This study evaluated the influence of a cola-type soft drink and a soy-based orange juice on the surface and subsurface erosion of primary enamel, as a function of the exposure time. Seventy-five primary incisors were divided for microhardness test (n=45) or scanning electron microscopy (SEM) analysis (n=30). The specimens were randomly assigned to 3 groups: 1 - artificial saliva (control); 2 - cola-type soft drink; and 3 - soy-based orange juice. Immersion cycles in the beverages were undertaken under agitation for 5 min, 3 times a day, during 60 days. Surface microhardness was measured at 7, 15, 30, 45 and 60 days. After 60 days, specimens were bisected and subsurface microhardness was measured at 30, 60, 90, 120, 150 and 200 µm from the surface exposed. Data were analyzed by ANOVA and Tukey’s test (a=0.05). Groups 2 and 3 presented similar decrease of surface microhardness. Regarding subsurface microhardness, group 2 presented the lowest values. SEM images revealed that after 60 days the surfaces clearly exhibited structural loss, unlike those immersed in artificial saliva. It may be concluded that erosion of the surfaces exposed to the cola-type soft drink was more accentuated and directly proportional to the exposure time.

This study evaluated in vitro the shear bond strength (SBS) of a resin-based pit-and-fissure sealant [Fluroshield (F), Dentsply/Caulk] associated with either an etch-and-rinse [Adper Single Bond 2 (SB), 3M/ESPE] or a self-etching adhesive system [Clearfil S3 Bond (S3), Kuraray Co., Ltd.] to saliva-contaminated enamel, comparing two curing protocols: individual light curing of the adhesive system and the sealant or simultaneous curing of both materials. Mesial and distal enamel surfaces from 45 sound third molars were randomly assigned to 6 groups (n=15), according to the bonding technique: I - F was applied to 37% phosphoric acid etched enamel. The other groups were contaminated with fresh human saliva (0.01 mL; 10 s) after acid etching: II - SB and F were light cured separately; III - SB and F were light cured together; IV - S3 and F were light cured separately; V - S3 and F were light cured simultaneously; VI - F was applied to saliva-contaminated, acid-etched enamel without an intermediate bonding agent layer. SBS was tested to failure in a universal testing machine at 0.5 mm/min. Data were analyzed by one-way ANOVA and Fisher's test (α=0.05).The debonded specimens were examined with a stereomicroscope to assess the failure modes. Three representative specimens from each group were observed under scanning electron microscopy for a qualitative analysis. Mean SBS in MPa were: I-12.28 (±4.29); II-8.57 (±3.19); III-7.97 (±2.16); IV-12.56 (±3.11); V-11.45 (±3.77); and VI-7.47 (±1.99). In conclusion, individual or simultaneous curing of the intermediate bonding agent layer and the resin sealant did not seem to affect bond strength to saliva-contaminated enamel. S3/F presented significantly higher SBS than the that of the groups treated with SB etch-and-rinse adhesive system and similar SBS to that of the control group, in which the sealant was applied under ideal dry, noncontaminated conditions.

Objective: To evaluate the association of bruxism phenotypes with single nucleotide polymorphisms in FKBP5, DRD2, ANKK1, and COMT. Methods: Clinical oral examination was performed to diagnose bruxism phenotypes in 150 children. DNA was collected from saliva. Logistic univariate regression, Chi-square, and Fisher’s exact tests were performed (p < 0.05). Results: Bruxism was associated with DRD2 (p = 0.02). Tooth grinding while awake was associated with ANKK1 (p < 0.001), and tooth grinding while asleep was associated with DRD2 in the additive (p = 0.030) and dominant (p = 0.008) model. Tooth clenching while awake was associated with ANKK1 in the additive (p = 0.005) and dominant (p = 0.008) models, whereas tooth clenching while asleep was associated with ANKK1 (p < 0.001) and with COMT in the additive (p = 0.001) and dominant (p = 0.003) models. Discussion: Polymorphisms in DRD2, ANKK1, and COMT are associated with bruxism phenotypes.

Epidermolysis bullosa (EB) is a heterogeneous group of rare genetic disorders characterized by marked fragility of the skin and mucous membranes in which vesiculobullous lesions occur in response to trauma, heat or no apparent cause. The recessive form of EB presents the greatest oral alterations including repeated blistering and scar formation leading to limited oral opening, ankyloglossia, tongue denudation, microstomia, vestibule obliteration and predisposition to oral carcinoma. Routine dental care may cause bullae formation on the lips and oral mucosa. Together with the ingestion of soft and frequently carbohydrate food, these anomalies lead to a high caries risk. This paper documents a case of a child diagnosed with recessive dystrophic epidermolysis bullosa (RDEB); describes the phases and difficulties of dental treatment and the measures that dentists and health care providers should adopt in order to provide a safe and effective dental treatment as well as earlier prevention to these patients.