Protein corona is immediately established on the surface of nanoparticles upon their introduction into biological milieu. Several studies have shown that the targeting efficiency of ligand-modified nanoparticles is attenuated or abolished owing to the protein adsorption. Here, transferrin receptor-targeting ligands, including LT7 (CHAIYPRH), DT7 (hrpyiahc, all d-form amino acids), and transferrin, were used to identify the influence of the ligand size and conformation on protein corona formation. The results showed that the targeting capacity of ligand-modified nanoparticles was lost after incubation with plasma in vitro, whereas it was partially retained after in vivo corona formation. Results from sodium dodecyl sulfate polyacrylamide gel electrophoresis and liquid chromatography-mass spectrometry revealed the difference in the composition of in vitro and in vivo corona, wherein the ligand size and conformation played a critical role. Differences were observed in cellular internalization and exocytosis profiles on the basis of the ligand and corona source.

(1) secondary caries was successfully produced in rats; (2) there was a correlation between the modified Keyes scoring method and micro-CT in the evaluation of the secondary caries; (3) the adhesive containing DMADDM significantly reduced both LD and ML (according to micro-CT), and also lowered the scores (based on the modified Keyes scoring method). This suggests that the novel DMADDM adhesive could perform an anticaries function in vivo via the secondary caries animal model which was also developed and testified in research. Secondary caries is one of the major reasons leading to the failure of caries restoration treatment. As a solution, anticaries adhesives perform well in biofilm inhibition in vitro. However, the lack of secondary caries animal models limits the evaluation of anticaries adhesives in vivo. Secondary caries is one of the main reasons for restoration failure with a heavy economic burden [Sakaguchi, 2005;Kasraei et al., 2017]. While many factors facilitate the development of secondary caries, oral bacteria and acid production are the initiators of dental caries [Mjor Keywords Antibacterial material · Bonding system · Dimethylaminododecyl methacrylate · Keyes animal model · Micro-CT · Tooth restoration AbstractWe investigated the anticaries properties of an adhesive containing dimethylaminododecyl methacrylate (DMADDM) in vivo via a secondary caries animal model. Cavities were prepared in the maxillary first molars of Wistar rats. DMADDM-containing adhesives were applied on one side and commercial adhesives on the opposite side as a control. After a 3-week feeding period to induce secondary caries, the molars were harvested for the evaluation of the secondary caries. Lesion depth (LD) and mineral loss (ML) were measured via a micro-CT method, and a modified Keyes scoring method yielded scores for the caries lesions. Statistical analysis was divided into 2 parts: a correlation analysis between 2 evaluations with one-way ANOVA and a least-significant differences (LSD) test, and an evaluation of anticaries adhesives with a paired samples t test. The results showed that:

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Background/purpose Streptococcus mutans is an important pathogen in the development of dental caries. Many studies have focused on the relationship between nicotine and S. mutans in vitro . The aim of this study was to investigate the effect of nicotine on the growth of S. mutans and its cariogenic potential in vivo . Materials and methods Sixteen male Specific-pathogen-free Wistar rats were divided into 2 groups (nicotine-treated and nicotine-untreated group) and infected with S. mutans . The S. mutans suspension was treated with 1 mg/mL nicotine in the nicotine-treated group. The Keyes method was used to evaluate sulcal caries of rats, and dental plaque on molar teeth was observed by scanning electron microscopy (SEM). Results Incidence of sulcal caries was higher in nicotine-treated group compared to nicotine-untreated group (42.7 ± 1.7 vs 37.3 ± 4.9, P = 0.009). Severity of caries increased with nicotine treatment. The slightly dentinal caries scores and moderate dentinal caries scores were higher in the presence of nicotine (P < 0.001). Increased number of S. mutans cells attached to dental surface was observed under SEM in the nicotine-treated group. Conclusion Nicotine would promote the attachment of S. mutans to dental surface, and further increase the incidence and severity of dental caries. Therefore, nicotine might be a risk factor for smoking-induced caries.