Fracture healing in protease-activated receptor-2 deficient mice

Kevin R. O'Neill, Christopher M. Stutz, Nicholas A. Mignemi, Heather Cole, Matthew R. Murry, Jeffry S. Nyman, Heidi Hamm, Jonathan G. Schoenecker

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1271-1276
Number of pages6
JournalJournal of Orthopaedic Research
Issue number8
StatePublished - Aug 2012


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

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine


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