New research that explains the function of a protein called osteocalcin in strengthening bones could one day help find new methods and therapeutics for fighting osteoporosis and lowering the risk of bone fracture. Prepared by engineering researchers at Rensselaer Polytechnic Institute and funded by the US National Institutes of Health, the study shows how fractures in healthy bones begin from tiny holes that measure 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 great—or if the bone is lacking osteopontin, osteocalcin, or both—the bone will crack and fracture. The multi-university study, led by Deepak Vashishth, head of the Department of Biomedical Engineering at Rensselaer Polytechnic Institute, 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,” said Mr Vashishth. “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 osteocalcin 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. The new study, however, is the first to explain the structural and mechanical importance of osteocalcin in bone.
Now that osteocalcin is known to participate in bone fracture, new strategies for strengthening the bond between osteocalin and osteopontin can be investigated, Mr Vashishth said. Augmenting the body’s natural supply of osteocalcin, for example, could be one possible strategy for treating osteoporosis and other conditions leading to increased fracture risk, he said. Osteocalin must be in its carboxylated form to get absorbed into bone, and the protein is carboxylated by vitamin K. He also explained that future studies could investigate the relation between vitamin K intake, osteocalcin, and bone strength.
“Currently, all of the advice for treating osteoporosis is related to calcium. We believe there’s more to the story than just calcium, and the results of this new study raise an important question about vitamin K. Leafy green vegetables are the best source of vitamin K—wouldn’t it be great if eating spinach and broccoli was not only healthy, but also good for your bones? We plan to investigate this link in future.”
Results of the new study, titled ΠΑΙΔΙΚΑ ΠΑΠΟΥΤΣΙΑ

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