Scientists are closing in on the solution to a persistent medical puzzle: why do high doses of cortisone, widely prescribed for asthma, rheumatoid arthritis and other inflammatory and autoimmune conditions, weaken bones?
Through studies of mice, researchers at Washington University School of Medicine in St. Louis have now identified osteoclasts, cells that dismantle old bone, as the essential link between osteoporosis and cortisone. As scientists flesh out the molecular-level details of this connection, they may be able to identify targets for therapy to prevent cortisone's damaging side effects on bone.
"High-dose cortisone is the second most common cause of osteoporosis, and we currently have no real treatment for this serious side effect," says senior author Steven L. Teitelbaum, M.D., Messing Professor of Pathology and Immunology. "Given how frequently these drugs are used to treat many different conditions, that's a major clinical problem."
Teitelbaum and colleagues including lead author Hyun-Ju Kim, Ph.D., a postdoctoral fellow, publish their results in the August issue of the Journal of Clinical Investigation.
Cortisone is a steroid produced naturally by the adrenal gland and synthesized by a number of pharmaceutical companies for clinical use. The drug is also used to treat lupus, multiple sclerosis and chronic obstructive pulmonary disease, and it is prescribed to transplant patients to prevent rejection of transplanted organs.
Earlier attempts to identify the connection between bone loss and cortisone produced seemingly contradictory results. In lab animal experiments, researchers found cortisone caused bone-building osteoblast cells to self-destruct, suggesting that cortisone disrupts the body's ability to form new bone after it is naturally dismantled by osteoclasts. However, experiments in the test tube also showed cortisone stimulates bone formation.