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US scientists have published the findings of a new study that challenges current understanding of how the healing process after a bone fracture works.
A team from Vanderbilt University Medical Center in Tennessee have made the discovery that fibrin - a protein that was thought to play a key role in fracture healing - is not required for this process at all.
Fibrin is involved in blood clotting, forming a mesh-like net that traps platelets to form a clot that stops bleeding. It is the main protein at the site of a fracture, so it was thought to promote repair by providing a scaffold for the initial phase of new bone formation.
However, new research published in the Journal of Clinical Investigation demonstrated that mice that lacked fibrinogen, a large protein that is usually converted into fibrin during blood clotting, were able to heal fractures normally even without fibrin.
In fact, the study offered evidence that an excess of fibrin at the fracture site can actually impair healing in many cases. Mice that were unable to get rid of fibrin were shown to find it harder to form blood vessels and heal the fractured bone, with subsequent depletion of fibrinogen restoring normal fracture repair processes.
The findings may explain why obesity, diabetes, smoking and advanced age - all conditions that damage the body's ability to get rid of fibrin - can impair fracture repair, while also suggesting that treatments to lower fibrinogen levels or increase the activity of enzymes that clear fibrin could aid bone healing processes.
Dr Jonathan Schoenecker, assistant professor of orthopaedic surgery and rehabilitation at Vanderbilt University Medical Center, said: "Many of the current pharmaceutical protocols are based on using fibrin to promote fracture healing. 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."
Original Article: New protein research challenges understanding of how bone fractures healNEXT ARTICLE
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