. She and her colleagues then began studying such lesions in segments of neck arteries removed from atherosclerosis patients to reduce the risk of strokes.

Examining the lesions, the team found that they contained traces of bone morphogenetic protein, or BMP--”the most potent bone-forming protein known,” she said. They could find no traces of the protein in healthy arterial tissue.

They grew cells from healthy arterial walls in the laboratory and found that within two weeks the cells spontaneously formed bone mineral similar to that observed in atherosclerosis. Those findings suggest that the artery wall cells have a hidden capacity to form bone that is apparently triggered during culturing of the cells--and during atherosclerosis. “That was completely to our surprise,” she said. “We expected we would have to apply something to them” for bone to form.

The next step, she said, will be to find what triggers the development of the calcium deposits and find some way to interfere with it.