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Although the propagation of fatigue cracks has been recognized as a problem of clinical significance in dentin, there have been few fracture mechanics-based studies that have investigated this issue. In the present study, in vitro cyclic fatigue experiments were conducted over a range of cyclic frequencies (1-50 Hz) on elephant dentin in order to quantify fatigue-crack growth behavior from the perspective of understanding the mechanism of fatigue in dentin. Specifically, results obtained for crack extension rates along a direction parallel to the dentinal tubules were found to be well described by the stress-intensity range, DeltaK, using a simple Paris power-law approach with exponents ranging from 12 to 32. Furthermore, a frequency dependence was observed for the crack-growth rates, with higher growth rates associated with lower frequencies. By using crack-growth experiments involving alternate cyclic and static loading, such fatigue-crack propagation was mechanistically determined to be the result of a "true" cyclic fatigue mechanism, and not simply a succession of static fracture events. Furthermore, based on the observed frequency dependence of fatigue-crack growth in dentin and observations of time-dependent crack blunting, a cyclic fatigue mechanism involving crack-tip blunting and re-sharpening is proposed. These results are deemed to be of importance for an improved understanding of fatigue-related failures in teeth.

The dentin-enamel junction (DEJ), which is the interfacial region between the dentin and outer enamel coating in teeth, is known for its unique biomechanical properties that provide a crack-arrest barrier for flaws formed in the brittle enamel1. In this work, we re-examine how cracks propagate in the proximity of the DEJ, and specifically quantify, using interfacial fracture mechanics, the fracture toughness of the DEJ region. Careful observation of crack penetration through the interface and the new estimate of the DEJ toughness ( approximately 5 to 10 times higher than enamel but approximately 75% lower than dentin) shed new light on the mechanism of crack arrest. We conclude that the critical role of this region, in preventing cracks formed in enamel from traversing the interface and causing catastrophic tooth fractures, is not associated with the crack-arrest capabilities of the interface itself; rather, cracks tend to penetrate the (optical) DEJ and arrest when they enter the tougher mantle dentin adjacent to the interface due to the development of crack-tip shielding from uncracked-ligament bridging.

Few studies have focused on a description of the fracture toughness properties of dentin in terms of resistance-curve (R-curve) behavior, i.e., fracture resistance increasing with crack extension, particularly in light of the relevant toughening mechanisms involved. Accordingly, in the present study, fracture mechanics based experiments were conducted on elephant dentin in order to determine such R-curves, to identify the salient toughening mechanisms and to discern how hydration may affect their potency. Crack bridging by uncracked ligaments, observed directly by microscopy and X-ray tomography, was identified as a major toughening mechanism, with further experimental evidence provided by compliance-based experiments. In addition, with hydration, dentin was observed to display significant crack blunting leading to a higher overall fracture resistance than in the dehydrated material. The results of this work are deemed to be of importance from the perspective of modeling the fracture behavior of dentin and in predicting its failure in vivo.