Thus, cerium oxide NPs are promising nanoparticles to interact with red blood cells in inflammatory situations where high ROS levels are present. In the study of [PERSON] et al., [27] CeO\({}_{2}\) NPs with different nanostructures (nanocube, nanorod, and nano-octahedra) were synthesized through hydrothermal methods, spin-coated on titanium grade IV disks, and evaluated for their hemolytic, anti-inflammatory, and antibacterial properties. Despite differences in their behavior, all NPs presented outstanding antimicrobial potential towards common peri-implantitis pathogens, such as _Porphyomonas gingivalis_ and _Fusobacterium nucleatum_. As the different physicochemical properties and degree of crystallinity might affect the antimicrobial, antioxidant, and hemolytic properties of CeO\({}_{2}\) NPs, [30] further research is needed to unravel the optimum materials for all biomedical applications where infection control is critical. The foremost prevalent bacteria that may create considerable amounts of lactic acid and demineralize teeth are _Streptococcus mutants_ and _Lactobacillus_[31]. Patients are more likely to develop caries after placement of fixed orthodontic appliances, due to the enhanced plaque and bacteria accumulation around brackets and bands [32]. This equipment makes it challenging for patients to maintain good oral hygiene, which raises the risk of caries. White spot lesions are caused by demineralization of the enamel (WSL) [33]. Within a month of bonding, WSL can be seen around the brackets, and by the time orthodontic treatment is complete, WSL prevalence has been estimated to reach 50% [34]. A literature investigation on CeO\({}_{2}\) nanoparticles reveals a positive effect against oral microbiota [20]. The antibacterial effectiveness of CeO\({}_{2}\) NPs depends on how well they interact with bacteria through electrostatic attraction to produce ROS, which causes bacterial cell death. These nanoparticles disrupt intracellular processes (DNA replication, mitosis, and cellular respiration) in bacterial cells, which results in the production of ROS and the elimination of both Gram-positive and Gram-negative bacteria [4]. On the other hand, according to [PERSON] et al., CeO\({}_{2}\) kills bacteria by a direct or an indirect contact mechanism. Thanks to the electrostatic contact, the positively charged CeO\({}_{2}\) is efficiently adhered onto the bacterial cell. In a direct mechanism, CeO\({}_{2}\) is directly deposited on the bacterial cell, causing damage to the outer cell wall and the formation of intracellular ROS. This contact renders the cellular proteins inert, allowing CeO\({}_{2}\) to enter the bacterial cell and inactivate the enzymes that cause the production of hydrogen peroxide. The resulting intracellular ROS damage to DNA, RNA, and protein eventually led to bacterial cell death [35]. Additionally, the reduction of CeO\({}_{2}\) from Ce\({}^{4+}\) to Ce\({}^{3+}\) on the cell surface following oxidation and adsorption of the bacterial wall induces oxidative stress [36]. In indirect contact, CeO\({}_{2}\) interacts most of the time with polysaccharide encapsulated bacteria whereas nanoparticles do not directly contact the cell wall. They react with the space around the bacteria and the resulting products cause more bacterial cell damage. Thus, in this contact, ROS are produced extracellularly and enter through the membrane to harm the bacterial cells by destroying nucleic acids and protein, eventually resulting in cell death [37]. The effectiveness of an antibacterial agent also depends on the CeO\({}_{2}\) nanoparticle concentration. Additionally, when CeO\({}_{2}\) nanoparticles are introduced to _E. coli_ bacterial cells, they are immediately taken up by the bacteria, resulting in oxidative stress and bacterial cell death [38]. Although, in general, ROS generation has been correlated with antibacterial properties [39], in some pathogens, ROS can exert opposite results by contributing to increased pathogen burden [40].