Research Article

Fracture healing in protease-activated receptor-2 deficient mice

  1. Kevin R. O'Neill1,
  2. Christopher M. Stutz1,
  3. Nicholas A. Mignemi1,
  4. Heather Cole1,
  5. Matthew R. Murry1,
  6. Jeffry S. Nyman1,2,3,4,
  7. Heidi Hamm5,
  8. Jonathan G. Schoenecker1,2,5,6,7,*

Article first published online: 13 JAN 2012

DOI: 10.1002/jor.22071

Issue

Journal of Orthopaedic Research

Journal of Orthopaedic Research

Volume 30, Issue 8, pages 1271–1276, August 2012

Additional Information

How to Cite

O'Neill, K. R., Stutz, C. M., Mignemi, N. A., Cole, H., Murry, M. R., Nyman, J. S., Hamm, H. and Schoenecker, J. G. (2012), Fracture healing in protease-activated receptor-2 deficient mice. J. Orthop. Res., 30: 1271–1276. doi: 10.1002/jor.22071

Author Information

  1. 1

    Department of Orthopaedics, Vanderbilt University Medical Center, Nashville, Tennessee 37232-9565

  2. 2

    Center for Bone Biology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-9565

  3. 3

    Department of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee 37232

  4. 4

    Department of Veterans' Affairs, Tennessee Valley Healthcare System, Nashville, Tennessee 37212

  5. 5

    Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-9565

  6. 6

    Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-9565

  7. 7

    Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee 37232-9565

*Department of Orthopaedics, Vanderbilt University Medical Center, Nashville, Tennessee 37232-9565. T: 1-615-936-3080; F: 1-615-343-2423

Publication History

  1. Issue published online: 20 JUN 2012
  2. Article first published online: 13 JAN 2012
  3. Manuscript Accepted: 20 DEC 2011
  4. Manuscript Received: 23 JUN 2011

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Keywords:

  • fracture;
  • protease-activated receptor;
  • mice;
  • bone biology;
  • inflammation

Abstract

Protease-activated receptor-2 (PAR-2) provides an important link between extracellular proteases and the cellular initiation of inflammatory responses. The effect of PAR-2 on fracture healing is unknown. This study investigates the in vivo effect of PAR-2 deletion on fracture healing by assessing differences between wild-type (PAR-2+/+) and knock-out (PAR-2−/−) mice. Unilateral mid-shaft femur fractures were created in 34 PAR-2+/+ and 28 PAR-2−/− mice after intramedullary fixation. Histologic assessments were made at 1, 2, and 4 weeks post-fracture (wpf), and radiographic (plain radiographs, micro-computed tomography (µCT)) and biomechanical (torsion testing) assessments were made at 7 and 10 wpf. Both the fractured and un-fractured contralateral femur specimens were evaluated. Polar moment of inertia (pMOI), tissue mineral density (TMD), bone volume fraction (BV/TV) were determined from µCT images, and callus diameter was determined from plain radiographs. Statistically significant differences in callus morphology as assessed by µCT were found between PAR-2−/− and PAR-2+/+ mice at both 7 and 10 wpf. However, no significant histologic, plain radiographic, or biomechanical differences were found between the genotypes. The loss of PAR-2 was found to alter callus morphology as assessed by µCT but was not found to otherwise effect fracture healing in young mice. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1271–1276, 2012

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