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, data suggests that increased remodeling precedes the occurrence of bone microdamage and stress fractures, suggesting a central role for increased intracortical 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 (BP) in the rabbit tibial stress fracture model, to test the hypothesis that reactive remodeling within the cortex drives the development of stress fractures. Ongoing studies suggest that BP antiresorptive therapy reduces the intensity of the stress fracture response, as indicated by technetium bone scans. This effect was most pronounced with short-term loading (3 weeks), with (99) technetium uptake in BP treated animals reduced approximately 25 percent from control levels; this effect was diminished by 6 weeks of loading. Reduction of bone 99technetium uptake at 3 weeks in drug-treated animals is consistent with suppression of the acute activation of new intracortical resorption foci by bisphosphonates. The implication of this suppression of the later accumulation of bone microcracks, and the evolution of final stress fracture, are unknown.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2001
- Accession Number
- ADA406161
Entities
People
- Mitchell B. Schaffler
- Robert W. Boyd
Organizations
- Henry Ford Health