The increase in bacterial resistance to one or several antibiotics has become a global health problem. Recently, nanomaterials have become a tool against multidrug-resistant bacteria. The metal and metal oxide nanoparticles are one of the most studied nanomaterials against multidrug-resistant bacteria. Several in vitro studies report that metal nanoparticles have antimicrobial properties against a broad spectrum of bacterial species. However, until recently, the bacterial resistance mechanisms to the bactericidal action of the nanoparticles had not been investigated. Some of the recently reported resistance mechanisms include electrostatic repulsion, ion efflux pumps, expression of extracellular matrices, and the adaptation of biofilms and mutations. The objective of this review is to summarize the recent findings regarding the mechanisms used by bacteria to counteract the antimicrobial effects of nanoparticles.
In recent years, the use and research in nanomaterials have increased considerably. In dentistry, nanomaterials have been investigated in all their specialties like dental prosthesis, implantology, dental operative, periodontics, and endodontics. The nanomaterials are investigated in the areas of dentistry due to their application in the improvement of the physical and chemical properties of conventional materials, as well as the use of the antimicrobial activity of nanomaterials such as silver nanoparticles. Recently, silver nanoparticles (AgNPs) have been studied for their use as an endodontic irrigator due to their high antimicrobial activity. But little is known about the possible mechanisms of the adaptation to AgNPs by endodontic bacteria. These mechanisms may be intrinsic (such as efflux pumps, downregulation of porins, and chromosomal resistance genes) or extrinsic (such as point and adaptive mutations and plasmids with resistance genes) adaptation systems. In addition to this, it has been reported that coselection or coregulation of metal resistance mechanisms, as in the case of nanoparticles, is accompanied by increased resistance to various antibiotics. For these reasons, the objective of this article is to do a review of the literature on the possible mechanisms used by endodontic bacteria to generate resistance to silver nanoparticles and the possible side effects of these mechanisms.
Background: The main microorganism associated with the failure of endodontic treatments is Enterococcus faecalis. Although several endodontic therapeutics have demonstrated antimicrobial activity against E. faecalis, the antimicrobial effectiveness of chitosan (CsNPs) and silver nanoparticles (AgNPs) included into conventional endodontic sealers for endodontic therapies is still unclear. Aim: The objective of this study was to evaluate the antibacterial activity increment (AAI) of endodontic sealers containing CsNPs and AgNPs as well as some chemical components against E. faecalis by direct contact assays. Methods: CsNPs and AgNPs were synthesized by reduction and ionic gelation methods, respectively. Nanoparticles were characterized by dynamic light scattering and energy dispersive X-ray analysis. The bactericidal activity was tested on monolayers on agar plates and collagen membrane surface assays against E. faecalis. Results: The size of CsNPs was 70.6±14.8 nm and zeta potential was 52.0±5.4 mV; the size of AgNPs was 54.2±8.5 nm, and zeta potential was –48.4±6.9 mV. All materials, single or combined, showed an AAI, especially when CsNPs, chlorhexidine (Chx), and the combination of CsNPs-Chx were added. However, the combination of CsNPs-Chx showed the highest (55%) AAI, followed by Chx (35.5%) and CsNPs (11.1%), respectively. There was a significant statistical difference in all comparisons ( p < 0.05). Tubliseal (40%) and AH Plus (32%) sealants showed a higher AAI on E. faecalis in the monolayer test and collagen membrane assay analyzed by scanning electron microscopy. Conclusions: Tubliseal and AH plus sealers combined with nanoparticles, especially CsNPs-Chx, could be used for conventional endodontic treatments in the control of E. faecalis bacteria.
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