Researchers observed fracture healing in three groups of mice:
- Fibrinogen-deficient mice developed by study author Jay Degen, PhD;
- Plasminogen-deficient mice;
- Control group.
Here are four points:
1. While mice lacking fibrinogen experienced greater bleeding following a fracture, their fractures otherwise healed normally.
2. Plasminogen-deficient mice that lacked the ability to clear fibrin from the site of injury faced impaired healing and also experienced heterotopic ossification in their muscle. Researchers aren’t sure why heterotopic ossification occurred and have made it a focal point for further research.
3. Derived from the plasma protein fibrinogen, fibrin is a key player in secondary hemostasis. According to a review published in Toxicologic Pathology, when normal vasculature is disrupted due to an injury, such as a bone fracture, the enzyme thrombin converts fibrinogen to fibrin, an insoluble protein that forms a cross-linked fiber mesh at the injury site.
More articles on orthopedics:
Orthopedic surgeon to know: Dr. David Bierbrauer of Cornerstone Orthopaedics & Sports Medicine
French Hospital Medical Center opens orthopedic patient wing: 4 points
Dr. Benjamin Robertson joins Essentia Health St. Joseph’s-Crosslake Clinic: 3 notes
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