Influence of Bone Remodeling Inhibition on the Development of Experimental Stress Fractures
Abstract
Stress fractures result from repetitive loading and have been regarded as a mechanical fatigue-driven process. However, a number of studies indicate implicate increased bone remodeling in the pathogenesis of stress fractures. Our experiments tested the hypothesis that pharmacological inhibition of bone remodeling will slow the accumulation of microdamage and diminish the severity of the stress fracture. Using a bisphosphonate (BIS) to suppress remodeling in the rabbit tibial stress fracture model, we found that antiresorptive therapy reduced the intensity of the stress fracture response in this model.(99mTechneitum uptake reduced by approximately 50 percent, size of the resulting fracture callus reduced by about 30-50% in BIS-treated animals) and a trend toward reduced bone microdamage accumulation. These data are consistent with the hypothesis that bone remodeling contributes to the pathogenesis of stress fracture. However, variability in this model was greater than expected, limiting our ability to move forward with this animal model. We also report on the results of novel model for stress fracture healing, using adult rats, developed under the aegis of this program.
Document Details
- Document Type
- Technical Report
- Publication Date
- Nov 01, 2005
- Accession Number
- ADA471385
Entities
People
- Mitchell B. Schaffler
Organizations
- Icahn School of Medicine at Mount Sinai