Effect of titanium tetrafluoride and amine fluoride treatment combined with carbon dioxide laser irradiation on enamel and dentin erosion

OBJECTIVE: This in vitro study aimed to analyze the influence of carbon dioxide (CO(2)) laser irradiation on the efficacy of titanium tetrafluoride (TiF(4)) and amine fluoride (AmF) in protecting enamel and dentin against erosion. METHODS: Bovine enamel and dentin samples were pretreated with carbon dioxide (CO(2)) laser irradiation only (group I), TiF(4) only (1% F, group II), CO(2) laser irradiation before (group III) or through (group IV) TiF(4) application, AmF only (1% F, group V), or CO(2) laser irradiation before (group VI) or through (group VII) AmF application. Controls remained untreated. Ten samples of each group were then subjected to an erosive demineralization and remineralization cycling for 5 days. Enamel and dentin loss were measured profilometrically after pretreatment, 4 cycles (1 day), and 20 cycles (5 days) and statistically analyzed using analysis of variance and Scheffe's post hoc tests. Scanning electron microscopy (SEM) analysis was performed in pretreated but not cycled samples (two samples each group). RESULTS: After 20 cycles, there was significantly less enamel loss in groups V and IV and significantly less dentin loss in group V only. All other groups were not significantly different from the controls. Lased surfaces (group I) appeared unchanged in the SEM images, although SEM images of enamel but not of dentin showed that CO(2) laser irradiation affected the formation of fluoride precipitates. CONCLUSION: AmF decreased enamel and dentin erosion, but CO(2) laser irradiation did not improve its efficacy. TiF(4) showed only a limited capacity to prevent erosion, but CO(2) laser irradiation significantly enhanced its ability to reduce enamel erosion

Antibacterial activity of medical-grade manuka honey against oral bacteria in vitro

Manuka honey (MH), derived from manuka shrub Leptospermum scoparium, native to New Zealand and Australia, contains elevated amounts of antimicrobial methylglyoxal1,2. Topical application of MH is effective in the treatment of burn and surgical wound infections3. Our aim was to assess the antibacterial effect of MH against oral microorganisms in order to explore its potential use in periodontal treatment

Dentin Hypersensitivity: Prevalence, Etiology, Pathogenesis, and Management

Dentin hypersensitivity is simply defined as a short sharply painful reaction of the exposed and innervated pulp-dentin complex in response to stimuli being typically thermal, evaporative, tactile, osmotic, or chemical and which reaction cannot be attributed to any dental defect or pathology. To be hypersensitive, dentin must be exposed and the exposed tubules must be open and patent to both the oral cavity and the pulp. Exposure of dentin through the loss of gingival and periodontal tissue may be caused by either too meticulous or by neglected oral hygiene. Exposure of dentin by the loss of the protecting enamel is mainly caused by erosion, abrasion, and abfraction or a combination thereof. Clinical examination for dentin hypersensitivity would include a pain provocation test by a tactile stimulus, an evaporative air stimulus, or a cold stimulus. A number of other dental conditions can give rise to pain symptoms, which may mimic those of dentin hypersensitivity. Therefore, careful examination is necessary to exclude the conditions, which need different treatment options. When the patients do suffer from dentin hypersensitivity, there is broad range of treatment options comprising home-use and professional approaches. It is advised to start with the less invasive home-use therapies and only expand to professional in-office treatments when the home-use treatments are not effective. When decided to continue with in-office treatments, again one should start with the least invasive ones. The working mechanisms fall under two basic categories being nerve desensitization (potassium salts and guanethidine) and occlusion of exposed dental tubules (chemically: strontium, fluoride, stannous, oxalate, calcium phospho silicate, arginine calcium carbonate, nano-hydroxyapatite, and glutaraldehyde; mechanically: pumice paste, glassionomers, dentin bondings, and resins; laser therapy). Regenerative mucogingival therapy also remains an alternative, where hard and soft tissue conditions allow

Protection of sound enamel and artificial enamel lesions against demineralisation: caries infiltrant versus adhesive

OBJECTIVE: To compare the protective potential of a conventional adhesive, a caries infiltrant and a combination of both against acidic challenge in vitro. METHODS: One-hundred-and-fifty discs from bovine lower central incisors were fabricated. Seventy-five samples remained untreated, whereas the other half was subjected to a demineralisation process (14 days, acidic buffer, and pH 5) to create artificial enamel lesions. Specimens were then radioactively irradiated, and each 15 sound and demineralised specimens were treated with a caries infiltrant (Icon, DMG), an unfilled adhesive (Heliobond, IvoclarVivadent) or a combination of infiltrant and adhesive. Specimens treated with the adhesive followed by a flowable composite (TetricEvoFlow, IvoclarVivadent) served as positive control, while untreated specimens served as negative control. All samples were then subjected to lactic acid for 3 weeks at pH 4. Loss of apatite was determined using the radiochemical method of liquid scintillation. Data were statistically analysed by Kruskal-Wallis-test, one-way ANOVA and Scheffe's post hoc tests (p ≤.05). RESULTS: In both sound enamel and artificial caries lesions, untreated specimens showed the highest rate of apatite loss, whereas enamel treated with the adhesive and the flowable composite showed almost complete protection surface against dissolution. The caries infiltrant, the adhesive and the combination of both were able to decrease enamel dissolution, but the adhesive and the combination of adhesive and infiltrant were more effective than the infiltrant alone. CONCLUSION: Within the limitations of this in vitro study, the application of an adhesive (alone or in combination with the caries infiltrant) is more effective to protect enamel dissolution than the infiltrant alone

Effect of short-time povidone-iodine application on osteoblast proliferation and differentiation

BACKGROUND AND OBJECTIVE: Povidone-iodine [polyvinylpyrrolidone-iodine complex (PVP-I)] is a broad-spectrum antimicrobial agent, frequently used in dentistry. In this study we investigated the short- and longterm effects on osteoblast number, viability, and function after short exposure to PVP-I with and without additional bone-morphogenetic protein-2 (BMP-2). MATERIAL AND METHODS: Confluent osteoblast-like cell line (MC3T3-E1, subclone 24) cultures were exposed to pure PVP-I solution (7.7 mg/ml) and dilutions of 1:10, 1:100 and 1:1000 for 10 seconds and washed with phosphate buffer solution. Cell proliferation and viability was determined by MTT and differentiation status by alkaline phosphatase (ALP) activity 6 days after initial plating. In a separate experiment, long-term cell proliferation, viability and function were assessed 4 weeks after PVP-I treatment by MTT and deposited calcium using an Alizarin-red staining test. RESULTS: PVP-I decreased ALP activity substantially. Stimulation by BMP-2 recovered ALP activity to near control levels at 1:100 and 1:1000 dilutions of PVP-I. The MTT assay showed reduced proliferation of the preosteoblastic cells for all treatments, irrespective whether BMP-2 was used or not. Only at PVP-I dilutions of 1:1000 proliferation rate was back to normal levels (95.6+/-2.4 %). No adverse long-term effect of PVP-I on mineralization of the extracellular matrix (Alizarinred) for dilutions higher than 1:100 was observed. Interestingly, undiluted and 1:10 diluted PVP-I even showed a significant increase in mineral deposition, especially in the presence of BMP-2. CONCLUSION: Short-time application of PVP-I in concentrations of 1:10 and higher lead to decreased viability and impaired differentiation. However, surviving cells showed good recovery and mineralization potential

Relationship between nanohardness and mineral content of artificial carious enamel lesions

The aim of this study was to compare cross-sectional nanohardness, measured using an ultra-microindentation system, with mineral content, from transversal microradiography, of artificial enamel caries lesions. Sections (85 +/- 10 microm) from 16 bovine enamel samples with artificial caries were prepared. The mineral content and cross-sectional nanohardness at known depths from the surface were compared. Both methods showed lesion profiles with a surface layer. The determination of nanohardness seems limited to lesions with a mineral content >45 vol%. There was a moderate linear relationship between mineral content and the square root of nanohardness (R2 = 0.81). It was concluded that the conversion of cross-sectional hardness into mineral content remains questionable and cannot be recommended

Five-Year Survival of Short Single-Tooth Implants (6 mm): A Randomized Controlled Clinical Trial

The aim of the present study was to evaluate whether 6-mm dental implants in the posterior segments of either jaw perform equally well in terms of clinical and radiographic outcomes when compared with 10-mm implants after 5 y of loading. Patients with single-tooth gaps in the posterior area who were scheduled for implant therapy were randomly assigned to a group receiving either a 6- or 10-mm implant. After a healing period of 10 wk, implants were loaded with a screw-retained single crown and followed up at yearly intervals. Of 96 patients, 86 could be recalled after 5 y. The implant survival rates amounted to 91% (95% confidence interval: 0.836 to 0.998) for the 6-mm group and 100% for the 10-mm group ( P = 0.036). Median crown-to-implant (C/I) ratios were 1.75 (interquartile range [IQR], 1.50 to 1.90) for the 6-mm group and 1.04 (IQR, 0.95 to 1.15) for the 10-mm group, whereas the median marginal bone levels measured -0.29 mm (IQR, -0.92 to 0.23) for the 6-mm group and -0.15 mm (IQR: -0.93 - 0.41) for the 10-mm group after 5 y. The C/I ratio turned out to be statistically significant ( P < 0.001), whereas marginal bone levels showed no significant difference between the groups. The 6-mm implants exhibited significantly lower survival rates than the 10-mm implants over 5 y, whereas there was no difference between upper and lower jaws in terms of survival ( P = 0.58). Lost implants did not show any sign of marginal bone loss or peri-implant infection previous to loss of osseointegration. High C/I ratio and implant length had no significant effect on marginal bone level changes or technical and biological complications (German Clinical Trials Registry: DRKS00006290)

Success of 6-mm Implants with Single-Tooth Restorations

The aim of the study was to test whether implants of 6 mm in length perform equally well as 10-mm implants in terms of survival and marginal bone-level changes when supporting single crowns. Patients with a posterior single-tooth gap were randomly allocated to either the placement of a 6-mm (test) or 10-mm implant (control). The treatment protocol allowed for internal sinus lift but not for lateral bone augmentation. After a healing period of 10 wk, implants were loaded with screw-retained single crowns. Survival rates, number of pockets ≥5 mm, and bleeding-on-probing were assessed clinically. The change of marginal bone level and crown-to-implant ratios were analyzed by 2 examiners. Longitudinal intragroup analyses for marginal bone levels were performed applying the Wilcoxon signed rank test. Intergroup differences at baseline and at 3 y were compared using the Mann-Whitney U test. The effect of implant length and crown-to-implant ratio on changes of marginal bone level also was determined. Of 94 implants placed (47 test and 47 control), 78 implants (40 test and 38 control) were available for follow-up examination at 3 y of loading. One test implant was lost during the second year. Hence, implant survival was not significantly different between the 2 groups after 3 y (98% test; 100% control). We found no significant change in the crestal bone level from baseline to 3 y for test and control implants with -0.19 ± 0.62 mm and -0.33 ± 0.71 mm, respectively. The intergroup difference was not significant. Crown-to-implant ratios were not associated with a statistically significant difference in marginal bone loss. However, the number of sites with pockets ≥5 mm was significantly higher in the test group. Based on the 3-y assessment, the use of 6-mm implants can be considered a viable option when reconstructing posterior single tooth gaps (German Clinical Trials Registry: DRKS00006290)

Non-canonical NRF2 activation promotes a pro-diabetic shift in hepatic glucose metabolism

Objective: NRF2, a transcription factor that regulates cellular redox and metabolic homeostasis, plays a dual role in human disease. While it is well known that canonical intermittent NRF2 activation protects against diabetes-induced tissue damage, little is known regarding the effects of prolonged non-canonical NRF2 activation in diabetes. The goal of this study was to determine the role and mechanisms of prolonged NRF2 activation in arsenic diabetogenicity. Methods: To test this, we utilized an integrated transcriptomic and metabolomic approach to assess diabetogenic changes in the livers of wild type, Nrf2−/−, p62−/−, or Nrf2−/−; p62−/− mice exposed to arsenic in the drinking water for 20 weeks. Results: In contrast to canonical oxidative/electrophilic activation, prolonged non-canonical NRF2 activation via p62-mediated sequestration of KEAP1 increases carbohydrate flux through the polyol pathway, resulting in a pro-diabetic shift in glucose homeostasis. This p62- and NRF2-dependent increase in liver fructose metabolism and gluconeogenesis occurs through the upregulation of four novel NRF2 target genes, ketohexokinase (Khk), sorbitol dehydrogenase (Sord), triokinase/FMN cyclase (Tkfc), and hepatocyte nuclear factor 4 (Hnf4A). Conclusion: We demonstrate that NRF2 and p62 are essential for arsenic-mediated insulin resistance and glucose intolerance, revealing a pro-diabetic role for prolonged NRF2 activation in arsenic diabetogenesis. © 2021 The Author(s)Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Cerium chloride reduces enamel lesion initiation and progression in vitro

Aim: Determination of the potential of cerium chloride to reduce artificial carious mineral loss and lesion depth progression. Methods: A total of 160 enamel samples were prepared from 40 bovine lower central incisors. Crowns were sectioned into four pieces, embedded in acrylic resin, ground flat and allocated to eight groups (S1-S4 and D1-D4; n = 20). Specimens of groups D1-D4 were stored (for 7 days) in a demineralizing buffer solution to induce caries-like lesions. Afterwards, samples were treated for 30 s with one of the following solutions: placebo (S1 and D1), amine fluoride (S2 and D2), cerium chloride (S3 and D3) and a combination of fluoride and cerium chloride (S4 and D4). After another 7 (D1-D4) or 14 (S1-S4) days in demineralizing buffer solution, integrated mineral loss and lesion depth were determined by transversal microradiography and compared by Scheffé's post hoc tests. Results: In groups S1-S4, the highest values for integrated mineral loss and lesion depth were observed for group S1 (placebo), the lowest values for group S4. The results in groups S2-S4 were not significantly different. In groups D1-D4, the highest values for integrated mineral loss and lesion depth were observed for group D1 (placebo), the lowest values in groups D3 and D4. In group D2, integrated mineral loss and lesion depth were significantly lower as compared to D1, but significantly higher compared to groups D3 and D4. Conclusion: Cerium chloride and its combination with fluoride are able to significantly reduce carious mineral loss and the progression of lesion depth. © 2013 S. Karger AG, Basel