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 that increased remodeling precedes the occurrence of bone microdamage and stress fractures, suggesting a central role for bone remodeling in the pathogenesis of stress fractures. Our ongoing experiments test the hypothesis by pharmacological inhibition of bone remodeling will slow the subsequent accumulation of microdamage, diminishing the severity of the stress fracture. We are using a bisphosphonate (BIS) in the rabbit tibial stress fracture model, to test the hypothesis that reactive remodeling within the cortex drives the development of stress fractures. Results to date indicate that BIS antiresorptive therapy reduces the intensity of the stress fracture response, as indicated by (99m)Techneitum bone scans, with the uptake of (99m)Techneitum reduced by approximately 50 percent in treated animals as compared to saline-treated controls. However, BIS treatment attenuated, but did not completely prevent the stress fracture response. These data are consistent with the hypothesis that bone remodeling contributes to the pathogenesis of stress fracture. The implication of this suppression on the later accumulation of bone microcracks and the evolution of final stress fracture are unknown are currently under investigation.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2002
- Accession Number
- ADA409742
Entities
People
- Mitchell B. Schaffler
- Robert D. Boyd
Organizations
- Case Western Reserve University