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Corrigendum Free access | 10.1172/JCI84059

Fibrinolysis is essential for fracture repair and prevention of heterotopic ossification

Masato Yuasa, Nicholas A. Mignemi, Jeffry S. Nyman, Craig L. Duvall, Herbert S. Schwartz, Atsushi Okawa, Toshitaka Yoshii, Gourab Bhattacharjee, Chenguang Zhao, Jesse E. Bible, William T. Obremskey, Matthew J. Flick, Jay L. Degen, Joey V. Barnett, Justin M.M. Cates, and Jonathan G. Schoenecker

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Published September 1, 2015 - More info

Published in Volume 125, Issue 9 on September 1, 2015
J Clin Invest. 2015;125(9):3723–3723. https://doi.org/10.1172/JCI84059.
Copyright © 2015, American Society for Clinical Investigation
Published September 1, 2015 - Version history
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Related article:

Fibrinolysis is essential for fracture repair and prevention of heterotopic ossification
Masato Yuasa, … , Justin M.M. Cates, Jonathan G. Schoenecker
Masato Yuasa, … , Justin M.M. Cates, Jonathan G. Schoenecker
Research Article Bone Biology Hematology Hepatology Nephrology Pulmonology

Fibrinolysis is essential for fracture repair and prevention of heterotopic ossification

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Abstract

Bone formation during fracture repair inevitably initiates within or around extravascular deposits of a fibrin-rich matrix. In addition to a central role in hemostasis, fibrin is thought to enhance bone repair by supporting inflammatory and mesenchymal progenitor egress into the zone of injury. However, given that a failure of efficient fibrin clearance can impede normal wound repair, the precise contribution of fibrin to bone fracture repair, whether supportive or detrimental, is unknown. Here, we employed mice with genetically and pharmacologically imposed deficits in the fibrin precursor fibrinogen and fibrin-degrading plasminogen to explore the hypothesis that fibrin is vital to the initiation of fracture repair, but impaired fibrin clearance results in derangements in bone fracture repair. In contrast to our hypothesis, fibrin was entirely dispensable for long-bone fracture repair, as healing fractures in fibrinogen-deficient mice were indistinguishable from those in control animals. However, failure to clear fibrin from the fracture site in plasminogen-deficient mice severely impaired fracture vascularization, precluded bone union, and resulted in robust heterotopic ossification. Pharmacological fibrinogen depletion in plasminogen-deficient animals restored a normal pattern of fracture repair and substantially limited heterotopic ossification. Fibrin is therefore not essential for fracture repair, but inefficient fibrinolysis decreases endochondral angiogenesis and ossification, thereby inhibiting fracture repair.

Authors

Masato Yuasa, Nicholas A. Mignemi, Jeffry S. Nyman, Craig L. Duvall, Herbert S. Schwartz, Atsushi Okawa, Toshitaka Yoshii, Gourab Bhattacharjee, Chenguang Zhao, Jesse E. Bible, William T. Obremskey, Matthew J. Flick, Jay L. Degen, Joey V. Barnett, Justin M.M. Cates, Jonathan G. Schoenecker

×

Original citation: J Clin Invest. 2015;125(8):3117–3131. doi:10.1172/JCI80313.

Citation for this corrigendum: J Clin Invest. 2015;125(9):3723. doi:10.1172/JCI84059.

A sentence was omitted from the Acknowledgments. The correct sentence is below.

μCT imaging and analysis were supported in part by the Center for Small Animal Imaging at the Vanderbilt University Institute of Imaging Sciences and by grant S10RR027631 from the NIH.

The authors regret the error.

Footnotes

See the related article beginning on page 3117.

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