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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.

Cracks and craze lines are often observed in the enamel of human teeth, but they rarely cause tooth fracture. The present study evaluates fatigue crack growth in human enamel, and compares that to the fatigue response of sintered hydroxyapatite (HAp) with similar crystallinity, chemistry and density. Miniature inset compact tension (CT) specimens were prepared that embodied a small piece of enamel (N=8) or HAp (N=6). The specimens were subjected to mode I cyclic loads and the steady state crack growth responses were modeled using the Paris Law. Results showed that the fatigue crack growth exponent (m) for enamel (m = 7.7±1.0) was similar to that for HAp (m = 7.9±1.4), whereas the crack growth coefficient (C) for enamel (C=8.7E-04 (mm/cycle)·(MPa·m 0.5 ) -m ) was significantly lower (p<0.0001) than that for HAp (C = 2.0E+00 (mm/cycle)·(MPa·m 0.5 ) -m ). Micrographs of the fracture surfaces showed that crack growth in the enamel occurred primarily along the prism boundaries. In regions of decussation, the microstructure promoted microcracking, crack bridging, crack deflection and crack bifurcation. Working in concert, these mechanisms increased the crack growth resistance and resulted in a sensitivity to crack growth (m) similar to bone and lower than that of human dentin. These mechanisms of toughening were not observed in the crack growth response of the sintered HAp. While enamel is the most highly mineralized tissue of the human body, the microstructural arrangement of the prisms promotes exceptional resistance to crack growth.

An understanding of the fatigue and fracture behavior of hard tissues (e.g., bone and tissues of the human tooth) is critical to the maintenance of physical and oral health. Recent studies suggest that there are a number of mechanisms contributing to crack extension and crack arrest in these materials, and that they appear to be a function of moisture and age of the tissue. An understanding of these processes can provide new ideas that are relevant to the design of multi-functional engineering materials. As a result, we have adopted the use of microscopic Digital Image Correlation (DIC) to examine the mechanisms of crack growth resistance and near-tip displacement distribution for cracks in human dentin that are subjected to opening mode loads. We have also developed a special compact tension (CT) specimen that permits evaluation of crack extension within small portions of tissue under both quasi-static and fatigue loads. The specimen embodies a selected portion of hard tissue within a resin composite restorative and enables an examination of diseased tissue, or portion with specific physiology, that would otherwise be impossible to evaluate. In this paper we describe application of these experimental methods and present some recent results concerning fatigue crack growth and stable crack extension in dentin and across the dentinenamel-junction (DEJ) of human teeth.

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