PAPER 5: BLOCKADE OF BETA-ADRENERGIC SIGNALLING DOES NOT INFLUENCE FRACTURE HEALING IN A MOUSE MODEL

Abstract

Introduction: Influence of beta-blockers against fracture is controversial. Role of beta-blockers in fracture treatment not explored.

Objective: to analyze influence of propranolol, a beta-blocker, on fracture healing in a mouse model.

Materials and Methods: Fracture and intramedullary nailing on right femur of 8 week, male C57BL/6 mice. Daily propranolol in drinking water: 0 (control), 4 (low dose) and 20 (high dose) mg/kg 3 week: microcomputed tomography (microCT), histological analyses 6 week: microCT, mechanical testing N = 5 üC 9/group Statistics: two-way ANOVA. Á = 0.05.

Results: From 3 to 6 weeks, callus volume and bone mineral content (BMC) decreased, and tissue mineral density increased significantly in control groups. Callus volume and BMC decreased significantly in low dose groups. No significance in high dose groups. No significance with treatment. At 3 weeks, callus area and woven bone percentage not different with treatment. At 6 weeks, ultimate torque not different with treatment or fracture. Within the control groups, twist at ultimate torque significantly lower in fractured bones. Torsional rigidity increased significantly in fractured bones, but not different with treatment.

Discussion: Most studies based on population observation or manipulation of sympathetic signaling using intact animal bones. The current fracture model may have created neural damage, thereby interrupting the sympathetic pathway and negating its regulation of bone metabolism. Whether neural signaling is compromised by fracture treatment requires further study and may be critical to the action of beta-blockers in bone.