Fracture healing in protease-activated receptor-2 deficient mice

J Orthop Res. 2012 Aug;30(8):1271-6. doi: 10.1002/jor.22071. Epub 2012 Jan 13.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomechanical Phenomena / physiology
  • Bony Callus / pathology
  • Female
  • Femoral Fractures / diagnostic imaging
  • Femoral Fractures / pathology*
  • Fracture Healing / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptor, PAR-2 / deficiency*
  • Receptor, PAR-2 / physiology
  • Tomography, X-Ray Computed


  • Receptor, PAR-2