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Resin-based pit-and-fissure sealants are often used to form a barrier on the occlusal surface of molars to treat caries lesions; however, bacteria can remain in the pit and fissures without detection, increasing the risk of secondary caries. Sealants with antimicrobial properties or microbial repellent actions might be advantageous. The aim of this study was to assess the inhibitory effect of a 2-methacryloxylethyl dodecyl methyl ammonium bromide (MAE-DB)-incorporated sealant against Streptococcus mutans. MAE-DB (4% wt) was incorporated into a commercially available sealant, Eco-S resin-based pit-and-fissure sealant (Vericom Co., Ltd., Korea); a sealant without MAE-DB served as a negative control, and Clinpro™ Sealant (3M™ ESPE™), a fluoride-releasing resin, was used as a commercial control. The effects of the cured sealants and their eluents on the growth of S. mutans were determined according to colony-forming unit counts and metabolic tests. The effects of the cured sealants on the adherence and membrane integrity of S. mutans were investigated using confocal laser-scanning microscopy (CLSM) in conjunction with fluorescent indicators. Compared with the negative control and commercial control, the cured MAE-DB-incorporated pit-and-fissure sealant exhibited a significant inhibitory effect on the growth of S. mutans (P < 0.05), whereas the eluents did not show any detectable antibacterial activity. The commercial control also showed no detectable bactericidal activity. Moreover, the aged experimental material retained its property of contact inhibition of biofilm formation. The fluorescence analysis of CLSM images demonstrated that the cured MAE-DB-incorporated sealant could hamper the adherence of S. mutans and exert a detrimental effect on bacterial membrane integrity. The incorporation of MAE-DB can render a pit-and-fissure sealant with contact antibacterial activity after polymerization via influencing the growth, adherence, and membrane integrity of S. mutans. Therefore, MAE-DB-containing pit-and-fissure sealant shows promise for preventing or controlling dental caries on occlusal pit and fissures of molars. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the involvement of intrinsic mitochondrial apoptosis in dental monomer-induced cytotoxicity and the influences of N-acetyl cysteine (NAC) on this process. Methods: Human dental pulp cells (hDPCs) were exposed to several dental monomers in the absence or presence of NAC, and cell viability, intracellular redox balance, morphology and function of mitochondria and key indicators of intrinsic mitochondrial apoptosis were evaluated using various commercial kits. Results: Dental monomers exerted dose-dependent cytotoxic effects on hDPCs. Concomitant to the over-production of reactive oxygen species (ROS) and depletion of glutathione (GSH), differential changes in activities of superoxide dismutase, glutathione peroxidase, and catalase were detected. Apoptosis, as indicated by positive Annexin V/propidium iodide (PI) staining and activation of caspase-3, was observed after dental monomer treatment. Dental monomers impaired the morphology and function of mitochondria, and induced intrinsic mitochondrial apoptosis in hDPCs via up-regulation of p53, Bax and cleaved caspase-3, and down-regulation of Bcl-2. NAC restored cell viability, relieved oxidative stress and blocked the apoptotic effects of dental monomers. Conclusions: Dental monomers induced oxidative stress and mitochondrial intrinsic apoptosis in hDPCs. NAC could reduce the oxidative stress and thus protect hDPCs against dental monomer-induced apoptosis. [ABSTRACT FROM AUTHOR]