Dental and skeletal effects after total arch distalization using modified C-palatal plate on hypo- and hyperdivergent Class II malocclusions in adolescents

ObjectivesTo compare the dental and skeletal treatment effects after total arch distalization using modified C-palatal plates (MCPPs) on adolescent patients with hypo- and hyperdivergent Class II malocclusion.Materials and MethodsThe study group included 40 patients with Class II malocclusion (18 boys and 22 girls, mean age = 12.2 ± 1.4 years) treated with MCPPs. Fixed orthodontic treatment started with the distalizing process in both groups. Participants were divided into hypo- or hyperdivergent groups based on their pretreatment Frankfort mandibular plane angle (FMA) ≤22° or ≥28°, respectively. Pre- and posttreatment lateral cephalograms were digitized, and 23 variables were measured and compared for both groups using paired and independent t-tests.ResultsThe hyper- and hypodivergent groups showed 2.7 mm and 4.3 mm of first molar crown distalizing movement, respectively (P < .001). The hypodivergent group had a slight 2.2° crown distal tipping of first molars compared with 0.3° in the hyperdivergent group. After distalization, the FMA increased 3.1° and 0.3°, in the hypodivergent and hyperdivergent groups, respectively (P < .001). SNA decreased in the hypodivergent group, while other skeletal variables presented no statistically significant differences in the changes between the groups.ConclusionsThe hypodivergent group showed more distal and tipping movement of the maxillary first molar and increased FMA than the hyperdivergent group. Therefore, clinicians must consider vertical facial types when distalizing molars using MCPPs in Class II nonextraction treatment.     

Computed tomography arterial portography for assessment of portal vein injury after blunt hepatic trauma

PURPOSE

Intrahepatic portal vein injuries secondary to blunt abdominal trauma are difficult to diagnose and can result in insidious bleeding. We aimed to compare computed tomography arterial portography (CTAP), reperfusion CTAP (rCTAP), and conventional computed tomography (CT) for diagnosing portal vein injuries after blunt hepatic trauma.

METHODS

Patients with blunt hepatic trauma, who were eligible for nonoperative management, underwent CTAP, rCTAP, and CT. The number and size of perfusion defects observed using the three methods were compared.

RESULTS

A total of 13 patients (seven males/six females) with a mean age of 34.5±14.1 years were included in the study. A total of 36 hepatic segments had perfusion defects on rCTAP and CT, while there were 47 hepatic segments with perfusion defects on CTAP. The size of perfusion defects on CT (239 cm³; interquartile range [IQR]: 129.5, 309.5) and rCTAP (238 cm³; IQR: 129.5, 310.5) were significantly smaller compared with CTAP (291 cm³; IQR: 136, 371) (both, P = 0.002).

CONCLUSION

Perfusion defects measured by CTAP were significantly greater than those determined by either rCTAP or CT in cases of blunt hepatic trauma. This finding suggests that CTAP is superior to rCTAP and CT in evaluating portal vein injuries after blunt liver trauma.The liver is one of the most frequently injured solid abdominal organs in the setting of blunt abdominal trauma (1). Fortunately, most patients with blunt hepatic trauma have relatively stable vital signs and need only supportive treatment or transarterial embolization (TAE) (1–9). Only 15% of patients, who present with hemodynamic instability or fail with nonoperative management, require operative intervention to manage their liver injury.Embolic therapy has been shown to have a high success rate in hemodynamically stable patients with blunt hepatic injury. TAE is associated with decreased abdominal infections, decreased transfusions, and decreased length of hospital stay compared with operative management (2, 3, 7). However, angiography can only detect bleeding from the hepatic artery; it cannot locate bleeding from the hepatic or portal vein. In the literature, portal vein injuries are not commonly described and most are the result of penetrating injuries to the extrahepatic portal veins. Mortality after a portal vein injury due to trauma is primarily due to hypovolemic shock and can be as high as 50% or greater (10, 11).Since the intrahepatic portions of the hepatic and portal veins are low pressure systems, they can bleed insidiously. Nevertheless, this subtle bleeding may require multiple transfusions and result in a prolonged hospital stay. Relative to an extrahepatic portal vein injury, patients with an intrahepatic portal vein injury may have relatively stable vital signs and slowly decreasing hemoglobin levels (10, 11). In addition, traumatic occlusion and/or thrombosis of the portal vein may cause large hepatic parenchymal infarction.Computed tomography arterial portography (CTAP) is a useful method based on portal enhancement of the liver by infusion of contrast material through the superior mesenteric artery for evaluating the portal venous system (12–15) and is widely used in patients with hepatic tumors with portal venous invasion (13, 16, 17). CTAP has a high sensitivity and specificity in the evaluation of portal vein thrombosis due to tumor (90% sensitivity, 99% specificity, 95% positive predictive value, 97% negative predictive value) (14). However, few studies have focused specifically on the utility of CTAP in the evaluation of portal vein injury as a result of trauma.The liver has a dual blood supply and receives between 66% and 75% of its blood supply from the hepatic portal vein with the remainder supplied by the hepatic artery (18). CTAP reflects only portal venous perfusion while reperfusion CTAP (rCTAP) reflects hepatic arterial reperfusion. Both rCTAP and conventional computed tomography (CT) are useful for determining certain liver injuries. However, they do not specifically evaluate the portal vein.The purpose of this study was to compare CTAP, rCTAP, and CT for diagnosing portal vein injuries after blunt hepatic trauma. We hypothesized that CTAP would be superior to rCTAP and CT in assessing portal vein injury after blunt hepatic trauma.     

Identification of glycoprotein Ib as a target for autoantibody in idiopathic (autoimmune) thrombocytopenic purpura

An antibody (DIL) from a patient with idiopathic thrombocytopenic purpura (ITP) was shown to have autospecificity on the basis of reactions with autologous platelets that were identical to those obtained with platelets from normal subjects. DIL antibody also reacted strongly in an immunofluorescence test with platelets from a patient with Glanzmann's thrombasthenia, but failed to react with platelets from a patient with the Bernard-Soulier syndrome who was known to be deficient in glycoprotein Ib (GPIb). Purified GPIb and control platelets, but not Bernard-Soulier platelets, inhibited the lytic activity of DIL. Using the GPIb-specific monoclonal antibody AP1 and one-dimensional rocket electrophoresis into gels containing rabbit antihuman platelet membrane antibody, it was shown that staphylococcal protein A-Sepharose beads coated with DIL antibody selectively remove GPIb from solubilized platelet preparations. By crossed immunoelectrophoresis it was found that DIL recognizes a determinant on GPIb on the membrane side of the cleavage site of the platelet calcium- activated protease (calpain). These studies provide direct evidence for binding of a platelet autoantibody to a determinant on GPIb relatively close to the site of insertion of this protein into the platelet membrane.     

BMP-driven NRF2 activation in esophageal basal cell differentiation and eosinophilic esophagitis

Tissue homeostasis requires balanced self-renewal and differentiation of stem/progenitor cells, especially in tissues that are constantly replenished like the esophagus. Disruption of this balance is associated with pathological conditions, including eosinophilic esophagitis (EoE), in which basal progenitor cells become hyperplastic upon proinflammatory stimulation. However, how basal cells respond to the inflammatory environment at the molecular level remains undetermined. We previously reported that the bone morphogenetic protein (BMP) signaling pathway is critical for epithelial morphogenesis in the embryonic esophagus. Here, we address how this pathway regulates tissue homeostasis and EoE development in the adult esophagus. BMP signaling was specifically activated in differentiated squamous epithelium, but not in basal progenitor cells, which express the BMP antagonist follistatin. Previous reports indicate that increased BMP activity promotes Barrett’s intestinal differentiation; however, in mice, basal progenitor cell–specific expression of constitutively active BMP promoted squamous differentiation. Moreover, BMP activation increased intracellular ROS levels, initiating an NRF2-mediated oxidative response during basal progenitor cell differentiation. In both a mouse EoE model and human biopsies, reduced squamous differentiation was associated with high levels of follistatin and disrupted BMP/NRF2 pathways. We therefore propose a model in which normal squamous differentiation of basal progenitor cells is mediated by BMP-driven NRF2 activation and basal cell hyperplasia is promoted by disruption of BMP signaling in EoE.