Damage Initiation at the Dentin/Adhesive Interface

The elastic stress-strain distribution could shed light on the likely damage initiation location and failure of the dentin/adhesive (d/a) interface. The interfacial microstructure and phase properties have a profound effect on the mechanical behavior of dentin/adhesive (d/a) interface. Both the interfacial microstructure and phase properties are influenced by the varying degree of demineralization of intertubular and peritubular dentin during etching as well as the depth of adhesive penetration into the hybrid layer. Objectives: The purpose of this investigation was to investigate the effect of interface geometry on load transfer at the d/a interface using a finite element model that utilizes the micro-structure/micro-property data collected from this laboratory. Methods: Computational unit cells, which are representative of the interface section, are identified and the distributions of micromechanical measures within the longitudinal section of the d/a are analyzed by considering the 2-dimensional FE models of these unit cells. Two possible realizations of computational unit cells with different tubule geometries are considered in the analysis. Elastic stress analyses of the 2-dimensional computational unit cells subjected to tensile loads were performed with a widely used commercial finite element (FE) package I-DEAS. Results: The results indicate that the morphological properties of the d/a interface affects both the stress concentration magnitude and the location near the hybrid/exposed-collagen layer. The change of location of stress concentration that occurs with the tapered geometry is further investigated by examining the maximum principal stress at three sections through the d/a interface. Conclusion: The results from this finite element model suggest that by increasing the widths of the peritubular and intertubular dentin decreases the stress concentrations and as the hybrid layer thickness increases the stress concentration increases for a linear infiltration mode. Supported in part: NIH/NIDCR: R01DE014392, K25DE015281 and NIH: R13DK069504.