In this study the crack growth resistance behavior and fracture toughness of human tooth enamel were quantified using incremental crack growth measures and conventional fracture mechanics. Results showed that enamel undergoes an increase in crack growth resistance (i.e. rising R-curve) with crack extension from the outer to the inner enamel, and that the rise in toughness is function of distance from the Dentin Enamel Junction (DEJ). The outer enamel exhibited the lowest apparent toughness (0.67 ± 0.12 MPa·m 0.5 ), and the inner enamel exhibited a rise in the growth toughness from 1.13 MPa·m 0.5 /mm to 3.93 MPa·m 0.5 /mm. The maximum crack growth resistance at fracture (i.e. fracture toughness (K c )) ranged from 1.79 to 2.37 MPa·m0.5. Crack growth in the inner enamel was accompanied by host of mechanisms operating from the micro-to the nano-scale. Decussation in the inner enamel promoted crack deflection and twist, resulting in a reduction of the local stress intensity at the crack tip. In addition, extrinsic mechanisms such as bridging by unbroken ligaments of the tissue and the organic matrix promoted crack closure. Microcracking due to loosening of prisms was also identified as an active source of energy dissipation. In summary, the unique microstructure of enamel in the decussated region promotes crack growth toughness that is approximately three times that of dentin and over ten times that of bone.

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An evaluation of the crack growth resistance of human coronal dentin was performed on tissue obtained from patients between ages 18 and 83. Stable crack extension was achieved over clinically relevant lengths (0 ≤ a ≤1 mm) under Mode I quasi-static loading and perpendicular to the nominal tubule direction. Results distinguished that human dentin exhibits an increase in crack growth resistance with extension (i.e. rising R-curve) and that there is a significant reduction in both the initiation (K o ) and plateau (K p ) components of toughness with patient age. In the young dentin (18≤age≤35) there was a 25 % increase in the crack growth resistance from the onset of extension (K o =1.34 MPa·m 0.5 ) to the maximum or "plateau" toughness (K p = 1.65 MPa·m 0.5 ). In comparison, the crack growth resistance of the old dentin (55≤age) increased with extension by less than 10 % from K o = 1.08 MPa·m 0.5 to K p = 1.17 MPa·m 0.5 . In young dentin toughening was achieved by a combination of inelastic deformation of the mineralized collagen matrix and microcracking of the peritubular cuffs. These mechanisms facilitated further toughening via the development of unbroken ligaments of tissue and posterior crack-bridging. Microstructural changes with aging decreased the capacity for near-tip inelastic deformation and microcracking of the tubules, which in turn suppressed the formation of unbroken ligaments and the degree of extrinsic toughening.

The enamel of human teeth is generally regarded as a brittle material with low fracture toughness. Consequently, the contributions of this tissue in resisting tooth fracture and the importance of its complex microstructure have been largely overlooked. In this study an experimental evaluation of the crack growth resistance of human enamel was conducted to characterize the role of rod (i.e. prism) orientation and degree of decussation on the fracture behavior of this tissue. Incremental crack growth was achieved in-plane, with the rods in directions longitudinal or transverse to their axes. Results showed that the fracture resistance of enamel is both inhomogeneous and spatially anisotropic. Cracks extending transverse to the rods in the outer enamel undergo a lower rise in toughness with extension, and achieve significantly lower fracture resistance than in the longitudinal direction. Though cracks initiating at the surface of teeth may begin extension towards the dentin–enamel junction, they are deflected by the decussated rods and continue growth about the tooth’s periphery, transverse to the rods in the outer enamel. This process facilitates dissipation of fracture energy and averts cracks from extending towards the dentin and vital pulp.

An evaluation of the fatigue crack resistance of human dentin was conducted to identify the degree of degradation that arises with aging and the dependency on tubule orientation. Fatigue crack growth was achieved in specimens of coronal dentin through application of Mode I cyclic loading and over clinically relevant lengths (0 ≤ a ≤ 2 mm). The study considered two directions of cyclic crack growth in which the crack was either in-plane (0°) or perpendicular (90°) to the dentin tubules. Results showed that regardless of tubule orientation, aging of dentin is accompanied by a significant reduction in the resistance to the initiation of fatigue crack growth, as well as a significant increase in the rate of incremental extension. Perpendicular to the tubules, the fatigue crack exponent increased significantly (from m=14.2±1.5 to 24.1±5.0), suggesting an increase in brittleness of the tissue with age. For cracks extending in plane with the tubules, the fatigue crack growth exponent does not change significantly with patient age (from m=25.4±3.03 to 22.9±5.3), but there is a significant increase in the incremental crack growth rate. Regardless of age, coronal dentin exhibits the lowest resistance to fatigue crack growth perpendicular to the tubules. While there are changes in the cyclic crack growth rate and mechanisms of cyclic extension with aging, this tissue maintains its anisotropy.