Fracture resistance of human cortical bone across multiple length-scales at physiological strain rates.

While most fracture-mechanics investigations on bone have been performed at low strain rates, physiological fractures invariably occur at higher loading rates. Here, at strain rates from 10(-5) to 10(-1) s(-1), we investigate deformation and fracture in bone at small length-scales using in situ small-angle x-ray scattering (SAXS) to study deformation in the mineralized collagen fibrils and at the microstructural level via fracture-mechanics experiments to study toughening mechanisms generating toughness through crack-tip shielding. Our results show diminished bone toughness at increasing strain rates as cracks penetrate through the osteons at higher strain rates instead of deflecting at the cement lines, which is a prime toughening mechanism in bone at low strain rates. The absence of crack deflection mechanisms at higher strain rates is consistent with lower intrinsic bone matrix toughness. In the SAXS experiments, higher fibrillar strains at higher strain rates suggest less inelastic deformation and thus support a lower intrinsic toughness. The increased incidence of fracture induced by high strain rates can be associated with a loss in toughness in the matrix caused by a strain rate induced stiffening of the fibril ductility, i.e., a "locking-up" of the viscous sliding and sacrificial bonding mechanisms, which are the origin of inelastic deformation (and toughness) in bone at small length-scales.