With the overall increase in oral health of the young, the number of fully dentate (or mostly dentate) seniors has increased. This group of patients poses a series of new challenges for the practicing dentist. Tooth fractures are most common in the restored teeth of senior patients and may be due to specific structural changes in dentin that take place with aging. This dissertation aims to develop a mechanistic understanding of crack growth in dentin, the major hard tissue of the human tooth, and to identify the effects from the age-dependent microstructure on fracture, energy dissipation and the mechanisms of toughening in human dentin. To achieve this understanding, a hybrid evaluation of crack extension in human dentin was employed where experimental measurements of crack extension and near-tip displacement fields were used as the solution for a finite element model simulating crack growth. The experiments consisted of an evaluation of stable crack growth in compact tension (CT) specimens of human dentin and use of micro Digital Image Correlation (DIC) to document the full-field displacement field with crack extension. A Nonlinear Finite Element Model (NLFEM) for the fracture process was developed to account for the intrinsic (ahead of the crack tip) and extrinsic (behind the crack tip) components of energy dissipation observed from experiments.;Results from investigation show that the fracture resistance of dentin increases with crack extension, that dentin exhibits rising R-curve behavior and that this behavior is a function of patient age. When quantified in terms of specific age groups, there was a 25% increase in the crack growth resistance for the young dentin (18 age 29) from initiation (K o = 1.35 MPa·m0.5) to the development of a plateau toughness (Kp = 1.60 MPa·m 0.5). In contrast, the increase in crack growth resistance of the old dentin (50 = age) from initiation (Ko = 1.10 MPa·m0.5) to plateau (Ko = 1.20 MPa·m0.5) was less than 10%. The difference in fracture toughness between the two age groups was approximately 30%. In young dentin toughening was found to result from crack bridging by unbroken ligaments, as well as microcracking of the peritubular dentin and separation between the intertubular and peritubular aspects. Toughening in old dentin was comprised of the same mechanisms as in young dentin, but occurred to lower extent than in the young tissue. The reduction in the fracture toughness with increasing patient age was found to be highly correlated with the degree of mineral filling the tubule lumens; the lowest toughness was obtained when the lumens were fully occluded by deposited mineral. Results from the NLFEM showed that the extrinsic and intrinsic mechanisms played equal roles in the degree of toughening achieved with crack extension. These findings indicate that strategies aimed at increasing the toughness of old dentin should focus on the development of methods for preventing deposition of mineral within the dentin tubules with age.
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