Abstract
Camphorquinone (CQ) is a popularly-used photosensitizer in composite resin restoration. In this study, the effects of CQ on cytotoxicity and inflammation-related genes and proteins expression of pulp cells were investigated. The role of reactive oxygen species (ROS), ATM/Chk2/p53 and hemeoxygenase-1 (HO-1) and MEK/ERK signaling was also evaluated. We found that ROS and free radicals may play important role in CQ toxicity. CQ (1 and 2 mM) decreased the viability of pulp cells to about 70% and 50% of control, respectively. CQ also induced G2/M cell cycle arrest and apoptosis of pulp cells. The expression of type I collagen, cdc2, cyclin B, and cdc25C was inhibited, while p21, HO-1 and cyclooxygenase-2 (COX-2) were stimulated by CQ. CQ also activated ATM, Chk2, and p53 phosphorylation and GADD45α expression. Besides, exposure to CQ increased cellular ROS level and 8-isoprostane production. CQ also stimulated COX-2 expression and PGE2 production of pulp cells. The reduction of cell viability caused by CQ can be attenuated by N-acetyl-L-cysteine (NAC), catalase and superoxide dismutase (SOD), but can be promoted by Zinc protoporphyin (ZnPP). CQ stimulated ERK1/2 phosphorylation, and U0126 prevented the CQ-induced COX-2 expression and prostaglandin E2 (PGE2) production. These results indicate that CQ may cause cytotoxicity, cell cycle arrest, apoptosis, and PGE2 production of pulp cells. These events could be due to stimulation of ROS and 8-isoprostane production, ATM/Chk2/p53 signaling, HO-1, COX-2 and p21 expression, as well as the inhibition of cdc2, cdc25C and cyclin B1. These results are important for understanding the role of ROS in pathogenesis of pulp necrosis and pulpal inflammation after clinical composite resin filling.
Highlights
In dentistry, resin composites are widely used as restorative materials because of their ease of handling and esthetic enhancement
The luminol reagents for western blotting and the primary antibodies Type I collagen, p-extracellular signal-regulated kinase (ERK), Glyceraldehyde 3-phosphate dehydrogenase (GAPDH), COX-2, HO-1, cdc2, cyclin B1, cdc25C, p-Ataxia telangiectasia mutated (ATM), p-Chk2, p-p53, GADD45α were obtained from Santa Cruz Biotechnology (Santa Cruz Biotechnology Inc., Santa Cruz, CA, USA), and p21 was from GeneTex (Irvine, California, USA)
Since pulpal inflammation was often noticed when exposed pulp or deep caries cavity is restored with dentin bonding agents (DBAs) and composite resins, we further studied and found that CQ stimulates prostaglandin E2 (PGE2) and PGF2α production of pulp cells
Summary
Resin composites are widely used as restorative materials because of their ease of handling and esthetic enhancement. The commonly used oligomers and monomers in organic polymer matrix of resin composites belong to dimethacrylates, which contain reactive carbon double bonds. They undergo free-radical polymerization that is a kind of addition polymerization, and polymerization initiators are contained to produce free radicals for initiating the reaction. The polymerization initiators used for light-cured resin composites usually consist of a photosensitizer, primarily camphorquinone (CQ), and a reducing agent which is often a tertiary amine such as dimethylaminoethyl methacrylate (DMAEMA) or dimethyl-para-toluidine (DMPT) [1]. The residual monomers and additives are free to diffuse out from the cured materials. They may be released into surrounding tissues, and may have potential toxic effects. CQ was identified as one of the main released components in extracts of resin-based materials [4,5]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
