By manipulating how sex steroids are processed in bone-building cells, it may be possible to increase the survival of these cells without causing many of the complications that come with hormone replacement therapy. The finding, published in the March 9 issue of Cell, could have important implications for the development of new drugs to prevent or treat osteoporosis in both men and women.
In cell culture experiments, a research team from the University of Arkansas for Medical Sciences in Little Rock used synthetic molecules that mimic some effects of estrogen to selectively activate the cell rescue pathway of estrogen and androgen receptors in mouse bone cells. By activating this pathway alone, the scientists were able to promote the longevity of osteoblasts, the cells that lay down new bone, without sparking other sex steroid activities within the cell. That could help prevent osteoporosis, a bone-thinning disease that is a major health risk for 28 million Americans, most of them older than 50.
In the United States, 10 million individuals have osteoporosis and 18 million more have low bone mass, placing them at increased risk for the disease. One of every two women and one in eight men over 50 will have a osteoporosis-related fracture over his or her lifetime. The disease accounts for more than 1.5 million fractures each year, including 300,000 hip fractures, about 700,000 spinal fractures, 250,000 wrist fractures and more than 300,000 fractures of other sites. In addition to hormone replacement therapy, exercise and adequate intake of calcium and vitamin D can help preserve bone mass and prevent slow osteoporosis.