Troy, N.Y. A new study from engineering researchers at Rensselaer Polytechnic Institute shows, for the first time, how the little-understood protein osteocalcin plays a significant role in the strength of our bones. The findings could lead to new strategies and therapeutics for fighting osteoporosis and lowering the risk of bone fracture.
Funded by the U.S. National Institutes of Health, the study details how fractures in healthy bones begin with the creation of incredibly tiny holes, each measuring only about 500 atoms in diameter, within the bone's mineral structure. In the case of a slip, trip, or fall, the force of the impact on a bone physically deforms a pair of joined proteins, osteopontin and osteocalcin, and results in the formation of nanoscale holes. These holes, called dilatational bands, function as a natural defense mechanism, and help to prevent further damage to the surrounding bone. However, if the force of the impact is too greator if the bone is lacking osteopontin, osteocalcin, or boththe bone will crack and fracture.
The multi-university study, led by Deepak Vashishth, head of the Department of Biomedical Engineering at Rensselaer, is the first to give evidence of fracture at the level of bone's nanostructure. Partnering with Rensselaer on the study were Villanova University, the Hospital for Special Surgery in New York, and Yale University.
"This study is important because it implicates, for the first time, the role of osteocalcin in giving bone the ability to resist fracture," Vashishth said. "Since osteocalcin is always the point of fracture, we believe that strengthening it could lead to a strengthening of the overall bone."
Long known but little understood, the protein osteocalin has been produced by and present in animal bones since before the dawn of humanity. Recently, abnormalities in ostoecalcin production have been associated with type 2 diabetes as well as problems in reproductive health.
|Contact: Michael Mullaney|
Rensselaer Polytechnic Institute