Characterization and effectiveness of a violet LED light for in-office whitening.

OBJECTIVES: This study characterized a violet LED light (V-LED; bright max whitening) tooth whitening device and evaluated its efficacy on stained enamel compared to hydrogen peroxide (HP). MATERIALS AND METHODS: Characterization of the V-LED beam profile was performed using a laser beam-profiler. The irradiance was measured throughout an exposure cycle at 0- and 8-mm distances using an integrating sphere and a spectral radiometer. Bovine enamel/dentin blocks stained with black tea (BT), cigarette smoke (CS), or without staining (CONT) were subjected to V-LED or 40% HP (n = 10/group). Color parameters (ΔL, Δa, Δb, and ΔE00) were measured using a digital spectrophotometer. Light transmission was estimated through 1-mm-thick bovine enamel slices (n = 5). ΔL, Δb, ΔE00, and irradiance were analyzed by two-way ANOVAs and Tukey's tests, Δa by Kruskal-Wallis and Mann-Whitney tests, and light transmission by t-test (α = 5%). RESULTS: Heterogeneous beam distribution was observed for the emitting V-LED chips. After 20 sequential exposures, irradiance levels were reduced 25-50%, regardless of the distance from V-LED. Localized irradiance values were statistically different between beam locations and different distances from the target. V-LED produced lower ΔE00, ΔL, Δa, and Δb values than HP for CONT and BT, with no differences for CS. Light transmittance decreased approximately 98% through 1-mm thick enamel. CONCLUSIONS: V-LED irradiance was heterogeneous and decreased throughout the exposure cycles and was also greatly reduced with increasing tip distance. V-LED produced a significantly lower whitening effect on BT and control teeth. CLINICAL RELEVANCE: This study contributes to the knowledge of V-LED and its clinical use.

Chagas disease is not associated with diabetes, metabolic syndrome, insulin resistance and beta cell dysfunction at baseline of Brazilian Longitudinal Study of Adult Health (ELSA-Brasil).

Chagas disease (ChD) affects millions of people worldwide, being endemic in Latin America and emerging in the United States and Europe. Classically described as targeting the heart and gastrointestinal tract, Trypanosoma cruzi parasitism leads to structural and pro-inflammatory changes in the adipose tissue and pancreas. The effects of these changes on insulin resistance (IR), beta cell dysfunction, diabetes mellitus (DM),and metabolic syndrome (MS) are unclear. We aim to evaluate the association of ChD with DM, IR, beta cell dysfunction and MS in the baseline of multi-centric cohort study 'Brazilian Longitudinal Study of Adult Health' (ELSA-Brasil). This cross-sectional analysis included 14,922 (98%) participants of ELSA-Brasil at baseline. To investigate the associations of ChD with DM, IR (assessed by HOMA-IR) and beta cell dysfunction (assessed by HOMA beta), and MS we fitted logistic regression models including socio-demographic and anthropometric variables, health-related conditions and laboratory results. ChD, defined by positive serology, was prevalent in 1.9% (n = 283) of the sample, 17.3% (n = 49) of whom had cardiomyopathy. DM prevalence was 17.25% (n = 2574) and was not different among those with and without ChD (20.5% vs 17.2%; p = 0.28). Fasting and 2 h-blood glucose after a 75 g anhydrous glucose were slightly higher among participants positive for ChD, when compared with those with negative serology (102 mg/dL versus 100 mg/dL, respectively; and 127 mg/dL versus 124 mg/dL, respectively), only in univariate analysis. There was no significant association between these variables and ChD after adjustments. In addition, there was no significant association between DM, IR, beta cell dysfunction or MS and ChD (without and with cardiomyopathy). Our results showed that ChD, regardless of the presence of cardiomyopathy, is not associated with DM, IR, beta cell dysfunction or MS. These findings suggest the parasitism of the adipose tissue and pancreas in Chagas disease do not translate into clinically relevant glucose abnormalities.

Use of antioxidants to restore bond strength after tooth bleaching with peroxides.

This review compiles the literature on the antioxidants used after tooth bleaching with either low or high-concentrated carbamide and hydrogen peroxide to recover the bond strength. Antioxidants used in bleached teeth are mainly natural and non-enzymatic, except for catalase. Commonly, antioxidants are applied to remove any reactive oxygen species (ROS) residues left from bleaching gels, which adversely affect adhesive procedures, such as restorations or orthodontic brackets bonding. Even though sodium ascorbate, the most thoroughly investigated antioxidant, showed the most efficient bond strength recovery at 10% concentration, its performance depends on the type of solution and the application time. Natural extracts, such as proanthocyanidins and green tea, showed satisfactory results in the reversal of bond strength at 5% and 10% concentrations, respectively. Sodium ascorbyl phosphate, α-tocopherol, and catalase exhibited promising results, but further research is required. The adhesive system type plays an important role in the outcome of enamel bond strength after the antioxidant application. The postponement of either restorations or orthodontic brackets cementation following bleaching procedures seems to be efficiently replaced by antioxidant application prior to bonding procedures. However, the efficacy of using an antioxidant to recover bond strength depends on its type and application time.

The contribution of FTO and UCP-1 SNPs to extreme obesity, diabetes and cardiovascular risk in Brazilian individuals.

BACKGROUND: Obesity has become a common human disorder associated with significant morbidity and mortality and adverse effects on quality of life. Sequence variants in two candidate genes, FTO and UCP-1, have been reported to be overrepresented in obese Caucasian population. The association of these genes polymorphisms with the obesity phenotype in a multiethnic group such as the Brazilian population has not been previously reported. METHODS: To assess the putative contribution of both FTO and UCP-1 to body mass index (BMI) and cardiovascular risk we genotyped SNPs rs9939609 (FTO) and rs6536991, rs22705565 and rs12502572 (UCP-1) from 126 morbidly obese subjects (BMI 42.9 ± 5.6 kg/m2, mean ± SE) and 113 normal-weight ethnically matched controls (BMI 22.6 ± 3.5 kg/m2, mean ± SE). Waist circumference, blood pressure, glucose and serum lipids were also measured. Each sample was also genotyped for 40 biallelic short insertion/deletion polymorphism (indels) for ethnic assignment and to estimate the proportion of European, African and Amerindian biogeographical ancestry in the Brazilian population. RESULTS: Cases did not differ from controls in the proportions of genomic ancestry. The FTO SNP rs9939609 and UCP-1 SNP rs6536991 were significantly associated with BMI (p= 0.04 and p<0.0001 respectively). An allele dose dependent tendency was observed for BMI for rs6536991 sample of controls. No other significant associations between any SNP and hypertension, hyperlipidemia and diabetes were noted after correction for BMI and no significant synergistic effect between FTO and UCP-1 SNPs with obesity were noted. There was not an association between rs9939609 (FTO) and rs6536991 (UCP-1) in with maximum weight loss after 1 year in 94 obese patients who underwent bariatric surgery. CONCLUSION: Our data are consistent with FTO rs9939609 and UCP-1 rs6536991 common variants as contributors to obesity in the Brazilian population.

Novel mutations of the BSCL2 and AGPAT2 genes in 10 families with Berardinelli-Seip congenital generalized lipodystrophy syndrome.

CONTEXT: Congenital generalized lipodystrophy, or Berardinelli-Seip syndrome, is a rare autosomal recessive disease caused by mutations in either the BSCL2 or AGPAT2 genes. This syndrome is characterized by an almost complete loss of adipose tissue usually diagnosed at birth or early infancy resulting in apparent muscle hypertrophy. Common clinical features are acanthosis nigricans, hepatomegaly with or without splenomegaly and high stature. Acromegaloid features, cardiomyopathy and mental retardation can also be present. DESIGN: We investigated 11 kindreds from different geographical areas of Brazil (northeast and southeast). All coding regions as well as flanking intronic regions of both genes were examined. Polymerase chain reaction (PCR) amplifications were performed using primers described previously and PCR products were sequenced directly. RESULTS: Four AGPAT2 and two BSCL2 families harboured the same set of mutations. BSCL2 gene mutations were found in the homozygous form in four kindreds (c.412C>T c.464T>C, c.518-519insA, IVS5-2A>G), and in two kindreds compound mutations were found (c.1363C>T, c.424A>G). In the other four families, one mutation of the AGPAT2 gene was found (IVS3-1G>C and c.299G>A). CONCLUSIONS: We have demonstrated four novel mutations of the BSCL2 and AGPAT2 genes responsible for Berardinelli-Seip syndrome and Brunzell syndrome (AGPAT2-related syndrome).