Evaluation of Enamel Roughness in Vitro After Orthodontic Bracket Debonding Using Different Methods of Residual Adhesive Removal

Objective:The aim of the present study was to compare different techniques for resin remnant removal (RRR) after orthodontic bracket debonding and to evaluate alterations on the dental enamel caused by these methods. The null hypothesis tested was that there is no difference between RRR techniques in relationship the changes caused on the dental enamel.Methods:A total of 75 bovine mandibular permanent incisors were used in the study. Brackets were bonded and debonded in each tooth in two experimental regions. Five RRR techniques were used in the experimental groups (n=15): Group 1-diamond bur (6-bladed), Group 2-diamond bur (12-bladed), Group 3-diamond bur (30-bladed), Group 4-aluminum oxide sandblasting (AOS), and Group 5-Er:YAG laser. Enamel surface was evaluated using profilometry, and surface roughness analysis was performed at three time intervals: before bracket bonding, after RRR techniques, and after final polishing. Qualitative analyses of the enamel surfaces were performed using scanning electron microscopy.Results:Multiblade burs showed the best results, and the 30-bladed bur created a less irregular enamel surface. AOS caused greater enamel wear, and Er:YAG laser caused more surface irregularity.Conclusion:The null hypothesis was rejected. The multiblade burs were the least harmful than the other techniques. Enamel surface roughness after using the 30-blade bur was similar to the original enamel. These results indicate that the type of bur tested (30-bladed) can be indicated to remove resin remnants after bracket debonding

Factors associated with prolonged non-nutritive sucking habits in two cohorts of Brazilian children

Abstract Background Non-nutritive sucking habits (NNSH) are very common during childhood. However, if these habits were maintained for 36 months of age or more, they are considered to be prolonged (PNNSH) and can cause occlusal, physiological and esthetic changes. There is controversy about their prevalence and whether perinatal, social, demographic and health characteristics influence their onset and duration. So, the objectives of this study are to estimate the prevalence of PNNSH and to evaluate perinatal, early life and school age factors associated with their occurrence in children. Methods A sample of 1,463 children aged 7–11 years born in Ribeirão Preto (RP-1994) and São Luís (SL-1997/98), Brazil, was reevaluated at school age in 2004/05. Birth weight, gestational age and perinatal variables were obtained at birth. Type of feeding, occurrence and duration of finger and pacifier sucking were recorded retrospectively at school age. PNNSH were defined when persisted for 36 months of age or more. Crude and adjusted prevalence ratios (PR) were estimated by Poisson regression (alpha = 5%). Results Prevalence of PNNSH was higher in RP (47.6%) than in SL (20.2%) – (p < 0.001). Perinatal variables were not associated to PNNSH, whilst female sex (PR = 1.27 in RP; PR = 1.47 in SL) and bottle feeding for 24 months or more (PR = 2.24 in RP; PR = 2.49 in SL) were risk factors in both locations. Breast feeding for 12 months or more (PR = 0.53 in RP; PR = 0.31 in SL) was associated with lower prevalence of PNNSH in both places. In SL, children whose mothers lived in consensual union (PR = 1.62) and worked outside the home (PR = 1.51) showed higher prevalence of PNNSH compared to their counterparts. Conclusions Prevalence of PNNSH was high especially in RP and was not associated with perinatal variables. In both cities there was an association between female sex, shorter breast-feeding duration, longer bottle feeding duration and higher prevalence of PNNSH.http://deepblue.lib.umich.edu/bitstream/2027.42/109521/1/12889_2013_Article_6874.pd

Novel Machado-Joseph disease-modifying genes and pathways identified by whole-exome sequencing

Machado-Joseph disease (MJD/SCA3) is a neurodegenerative polyglutamine disorder exhibiting a wide spectrum of phenotypes. The abnormal size of the (CAG)n at ATXN3 explains ~55% of the age at onset variance, suggesting the involvement of other factors, namely genetic modifiers, whose identification remains limited. Our aim was to find novel genetic modifiers, analyse their epistatic effects and identify disease-modifying pathways contributing to MJD variable expressivity. We performed whole-exome sequencing in a discovery sample of four age at onset concordant and four discordant first-degree relative pairs of Azorean patients, to identify candidate variants which genotypes differed for each discordant pair but were shared in each concordant pair. Variants identified by this approach were then tested in an independent multi-origin cohort of 282 MJD patients. Whole-exome sequencing identified 233 candidate variants, from which 82 variants in 53 genes were prioritized for downstream analysis. Eighteen disease-modifying pathways were identified; two of the most enriched pathways were relevant for the nervous system, namely the neuregulin signaling and the agrin interactions at neuromuscular junction. Variants at PARD3, NFKB1, CHD5, ACTG1, CFAP57, DLGAP2, ITGB1, DIDO1 and CERS4 modulate age at onset in MJD, with those identified in CFAP57, ACTG1 and DIDO1 showing consistent effects across cohorts of different geographical origins. Network analyses of the nine novel MJD modifiers highlighted several important molecular interactions, including genes/proteins previously related with MJD pathogenesis, namely between ACTG1/APOE and VCP/ITGB1. We describe novel pathways, modifiers, and their interaction partners, providing a broad molecular portrait of age at onset modulation to be further exploited as new disease-modifying targets for MJD and related diseases

Novel Machado-Joseph disease-modifying genes and pathways identified by whole-exome sequencing

Funding Information: This work was funded by FEDER - Fundo Europeu de Desenvolvimento Regional funds through the COMPETE 2020 - Operacional Programme for Competitiveness and Internationalisation (POCI), Portugal 2020 , and by Portuguese funds through FCT - Fundação para a Ciência e a Tecnologia / Ministério da Ciência, Tecnologia e Ensino Superior in the framework of the project PTDC/DTP-PIC/2638/2017 ( POCI-01-0145-FEDER-016592 ); GenomePT ( POCI-01-0145-FEDER-022184 ); ICVS Scientific Microscopy Platform , member of the national infrastructure PPBI - Portuguese Platform of Bioimaging ( PPBI-POCI-01-0145-FEDER-022122 ; by National funds , through the Foundation for Science and Technology (FCT) - project UIDB/50026/2020 and UIDP/50026/2020 ; and by the project NORTE-01-0145-FEDER-000013 , supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF) . MR is supported by FCT ( CEECIND/03018/2018 ). ARVM ( SFRH/BD/129547/2017 ) and AFF ( SFRH/BD/121101/2016 ) are supported by a PhD grant financed by FCT . CB is supported by the Multiple System Atrophy Trust and Alzheimer's Research UK . MDC received funding from National Ataxia Foundation (NAF) and from FCT ( SFRH/BPD/101925/2014 ); DV-C received a grant from FCT ( SFRH/BD/147826/2019 ). Publisher Copyright: © 2021Machado-Joseph disease (MJD/SCA3) is a neurodegenerative polyglutamine disorder exhibiting a wide spectrum of phenotypes. The abnormal size of the (CAG)n at ATXN3 explains ~55% of the age at onset variance, suggesting the involvement of other factors, namely genetic modifiers, whose identification remains limited. Our aim was to find novel genetic modifiers, analyse their epistatic effects and identify disease-modifying pathways contributing to MJD variable expressivity. We performed whole-exome sequencing in a discovery sample of four age at onset concordant and four discordant first-degree relative pairs of Azorean patients, to identify candidate variants which genotypes differed for each discordant pair but were shared in each concordant pair. Variants identified by this approach were then tested in an independent multi-origin cohort of 282 MJD patients. Whole-exome sequencing identified 233 candidate variants, from which 82 variants in 53 genes were prioritized for downstream analysis. Eighteen disease-modifying pathways were identified; two of the most enriched pathways were relevant for the nervous system, namely the neuregulin signaling and the agrin interactions at neuromuscular junction. Variants at PARD3, NFKB1, CHD5, ACTG1, CFAP57, DLGAP2, ITGB1, DIDO1 and CERS4 modulate age at onset in MJD, with those identified in CFAP57, ACTG1 and DIDO1 showing consistent effects across cohorts of different geographical origins. Network analyses of the nine novel MJD modifiers highlighted several important molecular interactions, including genes/proteins previously related with MJD pathogenesis, namely between ACTG1/APOE and VCP/ITGB1. We describe novel pathways, modifiers, and their interaction partners, providing a broad molecular portrait of age at onset modulation to be further exploited as new disease-modifying targets for MJD and related diseases.publishersversionpublishe

Occult hepatitis B infection by a recombinant D/C virus in an immunosuppressed patient

Approximately 300 million people worldwide were living with chronic hepatitis B virus infection as of 2016, however, this number does not account for those who might be living with occult hepatitis B virus infection due to difficulty diagnosing this condition. The multiple genotypes and the ability of the hepatitis B virus to acquire mutations that down-regulate its expression make occult hepatitis B virus infection a very elusive diagnosis. This is especially worrisome when there is a need to start immunosuppressive therapies, since there is a risk of reactivation in undiagnosed patients. We present a case of female patient who was referred to the consultation because she was about to start chemotherapy with an anti-CD20 agent and had a positive anti-HBc and anti-HBs. During routine workup an occult hepatitis B virus infection was diagnosed. Upon further study mutations in the PreCore and Basal Core Promoter regions were identified, as well as, a double genotype D/C. Therapy with tenofovir was initiated before the patient was started on chemotherapy. This case highlights the importance of comprehensive studying of patients who present with apparently resolved chronic hepatitis B virus infection, especially when they are about to start immunosuppressive therapies. Keywords: Hepatitis B, Recombinant genotype, Occult, Immunosuppressive therap