Beta-blockers can reverse the effects of osteoporosis—that's the surprising conclusion of a study by Shu Takeda, Florent Elefteriou and colleagues in the November 1 Cell. On the right is a cross-section of a vertebra from a mouse treated with beta-blockers, and on the left, one from a non-treated mouse. Beta-blockers increase the bone mass (black) in the vertebrae and other bones. These drugs also replace bone in mice that have had their ovaries removed to mimic the bone weakness that occurs commonly in post-menopausal women.

Credit: Reprinted with permission from Elsevier Science

The investigators launched their research with an analysis of the weight-regulating hormone leptin. They had known from previous studies that mice lacking leptin are extremely obese—but they also have greater bone mass than normal mice. This observation has its parallel in people, as obese individuals rarely suffer from osteoporosis. The authors found that leptin's effects on weight are regulated independently of its effects on bone mass. A division of the sympathetic nervous system receives leptin signals in the brain and transmits them to bone-forming cells, or osteoblasts, throughout the body.

Different types of adrenergic receptors mediate the functions of the sympathetic nervous system, which include timing the heart beat and breathing. Indeed, β2-adrenergic receptors stud the cells in heart muscle, and β2-adrenergic agonists—beta-blockers—are commonly prescribed to regulate blood pressure. The authors found that osteoblasts also expressed β2-adrenergic receptors and responded to beta-blocker treatment. If the approach works in people, it could offer hope to individuals afflicted with osteoporosis—which number about ten million in the United States alone. Currently prescribed drugs for osteoporosis arrest bone destruction, but cannot increase bone formation and reverse the effects of bone damage.