Researchers at Vanderbilt University Medical Center have concluded that fibrin, a protein involved in blood clotting and found abundantly around the site of new bone fractures, impedes rather than supports fracture healing.
Their recent study in The Journal of Clinical Investigation looked at mice that had experimentally induced deficits in either fibrin production or fibrin clearance. Researchers found normal fracture repair in mice without fibrin and impaired vascularization and fracture healing in mice with inhibited fibrin clearance. They also saw increased heterotopic ossification in the mice unable to remove fibrin.
In a Vanderbilt press release, study coauthor Jonathan Schoenecker, MD, commented that “any condition associated with vascular disease and thrombosis will impair fracture healing.” These findings, he suggested, may explain why obesity, diabetes, smoking, and old age—all of which are associated with impaired fibrin clearance—are also associated with impaired fracture healing. Dr. Schoenecker went on to speculate that anti-clotting drugs commonly used to treat cardiovascular conditions may find new applications in enhancing fracture repair.
Watch that pendulum. Fibrin provides the temporary scaffold that starts the healing process. And there is more to a clot than fibrin. Simply dosing a patient with anti-clotting factors threatens the healing process itself. Think of hemophiliacs. Caution advised.