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The present report is a study of the fracture behavior of the dentin-enamel complex, involving enamel, dentin, and the dentin-enamel junction (DEJ), that combines experimental design, computational finite element analysis, and fractography. Seven chevron-notched short-bar bovine DEJ specimens were utilized in this study. The general plane of the DEJ was approximately perpendicular to the fracture plane. All specimens were stored at 37 degrees C and 100% relative humidity for 24 h prior to being tested. A fracture test set-up was designed for application of tensile load on the DEJ specimens to initiate a crack at the vertex of the chevron in the enamel, across the DEJ zone and into the bulk dentin. During fracture testing, a water chamber was used to avoid dehydration of the specimen. The results showed that the lower boundary value of the fracture toughness of the DEJ perpendicular to its own plane was 3.38 +/- 0.40 MN/m1.5 and 988.42 +/- 231.39 J/m2, in terms of KIC and GKC, respectively. In addition, there was an extensive plastic deformation (83 +/- 12%) collateral to the fracture process at the DEJ zone. The fractography revealed that the deviation of the crak path involved an area which was approximately 50-100 microns deep. The parallel-oriented coarse collagen bundles with diameters of 1-5 microns at the DEJ zone may play a significant role in resisting the enamel crack. This reflects the fact, that in the intact tooth, the multiple full thickness cracks commonly found in enamel do not typically cause total failure of the tooth by crack extension into the dentin.

The dentin-enamel junction constitutes a unique boundary between two highly mineralized tissues with very different matrix composition and physical properties. The nature of the boundary between the ectoderm-derived enamel and mesoderm-derived dentin is not known. This study was undertaken to identify the presence, type, and distribution of collagen at the dentin-enamel junction as an initial step in understanding its structural-functional role in dental occlusion. Sections of human teeth were demineralized with 0.1 M neutral EDTA and examined by high-resolution field-emission scanning electron microscopy at low accelerating voltage. Enamel and dentin were observed to be linked by many parallel 80-120-nm diameter fibrils, which were inserted directly into the enamel mineral and also merged with the interwoven fibrillar network of the dentin matrix. Immunogold labeling for collagen was visualized by secondary electron imaging and backscatter electron imaging at low accelerating voltage. The collagen fibrils at the junctional zone as well as in the dentin matrix were identified as Type I collagen. Collagenase digestion led to loss of the fibrillar structures and prevented immunogold labeling with antibody specific to Type I collagen. Consequently, the dentin-enamel junction can be regarded as a fibril-reinforced bond which is mineralized to a moderate degree.

The results from network meta-analysis showed that most active treatment options had significantly better treatment outcome than placebo.

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Ethylenediaminetetraacetic acid (EDTA) is commonly used during the preparation of obstructed root canals that face a high risk of root perforation. Such perforations may be repaired with mineral trioxide aggregate (MTA). Due to EDTA's ability to chelate calcium ions, we hypothesized that EDTA may disrupt the hydration of MTA. Using scanning electron microscopy and energy-dispersive x-ray spectroscopy, we found that MTA specimens stored in an EDTA solution had no crystalline structure and a Ca/Si molar ratio considerably lower than those obtained for specimens stored in distilled water and normal saline. Poor cell adhesion in EDTA-treated MTA was also noted. X-ray diffraction indicated that the peak corresponding to portlandite, which is normally present in hydrated MTA, was not shown in the EDTA group. The microhardness of EDTA-treated specimens was also significantly reduced (p < 0.0001). These findings suggest that EDTA interferes with the hydration of MTA, resulting in decreased hardness and poor biocompatibility.