Browsing by Subject "plaque"

Now showing 1 - 3 of 3
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    Enhancing predicted fluoride varnish efficacy and post-treatment compliance by means of calcium-containing gummy bears
    (Elsevier, 2018) Lippert, Frank; Al Dehailan, Laila; Castiblanco, Gina A.; Tagelsir, Azza; Buckley, Christine; Eckert, George J.; Cariology, Operative Dentistry and Dental Public Health, School of Dentistry
    Objectives This study determined whether consumption of calcium-containing gummies prior to fluoride varnish application enhances plaque fluoride retention and compliance with post-varnish application instructions. Methods The present study followed a multi-center, parallel, randomized, and laboratory analyst-blind design. Following IRB approval, parent consent and child assent, 44 subjects (7–12 years), were randomized to either gummy or no-gummy study groups. A baseline plaque sample was obtained after a wash-out period. Fluoride varnish (5% NaF) was applied; subjects in the gummy group received two calcium-containing gummies prior to varnish application. Subjects were given two questionnaires to complete (subject and parent) to investigate adherence to post-treatment instructions. Three days later, a second plaque sample was obtained. Plaque was analyzed for plaque fluid and solid fluoride concentrations. Fluoride data were analyzed using Wilcoxon Rank Sum tests, questionnaire data using Pearson chi-square tests. Results Plaque fluid fluoride did not change pre- to post-treatment in the gummy group (mean ± sd: 8.8 ± 5.7 μmol/l vs. 10.0 ± 6.3 μmol/l; p = 0.265) or in the no-gummy group (8.1 ± 4.4 μmol/l vs. 16.1 ± 20.0 μmol/l; p = 0.058). Groups were not different for plaque fluid fluoride pre-treatment (p = 1.000), post-treatment (p = 0.904), or change (p = 0.904). Plaque solid fluoride did not change pre- to post-treatment in the gummy group (0.89 ± 1.10 μmol/g vs. 1.37 ± 1.77 μmol/g; p = 0.073) or in the no-gummy group (0.68 ± 0.77 μmol/g vs. 2.01 ± 5.00 μmol/g; p = 0.190). Groups were not different for plaque solid fluoride pre-treatment (p = 1.000), post-treatment (p = 0.466), or change (p = 0.874). No significant differences were found between groups for questionnaire responses. Conclusion This study failed to demonstrate an effect of calcium-containing gummies in enhancing plaque fluoride retention.
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    Nicotine Kill Time of Streptococcus Mutans
    (Office of the Vice Chancellor for Research, 2015-04-17) Cavazos, Ana; Gregory, Richard L.
    Cigarettes have thousands of components aside from tobacco and nicotine that are harmful to the smoker’s body. Smoking is considered a significant risk factor for cardiovascular disease (CVD) and periodontal disease. Yet smoking also plays a significant role in the buildup of plaque in the mouths of smokers. This is in part due to the formation of biofilm by Streptococcus mutans. S. mutans is an oral bacterium found in most humans that is considered to be the causative agent for dental caries. Particularly, S. mutans UA159 was used in this experiment. Biofilm formation regarding S. mutans and nicotine concentrations has previously been studied. It was found that at high concentrations of nicotine, biofilm formation of S. mutans decreased significantly. One of the aims of this study is to determine the time required to kill S. mutans.
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    Streptococcus mutans Binding to Collagen and Fibrinogen in Nicotine
    (Office of the Vice Chancellor for Research, 2015-04-17) Kristoff, Sylvie N.; Gomez, Grace; Gregory, Richard L.
    Introduction: Our overall goal is to find the mechanism for atherosclerosis. Smokers have increased incidence of atherosclerosis. Atherosclerosis occurs when there is a build up of plaque in the arteries. There is evidence that Streptococcus mutans help cause this blockage. We have already proven that S. mutans produces more biofilm in certain concentrations of nicotine. Also, we have found that nicotine upregulates S. mutans binding to proteins in certain concentrations; other labs have also demonstrated this. The intent of this study was to evaluate the binding of S. mutans to both collagen type I and fibrinogen, which are both proteins that are already present on the surface of endothelial cells lining arteries. Methods: S. mutans UA159 was cultured in 0.00-4.00 mg/mL nicotine. The cells were killed in formaldehyde and then coated with biotin. The proteins studied were plated (1 ug/ml) on 96-well microtiter plates. In order to block the empty spaces that the protein did not bind to, 1% BSA in sodium bicarbonate buffer was added to the plate. Each nicotine dilution of S. mutans was added to the plate and the amount of binding was assessed. Extra-avidin HRP and OPD were added to the plate and the intensity was measured at an absorbance of 490 nm using a spectrophotometer. Results: The intensity was directly related to the number of cells bound to the proteins. There was a significant increase in S. mutans binding when compared to the baseline for both collagen type I and fibrinogen. The binding was highest when S. mutans were cultured in 2 and 4 mg/mL nicotine. Conclusions: The data collected suggests that collagen type I and fibrinogen contribute to the mechanism of atherosclerosis. When S. mutans are cultured in moderately high concentrations of nicotine, more binding of the bacteria to these proteins occurs.