Cellular StreSS reaCtionS

et al., 2001). In deep cavities, the concentration of HEMA reaching the pulp would be in the range of 1.5-8 mmol/L, and about 4 mmol/L for TEGDMA (Noda et al., 2002). Inflammatory reactions (toxic reactions) are reported after the insertion of resin-based composites and adhesives in cavities very close to the pulp or when a (micro) perforation of the pulp had occurred. Consistently, the lack of new (osteo) dentin formation has been reported in humans when resin-based composites and the corresponding adhesives were in direct contact with the pulp, even when little inflammation was present (HörstedBindslev et al., 2003). Therefore, it is reasonable to assume from clinical observations that the released molecules (e.g., unreacted monomers) may interact with cell metabolism at concentrations that are not lethal to cells. Another important challenge for the dental pulp in the context of restorative therapy is bacteria in the cavity under the restoration, either left behind or migrating between the cavity floor and resin material through a marginal gap. Despite improved bonding materials/techniques, marginal gaps have been reported both in vitro and in vivo, mainly at cavity margins located below the cemento-enamel junction (Hahn et al., 2008) and especially in technically challenging situations, e.g., in posterior teeth. Bacteria, especially their toxins (e.g., lipopolysaccharides for Gram-negative bacteria being present in deep caries lesions), may elicit pulp inflammation. It is further known that bacterial invasion inhibits dentin bridge formation after pulp capping (Rutherford and Gu, 2000). Therefore, both bacteria and monomers imply environmental stress to dental pulp tissue, and they may influence target cell reactions in a combined way.