Does Preheating Influence the Cytotoxic Potential of Dental Resin Composites?

Resin-based dental composites (RBC) release cytotoxic components, however the extent of the elution from preheated RBCs is barely investigated. The aim was therefore to determine the cytotoxic effect of preheated conventional, bulk, and thermoviscous RBCs of clinically relevant sizes using different cell viability methods in a contact-free model. Samples (6 × 4 mm) were prepared from conventional [Estelite Sigma Quick (ESQ), Filtek Z250 (FZ)] and bulk-filled [Filtek One BulkFill Restorative (FOB), SDR Plus Bulk Flow (SDR), VisCalor Bulk (VCB)] RBCs. The pre-polymerization temperature was set to room temperature (RT) and 55/65 °C. Pulp cells were cultured, followed by a 2-day exposure to monomers released from solid RBC specimens suspended in the culture medium. Cytotoxicity was assessed using a WST-1, MTT, and LDH colorimetric viability assays. Data were analyzed using one-way ANOVA, Tukey's post hoc test, multivariate analysis, and independent t-test. The effect size (ƞp2) of material and temperature factors was also assessed. All the RBCs demonstrated cytotoxic effect upon exposure to pulp cells, but to a varying extent (ESQ >> VCB > FZ = FOB = SDR). The effect of pre-polymerization temperature was insignificant (ƞp2 < 0.03), except for the thermoviscous RBC, which showed inconsistent findings when subjected to distinct viability tests. Cell viability was predominantly dependent on the type of material used (p < 0.001) which showed a large effect size (ƞp2 > 0.90). Irrespective of the pre-polymerization temperature, RBC samples in a clinically relevant size can release monomers to such an extent, which can substantially decrease the cytocompatibility.

Defense Mechanisms Against Acid Exposure by Dental Enamel Formation, Saliva and Pancreatic Juice Production.

The pancreas, the salivary glands and the dental enamel producing ameloblasts have marked developmental, structural and functional similarities. One of the most striking similarities is their bicarbonate-rich secretory product, serving acid neutralization. An important difference between them is that while pancreatic juice and saliva are delivered into a lumen where they can be collected and analyzed, ameloblasts produce locally precipitating hydroxyapatite which cannot be easily studied. Interestingly, the ion and protein secretion by the pancreas, the salivary glands, and maturation ameloblasts are all two-step processes, of course with significant differences too. As they all have to defend against acid exposure by producing extremely large quantities of bicarbonate, the failure of this function leads to deteriorating consequences. The aim of the present review is to describe and characterize the defense mechanisms of the pancreas, the salivary glands and enamel-producing ameloblasts against acid exposure and to compare their functional capabilities to do this by producing bicarbonate.