Fracture healing in protease-activated receptor-2 deficient mice.

O'Neill KR, Stutz CM, Mignemi NA, Cole H, Murry MR, Nyman JS, Hamm H, Schoenecker JG
J Orthop Res. 2012 30 (8): 1271-6

PMID: 22247070 · DOI:10.1002/jor.22071

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.

Copyright © 2012 Orthopaedic Research Society.

MeSH Terms (11)

Animals Biomechanical Phenomena Bony Callus Female Femoral Fractures Fracture Healing Mice Mice, Inbred C57BL Mice, Knockout Receptor, PAR-2 Tomography, X-Ray Computed

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