This study was aimed to investigate the effects of Parathyroid hormone (PTH) and alendronate (ALN) on stress fracture repair. Stress fractures were induced in the ulnae of female adult rats. Animals were treated daily with vehicle, PTH (40 µg/kg) or alendronate (2µg/kg), respectively. Bone mineral content (BMC) and bone mineral density (BMD) of bilateral ulnae were measured at two, four and eight weeks following induction of stress fracture. Histology at the ulna midshaft was undertaken at 2 and 4weeks and mechanical testing was done at 8weeks after stress fracture. PTH increased BMC significantly by 7% at 4weeks and BMD and BMC significantly by 10% and 7% at 8weeks compared to the control. Alendronate did not change BMD or BMC in comparison with the control. PTH significantly stimulated bone formation by 114% at 2weeks, increased intracortical resorption area by 23% at 4weeks, and enhanced the ultimate force of the affected ulnae by 15% at 8weeks compared to the control. Alendronate significantly suppressed bone formation rate by 44% compared to the control at 4weeks. These data indicate that PTH may accelerate intracortical bone remodeling induced by microdamage and alendronate may delay intracortical bone remodeling during stress fracture repair in rats. This study suggests that PTH may be used to facilitate stress fracture repair whereas bisphosphonates may delay tissue level repair of stress fractures.