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, histopathological data and experimental data from our laboratory 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. Thus, we propose that stress fracture occurs through a positive feedback mechanism, in which increased mechanical usage stimulates focal bone turnover, resulting in a locally increased in porosity. Microdamage accumulation and stress fractures result from continued cyclic loading of this transiently osteopenic bone. The proposed experiments test the hypothesis by pharmacologically inhibiting the bone remodeling response, the subsequent accumulation of microdamage and the severity of the stress fracture can be diminished. In the proposed experiments, this hypothesis is being tested experimentally in the rabbit tibial stress fracture model, which was developed in our laboratory. To test the hypothesis that reactive remodeling within the cortex drives the development of stress fractures, the effect of remodeling suppression using a bisphosphonate on the accumulation of bone microdamage and diminishing the severity of stress fracture will be examined. Outcomes of these experiments will be assessed using bone scintigraphy, histomorphometry and biomechanical approaches.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2000
- Accession Number
- ADA389071
Entities
People
- Mitchell B. Schaffler
- Robert D. Boyd
Organizations
- Henry Ford Health