ObjectiveThis in situ study compared the effectiveness of two toothpastes containing hydroxyapatite or 500 ppm fluoride in promoting remineralization and inhibiting caries development.Materials and methodsTwo enamel blocks (human primary teeth), one sound and one with artificially-produced caries lesion, were exposed to toothpaste containing either 10% hydroxyapatite or 500 ppm F− (amine fluoride) via intra-oral appliance worn by 30 adults in two-arm double blind randomized crossover study lasting 14 days per arm (ClinicalTrials.gov: NCT03681340). Baseline and post-test mineral loss and lesion depth (LD) were quantified using microradiography. One-sided t-test of one group mean was used for intragroup comparison (baseline vs. post-test), while two-sided t-test of two independent means was used to compare the two toothpaste groups.ResultsPairwise comparison (baseline vs. test) indicated significant (p < 0.0001) remineralization and LD reduction by either toothpaste; however, when compared against each other, there was no statistically significant difference in remineralization or LD reduction between the two toothpastes. No demineralization could be observed in sound enamel blocks exposed to either toothpaste. While F− induced lesion surface lamination, HAP produced a more homogenous lesion remineralization.Conclusions10% hydroxyapatite achieved comparable efficacy with 500 ppm F− in remineralizing initial caries and preventing demineralization. Thus the HAP toothpaste is confirmed to be equal to the fluoride toothpaste in this study.
The present in vitro study investigated if simulated daily use of hydroxyapatite-based gel (15% HAP) remineralizes early caries lesions as effective as weekly use of high fluoride (12,500 ppm) concentration gel, comparing them with artificial saliva alone. MATERIALS AND METHODS: Three tooth blocks were produced from each of 20 bovine teeth. Caries-like lesion was created on each block by 4-day demineralization in acidified gel. The blocks were randomized into three remineralization groups (20 blocks/ group); Hydroxyapatite-based gel (Karex gelée, 15% HAP, fluoride-free), fluoride-based gel (Elmex gelée, 12,500 ppm F −), and artificial saliva (AS). Remineralization was conducted using pH-cycling model for 28 days with storage in AS. The pH cycling model consisted of 2 h demineralization once daily for all groups, and 3 min HAP gel application once daily, 3 min fluoride gel application once weekly, or remain in AS only respectively. Baseline and post-test mineral loss were quantified using microradiography. RESULTS: Paired t-tests (baseline vs. post-Test) indicated significant (p < 0.0001) remineralization in all groups. When compared against each other using Games-Howell's multiple comparison test, no significant difference in remineralization was observed between the two gels, but both gels exhibited significantly (p < 0.001) higher percentage mineral gain (HAP:39 ± 7%; fluoride:41 ± 11%) than AS alone (6 ± 2%). CONCLUSION: Hydroxyapatite-based gel (15% HAP) was as effective as fluoride-based gel (12,500 ppm F −) in remineralizing initial caries lesion.
Objectives:Using an established pH-cycling caries model, the authors evaluated the effectiveness of toothpastes containing Surface Pre-reacted Glass-ionomer filler (S-PRG) in preventing tooth surface demineralization.Materials and Methods:210 tooth blocks were randomly assigned to seven experimental groups (30 blocks/group): no treatment (A), and toothpaste containing either NaF (B), 0 wt% S-PRG (C), 1 wt% S-PRG (D), 5 wt% S-PRG (E), 20 wt% S-PRG (F) or 30 wt% S-PRG (G). Groups were subjected to 14-day demineralization for development of early caries lesions using a pH-cycling caries model. Demineralization was assessed using Quantitative Light-induced Fluorescence (QLF) and Transverse Microradiography (TMR). All pairwise contrasts (between treatments) were tested using Analysis of Variance (ANOVA), and then Tukey’s HSD for multiple comparisons. All p-values are considered significant if <0.05.Results:With QLF, there was a significant (ANOVA; p<0.001) difference in mean percent fluorescence loss (∆F) observed among the groups. Relative to control, all S-PRG-containing toothpastes significantly (Tukey’s; p<0.0001) inhibited demineralization at varying percentages (48.6%, 61.3%, 67.4% and 69.8% reduction with S-PRG 1%, 5%, 20% and 30% respectively). Demineralization reduction was not significant with either NaF (15.6% reduction) or 0% S-PRG (-2.5% reduction i.e. 2.5% more demineralization than the Control) when compared to control group. Mineral loss assessed using TMR followed a similar trend as fluorescence loss.Conclusion:Toothpaste containing S-PRG filler can serve as an effective caries control tool. S-PRG filler-containing dentifrice to be more effective in preventing tooth demineralization than 1100 ppm fluoride provided as sodium fluoride.
Background Current treatments for salivary gland (SG) hypofunction are palliative and do not address the underlying cause or progression of the disease. SG-derived stem cells have the potential to treat SG hypofunction, but their isolation is challenging, especially when the tissue has been damaged by disease or irradiation for head and neck cancer. In the current study, we test the hypothesis that multipotent bone marrow-derived mesenchymal stem cells (BM-MSCs) in a rat model are capable of trans-differentiating to the SG epithelial cell lineage when induced by a native SG-specific extracellular matrix (SG-ECM) and thus may be a viable substitute for repairing damaged SGs. Methods Rat BM-MSCs were treated with homogenates of decellularized rat SG-ECM for one hour in cell suspension and then cultured in tissue culture plates for 7 days in growth media. By day 7, the cultures contained cell aggregates and a cell monolayer. The cell aggregates were hand-selected under a dissecting microscope, transferred to a new tissue culture dish, and cultured for an additional 7 days in epithelial cell differentiation media. Cell aggregates and cells isolated from the monolayer were evaluated for expression of SG progenitor and epithelial cell specific markers, cell morphology and ultrastructure, and ability to form SG-like organoids in vivo. Results The results showed that this approach was very effective and guided the trans-differentiation of a subpopulation of CD133-positive BM-MSCs to the SG epithelial cell lineage. These cells expressed amylase, tight junction proteins (Cldn 3 and 10), and markers for SG acinar (Aqp5 and Mist 1) and ductal (Krt 14) cells at both the transcript and protein levels, produced intracellular secretory granules which were morphologically identical to those found in submandibular gland, and formed SG-like organoids when implanted in the renal capsule in vivo. Conclusions The results of this study suggest the feasibility of using autologous BM-MSCs as an abundant source of stem cells for treating SG hypofunction and restoring the production of saliva in these patients.
Nonalcoholic fatty liver disease (NAFLD) is a spectrum of disorders ranging from hepatic steatosis (excessive accumulation of triglycerides [TG]) to nonalcoholic steatohepatitis, which can progress to cirrhosis and hepatocellular carcinoma. The molecular pathogenesis of steatosis and progression to more severe NAFLD remains unclear. Obesity and aging, two principal risk factors for NAFLD, are associated with a hyperadrenergic state. β-Adrenergic responsiveness in liver increases in animal models of obesity and aging, and in both is linked to increased hepatic expression of β2-adrenergic receptors (β2-ARs). We previously showed that in aging rodents intracellular signaling from elevated hepatic levels of β2-ARs may contribute to liver steatosis. In this study we demonstrate that injection of formoterol, a highly selective β2-AR agonist, to mice acutely results in hepatic TG accumulation. Further, we have sought to define the intrahepatic mechanisms underlying β2-AR mediated steatosis by investigating changes in hepatic expression and cellular localization of enzymes, transcription factors and coactivators involved in processes of lipid accrual and disposition-and also functional aspects thereof-in livers of formoterol treated animals. Our results suggest that β2-AR activation by formoterol leads to increased hepatic TG synthesis and de novo lipogenesis, increased but incomplete β-oxidation of fatty acids with accumulation of potentially toxic long-chain acylcarnitine intermediates, and reduced TG secretion-all previously invoked as contributors to fatty liver disease. Experiments are ongoing to determine whether sustained activation of hepatic β2-AR signaling by formoterol might be utilized to model fatty liver changes occurring in hyperadrenergic states of obesity and aging, and thereby identify novel molecular targets for the prevention or treatment of NAFLD.
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