Nanoceria's unique redox characteristic may shield different tissues and organs from biological harm generated by various free radicals or reactive oxygen species (ROS) [5]. Superoxide radicals are common in mammalian cells, however, if their quantity rises, it can further cause several illnesses. Superoxide radical production is typically regulated by the SOD (superoxide dismutase), which finally eliminates the plethora of radicals. Ceria nanoparticles have the ability to mimic the regulation mechanism of SOD, switching between the two oxidation states of +3 and +4 and specifically when the +3/+4 ratio is high [16]. In terms of radical scavenging, the reaction between nanoceria and H\({}_{2}\)O\({}_{2}\) can have significant ramifications. This process comprises a catalase-like reaction between H\({}_{2}\)O\({}_{2}\) and Ce\({}^{4+}\), which reduces Ce\({}^{4+}\) to Ce\({}^{3+}\) while simultaneously oxidizing H\({}_{2}\)O\({}_{2}\) to molecular O\({}_{2}\), showing the catalase-mimetic activity of ceria. A low Ce\({}^{3+}\)/Ce\({}^{4+}\) ratio consequently favors this process [17]. Nanoceria may have an additional, fundamental antioxidant effect as a result of the interactions with superoxide and hydrogen peroxide, which might make it extremely desirable as a biological ROS scavenger. Combining the catalase- and SOD-mimetic activity of nanoceria may result in the display of a biorelated process for nanoceria regeneration [17]. Dental primers/adhesives, resin composite restorative materials, enamel-dentin adhesives, and other compounds with similar chemical compositions make up clinical restorative polymers [18]. Many studies have demonstrated that resin-based restorative materials encourage the development of cariogenic biofilms. Products of dental monomers' decomposition, such as bisphenol A-glycidyl dimethacrylate (BisGMA) and triethylene glycol dimethacrylate (TEGMA), which may alter the metabolic activity of caries-correlated bacteria like _Streptococcus mutans_ and increase their multiplication, are responsible for the formation of cariogenic biofilm [19]. Any tooth surface which is frequently exposed to sugar is destroyed by the succeeding cariogenic biofilm [20]. As a result, it affects the development of caries and causes caries around restorations (CARS) at the junction of the restoration and the prepared cavity. CARS is one major factor contributing to the failure of resin composite restorations. Thus, it is imperative to effectively manage the development of CARS in order to increase the success rate of composite resins [21; 22]. In a recent study, [PERSON] et al. reported that incorporating 3 wt.% of CeO\({}_{2}\) NPs into dental composite resulted in \(>\)99% potency against _Streptococcus mutans_, _Streptococcus mitis_, _Streptococcus aureus_, and _Lactobacillus_ spp. [20]  
In another area of the dental field, infection and inflammation, which suppress healing and soft tissue integration, are often linked to dental implant therapy failures [23]. After being surgically placed into the jawbone, dental implants undergo a process known as osseointegration that causes them to become biologically unified [24]. Preventing implant failures is one of the primary goals of surface modification for Ti-based implants [25]. Synthesizing a biocompatible material that has antibacterial properties increases the ratio of implant success [26]. New biomaterials for biomedical applications (dental implants) should satisfy ISO-10993 requirements to ensure that they are safe and homcompatible (ASTM-F756). The optimum innovative dental implant materials should have a variety of biological potentials under stress, including anti-inflammatory, antioxidative, angiogenic, and osteogenic properties [26; 27; 28]. In fact, it has been shown that cerium oxide nanoparticles behave favorably when they are in contact with erythrocytes. They work as potent antioxidants that dramatically improve damaged red blood cells caused by in vitro hyperthermia (anemia model) by reducing ROS production [29].