Characterizing gait induced normal strains in a murine tibia cortical bone defect model.

The critical role that mechanical stimuli serve in mediating bone repair is recognized but incompletely understood. Further, previous attempts to understand this role have utilized application of externally applied mechanical loads to study the tissue's response. In this project, we have therefore endeavored to capitalize on bone's own consistently diverse loading environment to develop a novel model that would enable assessment of the influence of physiologically engendered mechanical stimuli on cortical defect repair. We used an inverse dynamics approach with finite element analysis (FEA) to first quantify normal strain distributions generated in mouse tibia during locomotion. The strain environment of the tibia, as previously reported for other long bones, was found to arise primarily due to bending and was consistent in orientation through the stance phase of gait. Based on these data, we identified three regions within a transverse cross-section of the mid-diaphysis as uniform locations of either peak tension, peak compression, or the neutral axis of bending (i.e. minimal strain magnitude). We then used FEA to quantify the altered strain environment that would be produced by a 0.6mm diameter cylindrical cortical bone defect at each diaphyseal site and, in an in situ study confirmed our ability to accurately place defects at the desired diaphyseal locations. The resulting model will enable the exploration of cortical bone healing within the context of physiologically engendered mechanical strain.