Methacrylate monomers that are found to leach from cured resin-based dental materials induce biological effects in vitro. The underlying mechanisms have not been fully elucidated although involvement of increased cellular reactive oxygen species (ROS) and DNA-damage has been suggested. In this in vitro study we have elucidated the impact of a commonly used methacrylate monomer, HEMA, on the level and oxidation state of cellular glutathione, intracellular ROS level, as well as the formation of complex between HEMA and glutathione. HEMA exposure rapidly led to increased level of ROS and reduced level of GSH (reduced form of glutathione). Antioxidants effectively counteracted the ROS increase, but had no effect on the GSH depletion. No change in glutathione-disulphide (GSSG; oxidized form of glutathione) concentration was detected in the HEMA treated cells, showing that oxidation of glutathione was not responsible for the reduced GSH concentration. Further we demonstrated spontaneous formation of a complex between HEMA and GSH. In conclusion, we showed that exposure to HEMA led to drop in cellular glutathione level probably caused by complex formation with HEMA. A similar covalent binding of HEMA to macromolecules combined with increased level of cellular ROS due to lower levels of GSH is suggested to be important factors triggering the toxic response.
The lifespan of a resin‐based restoration is limited, with the main reason for failure being secondary caries. Biofilm formation at the tooth–material interface is a necessary etiological agent for caries development. Dental materials with antimicrobial properties may reduce formation of biofilm and thus increase the longevity of restorations. This study aimed to investigate the effect of methacrylated chitosan (CH‐MA), incorporated into the polymeric network of an experimental dental composite and adhesive, on biofilm growth of Streptococcus mutans and to assess the mechanical properties of the modified materials. The methacrylation of low‐molecular‐weight chitosan was achieved and biofilm studies confirmed the antibacterial effect of the modified polymer in solution. Methacrylated chitosan was incorporated into an experimental composite and adhesive, and the modified materials reduced the formation of S. mutans biofilm. The incorporation of CH‐MA did not alter the bond strength of the adhesives. However, the amount of CH‐MA in composite that is required to elicit an antibacterial response challenges the mechanical properties of the material. The hardness and flexural strength of the composite decreased with increasing amounts of CH‐MA. However, flexural strength values still met the requirement in the ISO standard.
Aim. The aim of this study was to investigate the antibacterial and antibiofilm properties of low viscosity chitosan on S. epidermidis growth and biofilm formation. Methods and Results. The antibacterial and antibiofilm properties were investigated, during both planktonic growth and biofilm formation. This was performed using different concentrations in media and by coating on polystyrene surfaces. In addition, the bactericidal effect was investigated using a modified direct contact test. The results showed that low viscosity chitosan in media had both a bacteriostatic and bactericidal effect on planktonic growth and biofilm formation of S. epidermidis in a concentration dependent manner. Polystyrene discs coated with chitosan reduced both early biofilm formation (6 h) and late biofilm formation (18 h), as confirmed by scanning electron microscopy. The modified direct contact test showed a bactericidal effect. Conclusion. This study demonstrated that low viscosity chitosan has a bacteriostatic and bactericidal activity against S. epidermidis and that the activity is dependent on the amount of chitosan added. In addition, low viscosity chitosan reduced biofilm formation both when added to media and when coated on polystyrene surfaces. Significance and Impact of Study. Low viscosity chitosan could be a contribution to new treatment approaches of biofilm-related infections of S. epidermidis.
Introduction: Coronal leakage and reinfection after root canal therapy is an important reason for endodontic failure. Zinc oxide-eugenol (ZOE) -based materials are often used as a coronal seal to prevent secondary infection. The antibacterial effect of ZOE cement is mainly due to leaching of eugenol from the material, but the effect is reported to decrease over time. Chitosan (CH) is a natural polymer with antibacterial properties. The aim of the study was to investigate if incorporation of (CH) and chitosan oligosaccharide (COS) in a ZOE-based material improved both the immediate and sustained antibacterial properties of the material. Methods: Enterococcus faecalis, Streptococcus mutans and Staphylococcus epidermidis was used to investigate the antibacterial effect of the materials in a modified direct contact test (MDCT) immediately after setting and after storage for 18 weeks in water. Leaching per week of eugenol from the materials was quantified using gas chromatography-mass spectrometry (GC-MS). The effect of eugenol on growth of bacteria was measured by reading of optical density at 600 nm after 18 h growth. Mechanical properties were investigated in a compressive strength test according to ISO 3107. Results: The present study showed that a ZOE-based material has antibacterial activity both as freshly prepared and after immersion in water for 18 weeks. Incorporating CH or COS may increase the antibacterial effect depending on the bacterial species investigated. The amount of leached eugenol did not differ between materials or during or after storage. S. mutans showed the highest susceptibility to eugenol of the three species investigated. Modification of the materials with CH or COS reduced the compressive strength, but the requirements in ISO 3017 were still met.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.