Mechanistic aspects of fracture and R-curve behavior in human cortical bone.

An understanding of the evolution of toughness is essential for the mechanistic interpretation of the fracture of cortical bone. In the present study, in vitro fracture experiments were conducted on human cortical bone in order to identify and quantitatively assess the salient toughening mechanisms. The fracture toughness was found to rise linearly with crack extension (i.e., rising resistance- or R-curve behavior) with a mean crack-initiation toughness, K0 of approximately 2 MPa square root m for crack growth in the proximal-distal direction. Uncracked ligament bridging, which was observed in the wake of the crack, was identified as the dominant toughening mechanism responsible for the observed R-curve behavior. The extent and nature of the bridging zone was examined quantitatively using multi-cutting compliance experiments in order to assess the bridging zone length and estimate the bridging stress distribution. Additionally, time-dependent cracking behavior was observed at stress intensities well below those required for overload fracture; specifically, slow crack growth occurred at growth rates of approximately 2 x 10(-9) m/s at stress intensities approximately 35% below the crack-initiation toughness. In an attempt to measure slower growth rates, it was found that the behavior switched to a regime dominated by time-dependent crack blunting, similar to that reported for dentin; however, such blunting was apparent over much slower time scales in bone, which permitted subcritical crack growth to readily take place at higher stress intensities.