Bone-building find hold hope for improved osteoporosis treatment
Washington: A team of American scientists claims to have uncovered an important step in hormone-triggered bone growth, paving the way 
for new osteoporosis drugs and better bone-building therapies.
The research from the University of Alabama at Birmingham (UAB) showed that parathyroid hormone (PTH) given intermittently enhances the body's own bone-building action through a specific "co-receptor" on the surface of bone cells.
While scientists have known for long that PTH stimulates bone formation, the exact mechanism underlying this effect has been unknown to date.
"Our study uncovers a novel mechanism for how parathyroid hormone signaling selectively stimulates bone formation. We have identified the protein co-receptor crucial to the whole process," said Dr. Xu Cao, UAB professor of pathology and senior author on the study.
During the study, the researchers focused on PTH signals in mice to see which cell receptors would actively recruit calcium from the blood.
Dr. Mei Wan, UAB associate professor of molecular and cellular pathology and first author on the study, said that the team's efforts helped uncover the one co-receptor responsible for turning on bone building.
Dr. Jay McDonald, pathology professor and director of UAB's Center for Metabolic Bone Disease, pointed out that the exact mechanism of PTH-signalled bone formation was previously shrouded by the joint production of osteoblasts and osteoclasts, two types of cells that are instrumental in regulating a healthy skeleton.
While osteoblasts regulate a healthy skeleton by forming new bone, and osteoclasts do so by resorbing old and brittle bone.
McDonald highlighted the fact that many existing osteoporosis drugs target both osteoblasts and osteoclasts, which can lead to zero or minimal bone formation.
"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," he said.
An article describing the new study has been published in the journal Genes and Development. [From Internet]
for new osteoporosis drugs and better bone-building therapies.The research from the University of Alabama at Birmingham (UAB) showed that parathyroid hormone (PTH) given intermittently enhances the body's own bone-building action through a specific "co-receptor" on the surface of bone cells.
While scientists have known for long that PTH stimulates bone formation, the exact mechanism underlying this effect has been unknown to date.
"Our study uncovers a novel mechanism for how parathyroid hormone signaling selectively stimulates bone formation. We have identified the protein co-receptor crucial to the whole process," said Dr. Xu Cao, UAB professor of pathology and senior author on the study.
During the study, the researchers focused on PTH signals in mice to see which cell receptors would actively recruit calcium from the blood.
Dr. Mei Wan, UAB associate professor of molecular and cellular pathology and first author on the study, said that the team's efforts helped uncover the one co-receptor responsible for turning on bone building.
Dr. Jay McDonald, pathology professor and director of UAB's Center for Metabolic Bone Disease, pointed out that the exact mechanism of PTH-signalled bone formation was previously shrouded by the joint production of osteoblasts and osteoclasts, two types of cells that are instrumental in regulating a healthy skeleton.
While osteoblasts regulate a healthy skeleton by forming new bone, and osteoclasts do so by resorbing old and brittle bone.
McDonald highlighted the fact that many existing osteoporosis drugs target both osteoblasts and osteoclasts, which can lead to zero or minimal bone formation.
"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," he said.
An article describing the new study has been published in the journal Genes and Development. [From Internet]
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