Most studies dealing with the caries preventive action of Nd:YAG laser have been done in permanent teeth and studies on primary teeth are still lacking. The aim of this study was to evaluate in vitro the effect of Nd:YAG laser combined or not with fluoride sources on the acid resistance of primary tooth enamel after artificial caries induction by assessing longitudinal microhardness and demineralization depth. Sixty enamel blocks obtained from the buccal/lingual surface of exfoliated human primary molars were coated with nail polish/wax, leaving only a 9 mm² area exposed on the outer enamel surface, and randomly assigned to 6 groups (n=10) according to the type of treatment: C-control (no treatment); APF: 1.23% acidulated phosphate fluoride gel; FV: 5% fluoride varnish; L: Nd:YAG laser 0.5 W/10 Hz in contact mode; APFL: fluoride gel + laser; FVL: fluoride varnish + laser. After treatment, the specimens were subjected to a des-remineralization cycle for induction of artificial caries lesions. Longitudinal microhardness data (%LMC) were analyzed by the Kruskal-Wallis test and demineralization depth data were analyzed by oneway ANOVA and Fisher's LSD test (á=0.05). APFL and APF groups presented the lowest percentage of microhardness change (p<0.05). Demineralization depth was smaller in all treated groups compared with the untreated control. In conclusion, Nd:YAG laser combined or not with fluoride gel/varnish was not more effective than fluoride alone to prevent enamel demineralization within the experimental period.

Microwave irradiation proved to be an effective alternative method to the disinfection of tongue cleaners and toothbrushes.

The aim of this study was to evaluate the effect of the Er:YAG laser and its association with fluoride (1.23% acidulate phosphate fluoride gel) on the prevention of enamel erosion. Sixty specimens were obtained from bovine enamel (4 × 4 mm), which were ground flat, polished, and randomly divided into five groups according to the preventive treatments: control-fluoride application; L--Er:YAG laser; L+F--laser + fluoride; F+L--fluoride + laser; L/F--laser/fluoride simultaneously. Half of the enamel surface was covered with nail varnish (control area), and the other half was pretreated with one of the preventive strategies to subsequently be submitted to erosive challenge. When the laser was applied, it was irradiated for 10 s with a focal length of 4 mm and 60 mJ/2 Hz. Fluoride gel was applied for 4 min. Each specimen was individually exposed to regular Coca-Cola® for 1 min, four times/day, for 5 days. Wear analysis was performed with a profilometer, and demineralization was assessed with an optical microscope. Data were analyzed using the Kruskal-Wallis test (wear)/Dunn test and ANOVA/Fisher's exact tests. The group L/F was similar to control group. The other groups showed higher wear, which did not present differences among them. In the demineralization assessment, the groups F+L and L/F showed lower demineralization in relation to the other groups. It can be concluded that none preventive method was able to inhibit dental wear. The treatments L/F and F+L showed lower enamel demineralization.

No abstract

The aim of this study was to evaluate by atomic force microscopy (AFM) the early phases and evolution of dental enamel erosion caused by hydrochloric acid exposure, simulating gastroesophageal reflux episodes. Polished bovine enamel slabs (4x4x2 mm) were selected and exposed to 0.1 mL of 0.01 M hydrochloric acid (pH=2) at 37 ?#61472;?#61616;C using five different exposure intervals (n=1): no acid exposure (control), 10 s, 20 s, 30 s and 40 s. The exposed area was analyzed by AFM in 3 regions to measure the roughness, surface area and morphological surface. The data were analyzed qualitatively. Roughness started as low as that of the control sample, Rrms=3.5 nm, and gradually increased at a rate of 0.3 nm/s, until reaching Rrms=12.5 nm at 30 s. After 40 s, the roughness presented increment of 0.40 nm only. Surface area (SA) increased until 20 s, and for longer exposures, the surface area was constant (at 30 s, SA=4.40 μm2 and at 40 s, SA=4.43 μm2). As regards surface morphology, the control sample presented smaller hydroxyapatite crystals (22 nm) and after 40 s the crystal size was approximately 60 nm. Short periods of exposure were sufficient to produce enamel demineralization in different patterns and the morphological structure was less affected by exposure to hydrochloric acid over 30 s.