Browsing by Subject "dental plaque"

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    Effect of titanium dioxide on Streptococcus mutans biofilm
    (Sage, 2023) Sanders, Molly K.; Duarte, Simone; Ayoub, Hadeel M.; Scully, Allison C.; Vinson, LaQuia A.; Gregory, Richard L.; Pediatric Dentistry, School of Dentistry
    Background: Streptococcus mutans (S. mutans) participates in the dental caries process. Titanium dioxide (TiO2) nanoparticles produce reactive oxygen species capable of disrupting bacterial DNA synthesis by creating pores in cell walls and membranes. Objective: The objective of this study was to determine the effect of TiO2 on the disruption of S. mutans biofilm. Methods: This study was conducted in four phases involving a TiO2-containing toothbrush and TiO2 nanoparticles. Each phase was completed using 24 h established S. mutans biofilm growth. Phase one data was collected through a bacterial plating study, assessing biofilm viability. Biofilm mass was evaluated in phase two of the study by measuring S. mutans biofilm grown on microtiter plates following crystal violet staining. The third phase of the study involved a generalized oxygen radical assay to determine the relative amount of oxygen radicals released intracellularly. Phase four of the study included the measurement of insoluble glucan/extracellular polysaccharide (EPS) synthesis using a phenol-sulfuric acid assay. Results: Both exposure time and time intervals had a significant effect on bacterial viability counts (p = 0.0323 and p = 0.0014, respectively). Bacterial counts after 6 min of exposure were significantly lower than after 2 min (p = 0.034), compared to the no treatment control (p = 0.0056). As exposure time increased, the amount of remaining biofilm mass was statistically lower than the no treatment control. Exposure time had a significant effect on oxygen radical production. Both the 30 and 100 nm TiO2 nanoparticles had a significant effect on bacterial mass. The silver nanoparticles and the 30 and 100 nm TiO2 nanoparticles significantly inhibited EPS production. Conclusion: The TiO2-containing toothbrush kills, disrupts, and produces oxygen radicals that disrupt established S. mutans biofilm. TiO2 and silver nanoparticles inhibit EPS production and reduce biofilm mass. The addition of TiO2 to dental products may be effective in reducing cariogenic dental biofilm.
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    Nicotine-Treated Fusobacterium nucleatum Binding to Collagen, Fibrinogen, and Fibronectin
    (Office of the Vice Chancellor for Research, 2016-04-08) Beshay, Y.S.; Gregory, R.L.
    Fusobacterium nucleatum, a gram-negative anaerobic bacterium found in dental plaque, causes periodontal diseases. Smoking is one of the risk factors that can increase periodontal problems and atherosclerosis. Atherosclerosis is initiated by oral bacteria (i.e., F. nucleatum) binding to surface proteins of endothelial cells, such as collagen, fibrinogen, and fibronectin. The main objective for this study was to test the binding of F. nucleatum to collagen, fibrinogen, and fibronectin under the effect of different concentrations of nicotine. F. nucleatum was grown overnight in brain-heart infusion (BHI) supplemented with yeast extract and 5% vitamin-K/hemin. Biofilm was grown for 48 hours in 0, 0.25, 0.5, 1, and 2 mg/mL of nicotine. Then, the biofilm cells were labeled with biotin 3-sulfo-N-hydroxy-succinimide ester sodium salt and fixed with 10% formaldehyde. A binding assay was conducted by coating a high-binding 96-well microtiter plate with 1 μg/mL of collagen, fibrinogen, or fibronectin. The plate was incubated overnight and blocked with 1% Bovine Serum Albumin (BSA), followed by the biotinylated and nicotine-treated F. nucleatum cells. ExtrAvidin-Peroxidase and OPD Peroxidase Substrate was used to visualize the binding. Optical density (OD) was measured with a spectrophotometer at 490 nm. Collagen, fibrinogen, and fibronectin binding assays demonstrated significantly higher absorbance with 2 mg/mL nicotine-treated F. nucleatum cells compared to untreated cells. The results indicated that an increase in nicotine concentration leads to an increase in F. nucleatum binding to collagen, fibrinogen, and fibronectin. This means that smokers may have an increased risk for atherosclerosis. Supported by Life-Health and Sciences Internship (LHSI).