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An understanding of how fatigue cracks grow in bone is of importance as fatigue is thought to be the main cause of clinical stress fractures. This study presents new results on the fatigue-crack growth behavior of small surface cracks (approximately 75-1000 microm in size) in human cortical bone, and compares their growth rates with data from other published studies on the behavior of both surface cracks and many millimeter, through-thickness large cracks. Results are obtained with a cyclically loaded cantilever-beam geometry using optical microscopy to examine for crack growth after every 100-500 cycles. Based on the current and previous results, small fatigue cracks appear to become more resistant to fatigue-crack growth with crack extension, analogous to the way the fracture resistance of cortical bone increases with crack growth. Mechanistically, a theory attributing such behavior to the development of bridges in the wake of the crack with crack growth is presented. The existence of such bridges is directly confirmed using optical microscopy.

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.

Age-related deterioration of the fracture properties of bone, coupled with increased life expectancy, is responsible for increasing incidence of bone fracture in the elderly, and hence, an understanding of how its fracture properties degrade with age is essential. The present study describes ex vivo fracture experiments to quantitatively assess the effect of aging on the fracture toughness properties of human cortical bone in the longitudinal direction. Because cortical bone exhibits rising crack-growth resistance with crack extension, unlike most previous studies, the toughness is evaluated in terms of resistance-curve (R-curve) behavior, measured for bone taken from wide range of age groups (34-99 years). Using this approach, both the ex vivo crack-initiation and crack-growth toughness are determined and are found to deteriorate with age; the initiation toughness decreases some 40% over 6 decades from 40 to 100 years, while the growth toughness is effectively eliminated over the same age range. The reduction in crack-growth toughness is considered to be associated primarily with a degradation in the degree of extrinsic toughening, in particular, involving crack bridging in the wake of the crack.