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.
Objective: To examine the risk of developing benign or malignant colorectal tumors in patients with periodontitis within 15 years using Taiwan’s National Health Insurance Database.
Background: Studies have shown that colorectal carcinoma often develops under inflammatory conditions and changes of microbiota in the gut. Recently, a link between Fusobacterium nucleatum, a periodontal pathogen, and colorectal carcinoma has been proposed. However, whether periodontitis is a risk of developing colorectal tumor remains uncertain.
Methods: In total, 35 124 participants were enrolled from 2000 to 2015 to examine the development risk of benign colorectal tumors, including 11 708 patients with periodontitis who received therapy (group 1), 11 708 patients with periodontitis not receiving periodontal treatment (group 2), and 11 708 non-periodontitis controls after matching for gender, age, and index year. To examine the risk of developing colorectal malignancy, 11 720 participants were assigned to each of the three groups. Cox proportional hazards model and Kaplan-Meier methods were used to compare the risks. Sensitivity analysis was performed, excluding the diagnoses during the first 1 or 5 years.
Results: After the follow-up, 177, 154, and 63 participants in group 1, group 2, and control group had benign colorectal tumors. Patients with periodontitis tended to be associated with a greater rate of having a benign colorectal tumor. The adjusted hazard ratios (aHRs) were 3.77 (95% confidence interval [CI] 2.01-4.82, p < .001) and 2.85 (95% CI 1.62-3.74, p < .001) for groups 1 and 2, respectively. Regarding the risk of malignant colorectal tumor, 20, 18, and 14 participants who developed malignant tumors were included in group 1, group 2, and control group; however, no significant increase in malignancy was observed in periodontitis groups (aHR1.92, 95% CI 0.74-2.36, p = .482; aHR 1.50, 95% CI 0.68-1.97, p = .529, for the two periodontitis groups, respectively).
Conclusions: The results of this study suggest that patients with periodontitis may have an increased risk of developing benign, but not malignant, colorectal tumors.
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.
This study concerns effects on water-borne lead from combinations of chlorine (CL) or chloramines (CA) with fluosilicic acid (FSA) or sodium fluoride (NaF). CL is known to corrode brass, releasing lead from plumbing devices. It is known that CA and CL in different ratios with ammonia (NH) mobilize copper from brass, which we have found also enhances elution of lead from leaded brass alloys. Phase I involved leaded-brass 1/4 in. elbows pre-conditioned in DI water and soaked in static solutions containing various combinations of CL, CA, FSA, NaF, and ammonium fluosilicate. In Phase II 20 leaded-brass alloy water meters were installed in pipe loops. After pre-conditioning the meters with 200 flushings with 1.0 ppm CL water, seven different solutions were pumped for a period of 6 weeks. Water samples were taken for lead analysis three times per week after a 16-h stagnation period. In the static testing with brass elbows, exposure to the waters with CA+50% excess NH3+FSA, with CA and ammonium fluosilicate, and with CA+FSA resulted in the highest estimated lead concentrations. In the flow-through brass meter tests, waters with CL+FSA, with CL+NaF, and with CL alone produced the highest average lead concentration for the first 3-week period. Over the last 3 weeks the highest lead concentrations were produced by CL+NaF, followed by CL alone and CA+NH3+FSA. Over the first test week (after CL flushing concentrations were increased from 1.0 to 2.0 ppm) lead concentrations nearly doubled (from about 100 to nearly 200 ppb), but when FSA was also included, lead concentrations spiked to over 900 ppb. Lead concentrations from the CL-based waters appeared to be decreasing over the study period, while for the CA+NH3+FSA combination, lead concentrations seemed to be increasing with time.
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.
Abstract
Objective
For more than 150 years, dental amalgam fillings (50% metallic mercury (Hg0) by weight) have been used in American dentistry. The US Food and Drug Administration (FDA) acknowledged that amalgams release Hg vapor that may be harmful to certain patients. This study examined the impact of Hg vapor exposure from amalgams in American adults.
Methods
Amalgam-Hg vapor exposure among 158,274,824 weighted-adult Americans was examined in the 2015–2018 National Health and Nutrition Examination Survey (NHANES). Beta (β)-coefficients were calculated for the correlation between the number of amalgam surfaces and daily micrograms (μg) of urinary Hg and daily μg of Hg vapor exposure from amalgams per kilogram (Kg) bodyweight.
Results
About 91 million (57.8%) adults had ≥1 amalgam surface and about 67 million (42.2%) had no amalgams. A β-coefficient = 0.041 significantly correlated the number of amalgam surfaces to daily amounts of urinary Hg. Differences were observed for gender and racial groups. Daily Hg vapor doses from amalgams were in excess of the most restrictive California’s Environmental Protection Agency (EPA) safety limit for about 86 million (54.3%) adults and in excess of the least restrictive US EPA safety limit among about 16 million (10.4%) adults. The mean allowable number of amalgam surfaces ranged from 1.28 for adult females under the California’s EPA safety limit to 16.23 for adult males under the US EPA safety limit.
Conclusion
Given that American adults are receiving significant, ongoing exposure to Hg vapor from amalgams, careful evaluation of the need to reduce use of amalgams should be considered.
The oral cavity is composed of about 300 million species of bacteria that occupy various ecological niches
Titanium is not only used in dental implants, but also in many dental materials and has shown to be toxic. Nickel braces, are often called “stainless steel”, as are nickel crowns. Nickel has been deemed to be carcinogenic, according to the National Toxicology Program, Department of Health and Human Services. When oral galvanism occurs, particles are released from the oral cavity and can translocate to other areas in the body, causing
potential toxicity and biological hazards