Dentin bonding agents and camphorquinone-induced cytotoxicity, 8-isoprostane and prostaglandin production is associated with CYP450, NQO1, NQO2, GST, and GSH peroxidase in human dental pulp cells.
Level 5 - mechanism / opinion, no new human data
In vitro bench research on cultured human cells
PubMed 41314882 · doi:10.1016/j.dental.2025.11.013
What was done
Cultured human dental pulp cells (HDPCs) were exposed for 24 hours to four commercial dentin bonding agents (DBAs) or the photo-initiator camphorquinone (CQ), with or without pharmacological inhibitors of CYP450, NQO1, NQO2, GST-P, GPx1, GPx4, or MEK/ERK. Measured outcomes included cell viability (MTT assay), oxidative stress (8-isoprostane ELISA), inflammatory mediator release (PGE2 ELISA), and enzyme expression (RT-PCR and immunofluorescence).
What was found
The abstract reports no numerical values, concentrations, or effect sizes. Qualitatively, all four DBAs stimulated 8-isoprostane and PGE2 production. CQ exposure upregulated mRNA and protein expression of CYP1A1, CYP1A2, NQO1, NQO2, GST-P, GPx1, and GPx4, with some upregulation attenuated by the MEK/ERK inhibitor U0126. Most enzyme inhibitors (α-naphthoflavone, dicoumarol, ES936, quercetin, melatonin, and a26) partially reduced CQ-induced 8-isoprostane and PGE2 production, whereas ethacrynic acid and cefoxitin did not; none significantly altered CQ-induced cytotoxicity.
Why it matters
It identifies specific drug-metabolizing and antioxidant enzymes involved in pulp cell inflammation and oxidative stress triggered by dental resin photo-initiators.
Limits
This is an in vitro cell culture model without the protective dentin thickness, pulp blood flow, or multicellular immune responses present in vivo. The abstract omits numerical data, baseline cell donor counts, and statistical significance values.
Cited by
- supports Acidic and toxic bonding materials placed deep at the base of dental fillings can cause the dental nerve to die.