Brushing associated with oral irrigation in maintaining implants and overdentures hygiene – a randomized clinical trial

Odontology - Evaluate, through a randomized clinical trial, the efficacy of brushing associated with oral irrigation in maintaining implant and overdenture hygiene. Thirty-eight participants, who...     

Diagnosis and management of hepatic artery in-stent restenosis after liver transplantation by optical coherence tomography:A case report

BACKGROUND Percutaneous transluminal angioplasty and stenting represent an effective treatment for hepatic artery stenosis after liver transplantation. In the first year after stenting, approximately 22% of patients experience in-stent restenosis, increasing the risk of artery thrombosis and related complications, and 50% experience liver failure. Although angiography is an important tool for diagnosis and the planning of therapeutic interventions, it may raise doubts, especially in small-diameter arteries, and it provides low resolution rates compared with newer intravascular imaging methods, such as optical coherence tomography(OCT).CASE SUMMARY A 64-year-old male developed hepatic artery stenosis one year after orthotropic liver transplantation and was successfully treated with percutaneous transluminal angioplasty with stenting. Five months later, the Doppler ultrasound results indicated restenosis. Visceral arteriography confirmed hepatic artery tortuosity but was doubtful for significant in-stent restenosis(ISR) and intrahepatic flow reduction. To confirm ISR, identify the etiology and guide treatment, OCT was performed. OCT showed severe stenosis due to four mechanisms: Focal and partial stent fracture, late stent malapposition, in-stent neointimal hyperplasia, and neoatherosclerosis.CONCLUSION Intravascular diagnostic methods can be useful in evaluating cases in which initial angiography results are not sufficient to provide a proper diagnosis of significant stenosis, especially with regard to ISR. A wide range of diagnoses are provided by OCT, resulting in different treatment options. Interventional radiologists should consider intravascular diagnostic methods as additional tools for evaluating patients when visceral angiography results are unclear.     

Specialized pro‐resolving lipid mediators in experimental periodontitis: A systematic review

Recently, several studies demonstrated the potential of using specialized pro‐resolving lipid mediators (SPMs), as a novel approach, in treating periodontitis in pre‐clinical models. This review aimed to systematically evaluate the biological actions of SPMs on periodontal tissues in animals with experimentally induced periodontitis. This systematic review was performed by following the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) guidelines. Studies were searched in three databases. Meta‐analysis was not performed because of the data heterogeneity. Study quality was assessed using Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE) Risk of Bias tool. Six studies using an experimental periodontitis model to test the efficacy of SPMs were selected. Resolvin E1 and lipoxins were topically applied to treat experimental periodontitis. Alveolar bone loss could be significantly prevented and regenerated by applying SPMs, when compared to the control group. The dosages of SPMs and the periods of disease induction varied based on the pre‐clinical model employed. Two studies further demonstrated the positive shift in microbial composition, in line with positive shift in inflammatory status, that are regulated by SPMs. Clinical studies are needed to optimize the application of SPMs in treating periodontal diseases in humans.     

The psychological impact of cryptic chromosomal abnormalities diagnosis announcement

This qualitative study aims to describe the psychological impact of the diagnosis announcement of pathogenic Copy Number Variations (pCNVs). We performed semi-structured interviews of 60 parents of 41 affected children and 5 geneticists who announced the diagnoses. The diagnosis of the best characterized microdeletion syndromes, often defined by patronymic names (e.g. Williams syndrome), is generally made on a clinical basis by geneticists and confirmed by fluorescence in situ hybridization analysis. Chromosomal microarray, on the contrary, can allow the disclosure of rare pCNVs named after cytogenetic formulas, with poorly known clinical consequences: this makes doctors feel less confident with these diagnosis announcements. The disclosure of pCNVs named after cytogenetic formulas does not facilitate the parental mental representation of the disease, leading some parents to call into question the genotype-phenotype correlation or the very notion of a diagnosis. The announcement of inherited pCNVs can increase the feeling of parental guilt; the disclosure of de novo pCNVs can induce a feeling of “breakage” in the mental representation of the parent-child vertical transmission. In conclusion, our study shows that the disclosure of pCNVs has a significant psychological impact: a multidisciplinary approach to the diagnosis announcement, including a psychological support, should be systematically warranted.     

Micro–Computed Tomography Analysis of the Root Canal Anatomy and Prevalence of Oval Canals in Mandibular Incisors

Introduction

This study aimed to describe the anatomy of the mandibular incisors by using micro–computed tomography.

Methods

Mandibular incisors (n = 340) were scanned at 19-μm voxel size resolution, and the numbers of canals were classified according to Vertucci classification, as well as the major and minor diameters of the root and root canals, presence of oval canals, and three-dimensional analysis of the apical third were also measured. Data were presented in terms of median and range for each anatomic classification.

Results

Overall, the specimens had 1 root canal (N = 257). The second most prevalent anatomy was Vertucci type III (N = 56). These anatomies represent 92% of the sample. The medians of the major diameter at the 1-, 2-, and 3-mm level of the most prevalent anatomies were 0.36, 0.39, and 0.47 mm for type I and 0.41, 0.51, and 0.66 mm for type III, respectively. The apical volume appears to be constant among these anatomies (0.63 and 0.59 mm³). Oval canals were found at the 1-mm apical level, with a prevalence of 16.7% for Vertucci type I and 37.5% for Vertucci type III. The presence of oval canals increased at the 3-mm apical level to 32.4% and 76.2% for Vertucci type I and III classifications, respectively.

Conclusions

Type I and III configurations represent 92% of the mandibular incisors studied. Within these anatomic configurations, oval-shaped canals in the apical third were not uncommon and more prevalent in the type III anatomy.     

Pancreatic Islet Vasculature Adapts to Insulin Resistance Through Dilation and Not Angiogenesis

Pancreatic islets adapt to insulin resistance through a complex set of changes, including β-cell hyperplasia and hypertrophy. To determine if islet vascularization changes in response to insulin resistance, we investigated three independent models of insulin resistance: ob/ob, GLUT4^+/−, and mice with high-fat diet–induced obesity. Intravital blood vessel labeling and immunocytochemistry revealed a vascular plasticity in which islet vessel area was significantly increased, but intraislet vessel density was decreased as the result of insulin resistance. These vascular changes were independent of islet size and were only observed within the β-cell core but not in the islet periphery. Intraislet endothelial cell fenestration, proliferation, and islet angiogenic factor/receptor expression were unchanged in insulin-resistant compared with control mice, indicating that islet capillary expansion is mediated by dilation of preexisting vessels and not by angiogenesis. We propose that the islet capillary dilation is modulated by endothelial nitric oxide synthase via complementary signals derived from β-cells, parasympathetic nerves, and increased islet blood flow. These compensatory changes in islet vascularization may influence whether β-cells can adequately respond to insulin resistance and prevent the development of diabetes.Pancreatic islets are highly vascularized, and this feature is critical for β-cells to rapidly sense the blood glucose and secrete insulin into the systemic circulation (1,2). Islet vascularization begins early in pancreas development and is maintained in adulthood as a consequence of islet cell production of angiogenic factors such as vascular endothelial growth factor-A (VEGF-A) and angiopoietin-1 (Ang-1) (3–6). These factors recruit endothelial cells (ECs), stimulate blood vessel growth and maturation, and in the case of VEGF-A, promote formation of EC fenestrations (5,6). In addition, ECs adjacent to pancreatic epithelium reciprocally influence islet cell differentiation and development (7,8).β-Cells have a remarkable ability to respond to changes in an organism’s metabolic state, such as changes in the blood glucose or increased insulin requirements. For example, when insulin resistance develops, β-cells of the pancreatic islet can dramatically increase insulin production and secretion with an increase of β-cell mass, thus maintaining normoglycemia (9,10). In this way, mouse models with marked insulin resistance and humans with obesity-related insulin resistance are hyperinsulinemic but not hyperglycemic. The mechanisms underlying this β-cell adaptation to insulin resistance and their subsequent failure in some individuals who develop type 2 diabetes are incompletely understood.Because of the highly vascularized state of pancreatic islets and the marked changes in β-cell size and number in the setting of insulin resistance, we hypothesized that the islet vasculature must adapt to these changes in β-cell mass and insulin requirements. We envisioned that a hyperplastic islet, like a growing tumor mass, would increase production of angiogenic factors to increase its vascular supply with expanding β-cell mass (11). To test this hypothesis, we examined islet vascularization in three mouse models of insulin resistance and found, unexpectedly, that islet vessel density was decreased, not increased, and that the intraislet vasculature became markedly dilated whereas vessels in the exocrine tissue were unchanged. The dilation of intraislet capillaries was independent of islet size, suggesting the vascular adaptation may primarily support increased β-cell insulin secretory demand rather than β-cell mass expansion. Moreover, these vascular changes were accompanied by an increase in islet parasympathetic innervation. Our results indicate that the metabolic state influences islet angioarchitecture and innervation, suggesting that islet neurovascular remodeling may influence whether β-cells can adequately respond to insulin resistance and maintain normoglycemia.