Scientists have identified a crucial step in hormone-triggered bone growth that could lead to development of new and better bone-building therapies, according to UAB research published in the November issue of the journal Genes and Development.
The study demonstrated that parathyroid hormone (PTH) — given intermittently — enhances the body’s own bone-building action, said pathology Professor Xu Cao, Ph.D., senior author on the study. “We have identified the protein co-receptor crucial to the whole process.”
Researchers examined PTH signals in mice to identify the cell receptors that actively recruited calcium from the blood, and they uncovered the co-receptor responsible for turning on the bone-building process, said Associate Professor Mei Wan, Ph.D., first author on the study.
Previously, the mechanism of PTH-signaled bone formation had been unknown and complicated by the joint production of osteoblasts and osteoclasts, said Professor Jay McDonald, M.D., director of UAB’s Center for Metabolic Bone Disease. Both types of cells help regulate the skeleton – osteoblasts by forming new bone and osteoclasts by resorbing old and brittle bone. Many osteoporosis drugs target both osteoblasts and osteoclasts, which can lead to zero or minimal bone formation, he said.
“The ideal would be to have one drug to shut down the osteoclasts and turn on the osteoblasts to effectively build bone. We don’t have that yet, but this study shows us the path to get there,” McDonald said.