Abstract

Microdamage induced by falls or other abnormal loads that cause shear stress in trabecular bone could impair the mechanical properties of the proximal femur or spine. Existing microdamage may also increase the initiation and propagation of further microdamage during subsequent normal, on-axis, loading conditions, resulting in atraumatic or “spontaneous” fractures. Microdamage formation due to shear and compressive strains was studied in 14 on-axis cylindrical bovine tibial trabecular bone specimens. Microdamage was induced by a torsional overload followed by an on-axis compressive overload and quantified microscopically. Fluorescent agents were used to label microdamage and differentiate damage due to the two loading modes. Both the microcrack density and diffuse damage area caused by the torsional overload increased with increasing shear strain from the center to the edge of the specimen. However, the mean microcrack length was uniform across the specimen, suggesting that microcrack length is limited by microstructural features. The mean density of microcracks caused by compressive overloading was slightly higher near the center of the specimen, and the diffuse damage area was uniform across the specimen. Over 20% of the microcracks formed in the initial torsional overloading propagated during compression. Moreover the propagating microcracks were, on average, longer than microcracks formed by a single overload. As such, changes in loading mode can cause propagation of microcracks beyond the microstructural barriers that normally limit the length. Damage induced by in vivo off-axis loads such as falls may similarly propagate during subsequent normal loading, which could affect both remodeling activity and fracture susceptibility.

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