Even though fluoride toothpaste may be diluted by saliva, the results of the present study indicate that use of 5000 ppm fluoride toothpaste might lead to improved caries control.
The aim was to measure and compare fluoride concentrations in oral mucosa and saliva following a single brushing with either 1,450 or 5,000 ppm fluoride toothpaste. Fourteen healthy participants provided saliva and oral mucosa samples in the morning before tooth brushing. Then participants brushed their teeth with 1,450 ppm fluoride toothpaste, and saliva and mucosa samples were collected after 1, 2, 4, and 6 h. The experiment was repeated 3–7 days later with 5,000 ppm fluoride toothpaste. All samples were analyzed for fluoride using an ion-selective electrode adapted for microanalysis. Pre-brushing fluoride concentrations were higher in mucosa (mean1,450 0.26 ppm and mean5,000 0.20 ppm) than in saliva (mean1,450 0.08 ppm and mean5,000 0.07 ppm). The mean fluoride concentrations increased in both mucosa and saliva following a single brushing with both 1,450 ppm (meanmuc1,450 (1 h) 1.15 ppm, meansal1,450 (1 h) 0.33 ppm) and 5,000 ppm fluoride toothpaste (meanmuc5,000 (1 h) 3.21 ppm and meansal5,000 (1 h) 0.90 ppm). At 6 h, the fluoride concentrations had returned to pre-brushing levels. Across the 6-h sampling period the fluoride concentration in saliva was statistically significantly 1.4 times higher following brushing with 5,000 ppm compared with 1,450 ppm fluoride toothpaste. For mucosa, this ratio was only 1.1 and not statistically significant. In conclusion, the fluoride level in oral buccal mucosa is higher than in saliva and follows the same fluoride clearance pattern as in saliva. Over the initial 6-h period following a single tooth brushing, the ratio of the fluoride concentration in mucosa to that in saliva is independent of the fluoride concentrations in the toothpastes used.
Angiogenesis, the formation of new blood vessels from existing vessels is required for many physiological processes and for growth of solid tumors. Initiated by hypoxia, angiogenesis involves binding of angiogenic factors to endothelial cell (EC) receptors and activation of cellular signaling, differentiation, migration, proliferation, interconnection and canalization of ECs, remodeling of the extracellular matrix and stabilization of newly formed vessels. Experimentally, these processes can be studied by several in vitro and in vivo assays focusing on different steps in the process. In vitro, ECs form networks of capillary-like tubes when propagated for three days in coculture with fibroblasts. The tube formation is dependent on vascular endothelial growth factor (VEGF) and omission of VEGF from the culture medium results in the formation of clusters of undifferentiated ECs. Addition of angiogenesis inhibitors to the coculture system disrupts endothelial network formation and influences EC morphology in two distinct ways. Treatment with antibodies to VEGF, soluble VEGF receptor, the VEGF receptor tyrosine kinase inhibitor SU5614, protein tyrosine phosphatase inhibitor (PTPI) IV or levamisole results in the formation of EC clusters of variable size. This cluster morphology is a result of inhibited EC differentiation and levamisole can be inferred to influence and block VEGF signaling. Treatment with platelet factor 4, thrombospondin, rapamycin, suramin, TNP-470, salubrinal, PTPI I, PTPI II, clodronate, NSC87877 or non-steriodal anti-inflammatory drugs (NSAIDs) results in the formation of short cords of ECs, which suggests that these inhibitors have an influence on later steps in the angiogenic process, such as EC proliferation and migration. A humanized antibody to VEGF is one of a few angiogenesis inhibitors used clinically for treatment of cancer. Levamisole is approved for clinical treatment of cancer and is interesting with respect to anti-angiogenic activity in vivo since it inhibits ECs in vitro with a morphology resembling that obtained with antibodies to VEGF.
Information on differences in biofilm fluoride concentration across intra-oral regions may help explain the distribution of caries within the dentition. The aim of this cross-sectional study was to describe the fluoride concentration in saliva and in biofilm fluid and biofilm solids across 6 intra-oral regions. Unstimulated whole saliva was collected from 42 participants and biofilm harvested from the buccal sites in the 4 molar and 2 anterior regions. Samples were collected at least 1 h after use of fluoride dentifrice. No attempt was made to control the participants' food consumption or use of other topical agents. Centrifuged saliva, biofilm fluid, and biofilm solids were analysed for fluoride using a fluoride ion-selective electrode, adapted for microanalysis. Fluoride in biofilm varied across intra-oral regions. The mean biofilm fluid fluoride concentrations across the oral cavity ranged from 11.6 to 16.8 µ
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