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This case highlights the problem of the deceptive reassurance that radiographs appear to provide in relation to the fact that there is possible release of Ti particles in the peri-implant environment.

E-cigarettes (e-cigs) have drastically increased in popularity during the last decade, especially among teenagers. While recent studies have started to explore the effect of e-cigs in the oral cavity, little is known about their effects on the oral microbiota and how they could affect oral health and potentially lead to disease, including periodontitis and head and neck cancers. To explore the impact of e-cigs on oral bacteria, we selected members of the genus Streptococcus, which are abundant in the oral cavity. We exposed the commensals Streptococcus sanguinis and Streptococcus gordonii and the opportunistic pathogen Streptococcus mutans, best known for causing dental caries, to e-liquids and e-cig aerosols with and without nicotine and with and without menthol flavoring and measured changes in growth patterns and biofilm formation. Our results demonstrate that e-cig aerosols hindered the growth of S. sanguinis and S. gordonii, while they did not affect the growth of S. mutans. We also show that e-cig aerosols significantly increased biofilm formation by S. mutans but did not affect the biofilm formation of the two commensals. We found that S. mutans exhibits higher hydrophobicity and coaggregation abilities along with higher attachment to OKF6 cells than S. sanguinis and S. gordonii. Therefore, our data suggest that e-cig aerosols have the potential to dysregulate oral bacterial homeostasis by suppressing the growth of commensals while enhancing the biofilm formation of the opportunistic pathogen S. mutans. This study highlights the importance of understanding the consequences of e-cig aerosol exposure on selected commensals and pathogenic species. Future studies modeling more complex communities will provide more insight into how e-cig aerosols and vaping affect the oral microbiota. IMPORTANCE Our study shows that e-cigarette aerosol exposure of selected bacteria known to be residents of the oral cavity hinders the growth of two streptococcal commensals while enhancing biofilm formation, hydrophobicity, and attachment for the pathogen S. mutans. These results indicate that e-cigarette vaping could open a niche for opportunistic bacteria such as S. mutans to colonize the oral cavity and affect oral health.

Porphyromonas gingivalis, a keystone periodontal pathogen, has emerged as a risk factor for systemic chronic diseases, including non-alcoholic fatty liver disease (NAFLD). To clarify the mechanism by which this pathogen induces such diseases, we simultaneously analyzed the transcriptome of intracellular P. gingivalis and infected host cells via dual RNA sequencing. Pathway analysis was also performed to determine the differentially expressed genes in the infected cells. Further, the infection-induced notable expression of P. gingivalis livk and livh genes, which participate in branched-chain amino acid (BCAA) transfer, was also analyzed. Furthermore, given that the results of recent studies have associated NAFLD progression with elevated serum BCAA levels, which reportedly, are upregulated by P. gingivalis, we hypothesized that this pathogen may induce increases in serum BCAA levels and exacerbate liver injury via livh/livk. To verify this hypothesis, we constructed P. gingivalis livh/livk-deficient strains (Δlivk, Δlivh) and established a high-fat diet (HFD)-fed murine model infected with P. gingivalis. Thereafter, the kinetic growth and exopolysaccharide (EPS) production rates as well as the invasion efficiency and in vivo colonization of the mutant strains were compared with those of the parental strain. The serum BCAA and fasting glucose levels of the mice infected with either the wild-type or mutant strains, as well as their liver function were also further investigated. It was observed that P. gingivalis infection enhanced serum BCAA levels and aggravated liver injury in the HFD-fed mice. Additionally, livh deletion had no effect on bacterial growth, EPS production, invasion efficiency, and in vivo colonization, whereas the Δlivk strain showed a slight decrease in invasion efficiency and in vivo colonization. More importantly, however, both the Δlivk and Δlivh strains showed impaired ability to upregulate serum BCAA levels or exacerbate liver injury in HFD-fed mice. Overall, these results suggested that P. gingivalis possibly aggravates NAFLD progression in HFD-fed mice by increasing serum BCAA levels, and this effect showed dependency on the bacterial BCAA transport system.

This study investigated the bleaching effectiveness and the physicochemical effects on enamel of violet light and ozone, associate or not to hydrogen peroxide, compared to 35%-hydrogen peroxide. Enamel-dentin blocks from human molars were randomly allocated to receive one of the following bleaching protocols (n=15): (HP) 35%-hydrogen peroxide, (VL) violet light, (OZ) ozone, the association between hydrogen peroxide with ozone (OZ+HP) or violet light (VL+HP). All protocols were performed in two sessions with a 48h interval. Color (spectrophotometer) and mineral composition (Raman spectroscopy) were measured before and after the bleaching. Color changes were calculated by ΔEab, ΔE00, and whitening index (WI). The surface roughness was measured with an atomic force microscope. Data were analyzed by One-way or Two-way repeated measure ANOVA followed by the Tukey’s test (α = 0.05). The lowest color change values (either measured by WI, ΔEab, or ΔE00) were observed for VL and OZ used with no HP. Violet light associate with HP was unable to improve the color changes observed for the peroxide alone, in combination with OZ and HP, the highest color changes were verified. Regardless of bleaching protocol, the bleached enamel presented higher contents of PO4 and CO3 -2 than those observed at baseline. All bleaching protocols resulted in similar enamel surface roughness. Both the VL and the OZ caused reduced effects on the enamel color change when used alone. The ozone therapy improved the bleaching effect in the group that received the association of HP.

Aim

Vitamin D3 plays an important role in affecting the overall remineralization process of the dentition. The use of supplements help to keep the levels at optimum and thus reduce the chances of treating very early lesion of caries. Hence the aim was to investigate the indirect effects of oral vitamin D3 on microhardness and elemental weight percentage of Calcium (Ca) and Phosphorous (P) in enamel surface with an artificially initiated carious lesion.

Methods

The 120 extracted premolars were randomly divided into five groups according to salivary immersion. Each group had a total of twenty-four participants, with the following characteristics: control +ve: sound enamel; control -ve: only subjected to pH cycle; A: pH cycle and immersion in control saliva; B: pH cycle and saliva collected after three weeks; and C: pH cycle and saliva collected after six weeks. The unstimulated saliva was collected from (40) adult volunteers receiving vitamin D3 1000IU gel capsules daily for six weeks. Before each vitamin D3 intake, 10 mL of unstimulated control saliva was collected from each participant. Then other 10 ml. were collected after three and six weeks of vitamin D receiving periods. Saliva immersion time (12 hours). Enamel surface was assessed by Vicker’s Microhardness machine and (X-ray fluorescence – XRF) spectrometer.

Results

For all specimens, there was a significant decrease in both (Ca and P weight %) after demineralization and then they significantly increased after receiving vitamin D3. The microhardness and elemental analysis provide confirmed results that were represented as a statistically significant difference at (P≤ 0.05) between groups that received vitamin D3 and those without vitamin D3 dosage.

Conclusions

Oral vitamin D3 has a significant potential in motivating remineralization of early lesions on the enamel surfaces representing improved surface microhardness and minerals content (Ca and P weight %) of demineralized tooth surfaces.