New discovery of how bone fractures heal may lead to new ways of treatment. “A team of Vanderbilt investigators has discovered that fibrin, a protein that was thought to play a key role in fracture healing, is not required. Instead, the breakdown of fibrin is essential for fracture repair.
The findings, reported in the August issue of the Journal of Clinical Investigation, shift understanding of how fractures heal and have implications for efforts to promote fracture repair.
“Many of the current pharmaceutical protocols are based on using fibrin to promote fracture healing,” said Jonathan Schoenecker, M.D., Ph.D., assistant professor of Orthopaedic Surgery and Rehabilitation. “In certain instances it may help, but we’ve shown for sure that you don’t need it. Bone biology does not require fibrin to heal a fracture.”
Fibrin is involved in blood clotting; it forms a meshlike net that traps platelets to form a clot. When bones break, so do blood vessels, and clots form to stop the bleeding.
“Most people don’t realize that bone is the most vascular organ in our bodies,” Schoenecker said. “When you have a fracture, you have a huge disruption of that vascularity.”
Since fibrin is the main protein at the site of a fracture, it was thought to promote repair by providing a scaffold for the initial phase of new bone formation. Schoenecker and colleagues found, however, that fracture repair was normal in mice missing the fibrin precursor fibrinogen.
The investigators had previously reported the importance of vascular re-connection for bone fracture healing. Using imaging techniques they developed to simultaneously study angiogenesis (new blood vessel growth) and bone formation after fracture, they found that blood vessels grow first at the ends of the fracture, extend and reconnect. Then new bone forms.
“Therefore, any condition associated with vascular disease and thrombosis will impair fracture healing,” Schoenecker said.”
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