Bone fracture risk may increase when critical enzymatic processes decline

"This is the first study that lays down that phosphorylation in bone matters, particularly how it assists bone in releasing energy, and that loss of this modification is bad for bone," Vashishth said.

The team also studied the effect of osteopontin phosphorylation levels in the rare bone diseases hypophosphatemia and hyperphosphatemia, which are associated with skeletal deformities. In both diseases, Vashishth said, osteopontin phosphorylation levels decreased, a finding that lays the groundwork for further exploration.

"Another promising discovery was that these levels do change with diseases in bone," Vashishth said. "Is phosphorylation directly affecting the fracture propensity of bones in these diseased conditions? And what therapeutic tools can we use to fix this? These are the questions that we want to investigate."

In the spirit of the New Polytechnic, the model that drives research and education at Rensselaer, this research was highly collaborative across multiple disciplines. Vashishth and his lab worked with researchers at McGill University in Canada, the University of Southampton in the United Kingdom, the University of Patras in Greece, Aarhus University in Denmark, and Vienna University of Technology in Austria. Each research team brought a different expertise and piece of this puzzle to the work.

The team's findings may also be applied to similar processes within other connective tissues and possible therapeutics to counteract abnormal osteopontin phosphorylation levels.

"This is not just specific to bone, because phosphorylation is a more ubiquitous change in other tissues in the body," Vashishth said. "Osteopontin is not only in bone, it's in other tissues in our body, like our kidneys and several other places. This research can also shed light on other things that can happen throughout the body."