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.     

Muscle strength and ankle mobility for the gait parameters in diabetic neuropathies

AimsTo evaluate the spatio-temporal variables of gait and the isometric muscle strength component of the ankle in patients with peripheral diabetic neuropathy. Also, verify the relationship between these variables and gait parameters.MethodsThis study involved 25 diabetic peripheral neuropathy (DPN) participants (62.4 ± 8.36 years) and 27 age-matched healthy control individuals (64.48 ± 6.21 years). The assessment of the spatio-temporal parameters of gait was performed using an electronic baropodometry treadmill. Prior to the collection data, each participant was instructed to walk on the treadmill in her/his habitual self-selected speed.ResultsDiabetic neuropathy group showed impairment of gait, with a smaller stride and length speed of the cycle, and increased duration of support time. Restricted dorsiflexion mobility and increased plantarflexion mobility were found, with a decrease in muscle strength of the dorsiflexors and plantiflexors. There was a significant relationship between plantiflexor muscle strength and the length and speed of the gait cycle. Also the muscle strengths of the plantiflexors and dorsiflexors, and the range of motion of dorsiflexion were predictors of gait performance.ConclusionsThe ankle, muscle strength and ankle mobility variables could explain changes in gait speed and range of motion in patients with DPN, allowing for the application of preventive strategies.     

The Impact of MRSA Colonization on Surgical Site Infection Following Major Gastrointestinal Surgery

Purpose

The purpose of this study is to determine whether methicillin-resistant Staphylococcus aureus (MRSA) colonization affects surgical site infections (SSI) after major gastrointestinal (GI) operations.

Methods

We retrospectively reviewed the charts of all patients undergoing major GI surgery from December 2007 to August 2009. All patients were tested for MRSA colonization and grouped according to results (MRSA+, methicillin-sensitive S. aureus [MSSA]+, and negative). Data analyzed included demographics, incidence of SSI, and wound culture results.

Results

A total of 1,137 patients were identified; 78.9 % negative, 14.7 % MSSA+, and 6.4 % MRSA+. The mean age was 59.5 years, 44.5 % of the patients were men, and 47.9 % of the patients underwent colorectal operation. SSI was identified in 101 (8.9 %) patients and was higher in the MRSA+ group than the negative and MSSA+ groups (13.7 vs. 9.4 vs. 4.2 %; p?<?0.05). Although MRSA colonization had an odds ratio of 1.43 for developing an SSI, it was not a significant independent risk factor. However, the MRSA+ group was strongly associated with MRSA cultured from the wound when SSI was present (70 vs. 8.5 %; p?<?0.0001).

Conclusions

MRSA colonization is not an independent risk factor for SSI following major GI operations; however, it is strongly predictive of MRSA-associated SSI in these patients. Preoperative MRSA nasal swab test with decolonization may reduce the incidence of MRSA-associated SSI after major GI surgery.     

Loss of p53 cooperates with K‐ras activation to induce glioma formation in a region‐independent manner

Gliomas are recognized as a heterogeneous group of neoplasms differing in their location and morphological features. These differences, between and within varying grades of gliomas, have not been explained solely on the grounds of an oncogenic stimulus. Interactions with the tumor microenvironment as well as inherent characteristics of the cell of origin are likely a source of this heterogeneity. There is an ongoing debate over the cell of origin of gliomas, where some suggest a progenitor, while others argue for a stem cell origin. Thus, it is presumed that neurogenic regions of the brain such as the subventricular zone (SVZ) containing large numbers of neural stem and progenitor populations are more susceptible to transformation. Our studies demonstrate that K‐ras^G12D cooperates with the loss of p53 to induce gliomas from both the SVZ and cortical region, suggesting that cells in the SVZ are not uniquely gliomagenic. Using combinations of doxycycline‐inducible K‐ras^G12D and p53 loss, we show that tumors induced by the cooperative actions of these genes remain dependent on active K‐ras expression, as deinduction of K‐ras^G12D leads to complete tumor regression despite absence of p53. These results suggest that the interplay between specific combinations of genetic alterations and susceptible cell types, rather than the site of origin, are important determinates of gliomagenesis. Additionally, this model supports the view that, although several genetic events may be necessary to confer traits associated with oncogenic transformation, inactivation of a single oncogenic partner can undermine tumor maintenance, leading to regression and disease remission. GLIA 2013;61:1862–1872     

Fluorescence, birefringence and confocal microscopy of the abdominal aorta from nonobese diabetic (NOD) mice

In this study, nonenzymatic glycosylation was assessed in aorta extracellular matrix (ECM) from nonobese diabetic (NOD) mice, using nitroblue tetrazolium (NBT). Molecular and structural changes were investigated in elastic lamellae and collagen fibers of diabetic mice aortas after staining with dansyl chloride and anilinonaphthalene sulfonate (ANS). Alterations in arterial autofluorescence and birefringence of collagen fibers were investigated in unstained aortas. Proliferation of smooth muscle cells (SMC) was also investigated by Feulgen reaction staining assessed by confocal microscopy and image analysis. Assessment of nonenzymatic glycosylation demonstrated glycosylation products in the aorta ECM of NOD mice. Elastic lamellae and collagen fibers from NOD mouse aortas presented less intense fluorescence after staining with dansyl chloride and ANS when compared to aortas of control nondiabetic mice. However, unstained NOD aortas showed more intense autofluorescence when compared to controls. Birefringence analysis suggests alterations in the higher molecular packing of the arterial collagen fibers in NOD aortas. In aortas stained by Feulgen reaction, no evidence of SMC proliferation was observed in diabetic aortas.     

Effects of a combined application of potassium oxalate gel/adhesive agent on dentin permeability in vitro

PURPOSE: To test the effects of sequential application of potassium oxalate gel/adhesive agent on in vitro dentin permeability. MATERIALS AND METHODS: Full crown preparations were made in extracted human molars to expose deep coronal dentin. The roots and pulp were removed and the resulting crown segments were connected to a special device (Flodec) to permit the measurement of the permeability of the specimens before and after treatments. Minimum and maximum permeability were recorded after smear layer and phosphoric acid treatment. A new smear layer was created and the permeability measured after the crowns were bonded with Single Bond (3M ESPE), One-Up Bond F (Tokuyama), and AdheSE (Ivoclar Vivadent), either according to manufacturer's instructions or after treating the acid-etched dentin with a 3 wt% potassium oxalate gel. The results were expressed as a percentage of maximum permeability values. Impressions and epoxy resin replicas from the crown segments were produced for SEM examination. RESULTS: None of the adhesives were able to eliminate the fluid flow through dentin. Two-way ANOVA revealed that the application of potassium oxalate prior to the bonding procedures was the most effective technique in reducingthe dentin permeability (p < 0.05), regardless of the adhesive used. SEM micrographs showed that transudation of dentinal fluid could be identified on the surfaces of all replicas. CONCLUSION: The use of potassium oxalate gel was effective in reducing the permeability of bonded dentin.