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Aim: The aim of this study was to evaluate demographic and clinical factors involved in the immediate seeking of care after traumatic dental injury (TDI) in Brazilian children.Materials and Methods: Records from 74 patients, age ranged 1-11 years, who sought treatment at the School of Dentistry of Ribeirão Preto at University of São Paulo, Brazil, were collected. Data was analyzed using the Epi Info 7.0 software by t-test, odds ratio calculation, Chi-square, or Fisher's exact tests.Results: Twenty-three (31.1%) sought dental treatment immediately and 51 (68.9%) did not seek dental treatment immediately. The most common type of trauma was lateral luxation (44.6%). In primary teeth, 31 cases (60.78%) involved the soft tissue and 16 (39.2%) involved hard tissue injuries. While in permanent teeth, 20 cases (40%) involved soft tissue and 24 (60%) involved hard tissue injuries had more traumas in the hard tissue (P = 0.04). The type of injury and dentition was not associated with the time that the guardians sought dental treatment (P > 0.05). None of the factors were involved in immediately seeking care after TDI.Conclusion: Moreover, the majority of parents/caregivers did not immediately seek dental treatment after TDI, regardless of the type of injury. [ABSTRACT FROM AUTHOR]

Background Phospholipases C (PLCs) are virulence factors found in several bacteria. In Mycobacterium tuberculosis (Mtb) they exhibit cytotoxic effects on macrophages, but the mechanisms involved in PLC-induced cell death are not fully understood. It has been reported that induction of cell necrosis by virulent Mtb is coordinated by subversion of PGE2, an essential factor in cell membrane protection. Results Using two Mtb clinical isolates carrying genetic variations in PLC genes, we show that the isolate 97-1505, which bears plcA and plcB genes, is more resistant to alveolar macrophage microbicidal activity than the isolate 97-1200, which has all PLC genes deleted. The isolate 97-1505 also induced higher rates of alveolar macrophage necrosis, and likewise inhibited COX-2 expression and PGE2 production. To address the direct effect of mycobacterial PLC on cell necrosis and PGE2 inhibition, both isolates were treated with PLC inhibitors prior to macrophage infection. Interestingly, inhibition of PLCs affected the ability of the isolate 97- 1505 to induce necrosis, leading to cell death rates similar to those induced by the isolate 97- 1200. Finally, PGE2 production by Mtb 97-1505-infected macrophages was restored to levels similar to those produced by 97-1200-infected cells. Conclusions Mycobacterium tuberculosis bearing PLCs genes induces alveolar macrophage necrosis, which is associated to subversion of PGE2 production. [ABSTRACT FROM AUTHOR]

Purpose: Radiation-related caries is characterized by enamel delamination near the dentinoenamel junction (DEJ). We investigated the activity and expression of the matrix metalloproteinases (MMPs) -2 and -9 in order to understand disease pathogenesis in teeth submitted or not to radiotherapy (RT). Methods: In situ zymography and immunofluorescence assays were performed to evaluate the activity and expression of MMPs -2 and -9, respectively. Twelve primary second molars were randomly assigned into two experimental subgroups: irradiated and nonirradiated. Dental fragments were exposed to radiation at a dose fraction of two Gy for five consecutive days until reaching the total dose of 60 Gy. The percentage of fluorescence in the DEJ was evaluated in three distinct regions of the tooth (cervical, cusp, and pit). The regions were photographed under fluorescence microscopy at 1.25x and 5x magnification. Results: The intensity of fluorescence per mm2 in the DEJ was higher in the cervical region of irradiated primary teeth (P<0.05) versus nonirradiated ones. In these areas, immunofluorescence revealed expression of MMPs -2 and -9. Conclusion: Radiotherapy can increase the activity of MMPs -2 and -9 in the cervical region of the DEJ of primary teeth. [ABSTRACT FROM AUTHOR]

A solitary median maxillary central incisor (SMMCI) is rare and affected individuals may carry a potentially serious condition known as SMMCI syndrome. However, many of these cases do not receive proper attention because they are misdiagnosed as agenesis of the maxillary central incisor. The purpose of this manuscript is to report two cases of children with only one maxillary central incisor and draw diagnostic differences between the entities. A correct diagnosis is very important because if an SMMCI is confirmed, the patient should be referred for genetic counseling. [ABSTRACT FROM AUTHOR]

Proanthocyanidin (PA) is a promising dentin biomodifier due to its ability to stabilize collagen fibrils against degradation by matrix metalloproteinases (MMPs); however, the most effective protocol to incorporate PA into bonding procedures is still unclear. This study evaluated the effect of dentin biomodification with a PA acid etchant on MMP activity, adhesive interface morphology and resin-dentin microtensile bond strength. Sound extracted human molars were flattened to expose dentin and acid-etched for 15 s according to the groups: EXP - experimental phosphoric acid; EXP+PA - experimental phosphoric acid 10% PA; TE - total-etching system; SE - self-etching system. Samples were restored with composite resin and stored in distilled water (37ºC). MMP activity and interface morphology were analyzed after 24 h by in situ zymography (n=6) and scanning electron microscopy (n=3), respectively. The resin-dentin microtensile bond strength (μTBS) was evaluated after 24 h and 6 months storage (n=6). Significantly higher MMP activity was detected in etched dentin compared with untreated dentin (p<0.05), but no difference among acid groups was found. Resin tags and microtags, indicative of proper adhesive system penetration in dentinal tubules and microtubules, were observed along the hybrid layer in all groups. There was no difference in μTBS between 24 h and 6 months for EXP+PA; moreover, it showed higher long-term μTBS compared with TE and EXP (p<0.05). The results suggest that 15 s of biomodification was not sufficient to significantly reduce MMP activity; nonetheless, EXP+PA was still able to improve resin-dentin bond stability compared with total- and self-etching commercial systems.

Histoplasma capsulatum is the agent of histoplasmosis, one of the most frequent mycoses in the world. The infection initiates with fungal spore inhalation, transformation into yeasts in the lungs and establishment of a granulomatous disease, which is characterized by a Th1 response. The production of Th1 signature cytokines, such as IFN-γ, is crucial for yeast clearance from the lungs, and to prevent dissemination. Recently, it was demonstrated that IL-17, a Th17 signature cytokine, is also important for fungal control, particularly in the absence of Th1 response. IL-22 is another cytokine with multiple functions on host response and disease progression. However, little is known about the role of IL-22 during histoplasmosis. In this study, we demonstrated that absence of IL-22 affected the clearance of yeasts from the lungs and increased the spreading to the spleen. In addition, IL-22 deficient mice ( Il22 -/- ) succumbed to infection, which correlated with reductions in the numbers of CD4 + IFN-γ + T cells, reduced IFN-γ levels, and diminished nitric oxide synthase type 2 (NOS2) expression in the lungs. Importantly, treatment with rIFN-γ mitigated the susceptibility of Il22 -/- mice to H. capsulatum infection. These data indicate that IL-22 is crucial for IFN-γ/NO production and resistance to experimental histoplasmosis.

Prostaglandin E 2 (PGE 2 ) suppresses macrophage effector mechanisms; however, little is known about the function of PGD 2 in infected alveolar macrophages (AMs). Using serum-opsonized Histoplasma capsulatum (Ops- H. capsulatum ) in vitro, we demonstrated that AMs produced PGE 2 and PGD 2 in a time-dependent manner, with PGE 2 levels exceeding those of PGD 2 by 48 h postinfection. Comparison of the effects of both exogenous PGs on AMs revealed that PGD 2 increased phagocytosis and killing through the chemoattractant receptor-homologous molecule expressed on Th2 lymphocytes receptor, whereas PGE 2 had opposite effects, through E prostanoid (EP) receptor 2 (EP2)/EP4-dependent mechanisms. Moreover, PGD 2 inhibited phospholipase C-γ (PLC-γ) phosphorylation, reduced IL-10 production, and increased leukotriene B4 receptor expression. In contrast, exogenous PGE 2 treatment reduced PLC-γ phosphorylation, p38 and nuclear factor κB activation, TNF-α, H 2 O 2 , and leukotriene B 4 , but increased IL-1β production. Using specific compounds to inhibit the synthesis of each PG in vitro and in vivo, we found that endogenous PGD 2 contributed to fungicidal mechanisms and controlled inflammation, whereas endogenous PGE 2 decreased phagocytosis and killing of the fungus and induced inflammation. These findings demonstrate that, although PGD 2 acts as an immunostimulatory mediator to control H. capsulatum infection, PGE 2 has immunosuppressive effects, and the balance between these two PGs may limit collateral immune damage at the expense of microbial containment., (Copyright © 2018 by the American Society for Biochemistry and Molecular Biology, Inc.)

Leukotriene B 4 (LTB 4 ) is essential for host immune defence. It increases neutrophil recruitment, phagocytosis and pathogen clearance, and decreases oedema and inflammasome activation. The host response and the role of LTB 4 during Achromobacter xylosoxidans infection remain unexplored. Wild-type (129sv) and LTB 4 deficient (Alox5 -/- ) mice were intratracheally infected with A. xylosoxidans. Wild-type 129sv infected mice survived beyond the 8 th day post-infection, exhibited increased levels of LTB 4 in the lung on the 1 st day, while levels of PGE 2 increased on the 7 th day post-infection. Infected Alox5 -/- mice showed impaired bacterial clearance, increased lung inflammation, and succumbed to the infection by the 7 th day. We found that exogenous LTB 4 does not affect the phagocytosis of A. xylosoxidans by alveolar macrophages in vitro. However, treatment of infected animals with LTB 4 protected from mortality, by reducing the bacterial load and inflammation via BLT 1 signalling, the high affinity receptor for LTB 4 . Of importance, we uncovered that LTB 4 induces gene and protein expression of α-defensin-1 during the infection. This molecule is essential for bacterial clearance and exhibits potent antimicrobial activity by disrupting A. xylosoxidans cell wall. Taken together, our data demonstrate a major role for LTB 4 on the control of A. xylosoxidans infection.

A solitary median maxillary central incisor (SMMCI) is rare and affected individuals may carry a potentially serious condition known as SMMCI syndrome. However, many of these cases do not receive proper attention because they are misdiagnosed as agenesis of the maxillary central incisor. The purpose of this manuscript is to report two cases of children with only one maxillary central incisor and draw diagnostic differences between the entities. A correct diagnosis is very important because if an SMMCI is confirmed, the patient should be referred for genetic counseling.