Objective: To assess the in vivo release of nickel, chromium, and iron ions into saliva by different metallic brackets. Materials and Methods: Thirty volunteers wore removable appliances with bonded brackets and were divided according to the brand of brackets: group A, 3M/Unitek (AISI 303); group B, American Orthodontics (AISI 316L); and group C, Dentaurum (AISI 316L). The appliances were worn for 60 days, and saliva samples were collected at the following time points: T1, before placement of the appliance; T2, after 10 minutes; T3, 24 hours; T4, 7 days; T5, 30 days; and T6, 60 days after insertion of the removable appliance. Saliva samples were analyzed for nickel, chromium, and iron by atomic absorption spectrophotometry. Statistical analysis was performed by nonparametric tests (Friedman, Mann-Whitney, Kruskal-Wallis). Results: Saliva evaluation revealed a large variation in concentration of these ions between individuals. The results also appeared to indicate an increase in nickel and chromium ions immediately after placement of the appliance (T2), but this was statistically significant only for groups B and C. There was no increase in iron levels. A tendency for increases in nickel and chromium concentrations was verified immediately after placement of the appliance, but these values are probably reduced because of biofilm formation regardless of the bracket used. Conclusion: Nickel and chromium ion concentrations increased immediately after placement of the appliance in the mouth for all study groups. There were no significant differences in the nickel, chromium, and iron levels released by the three groups of appliances at all study periods.

Our results suggest that extracellular DNA in mucus play a role in lower airways obstruction in OVA asthma protocol and that the treatment with rhDNase improved lung function and DNA extracellular traps, with no direct cellular anti-inflammatory effects.

In this retrospective report, the use of omalizumab in Brazilian children with STRA significantly improved disease control, decreased hospitalizations, and allowed suspension of continuous oral corticosteroids.

Objective: To describe the clinical characteristics, lung function, radiological findings, and the inflammatory cell profile in induced sputum in children and adolescents with severe therapy-resistant asthma (STRA) treated at a referral center in southern Brazil. Methods: We retrospectively analyzed children and adolescents (3-18 years of age) with uncontrolled STRA treated with high-dose inhaled corticosteroids and long-acting ß2 agonists. We prospectively collected data on disease control, lung function, skin test reactivity to allergens, the inflammatory cell profile in induced sputum, chest CT findings, and esophageal pH monitoring results. Results: We analyzed 21 patients (mean age, 9.2 ± 2.98 years). Of those, 18 (86%) were atopic. Most had uncontrolled asthma and near-normal baseline lung function. In 4 and 7, induced sputum was found to be eosinophilic and neutrophilic, respectively; the inflammatory cell profile in induced sputum having changed in 67% of those in whom induced sputum analysis was repeated. Of the 8 patients receiving treatment with omalizumab (an anti-IgE antibody), 7 (87.5%) showed significant improvement in quality of life, as well as significant reductions in the numbers of exacerbations and hospitalizations. Conclusions: Children with STRA present with near-normal lung function and a variable airway inflammatory pattern during clinical follow-up, showing a significant clinical response to omalizumab. In children, STRA differs from that seen in adults, further studies being required in order to gain a better understanding of the disease mechanisms.

Asthma is associated with a loss of the structural integrity of airway epithelium and dysfunction of the physical barrier, which protects airways from external harmful factors. Granulocyte activation causes the formation of extracellular traps, releasing web-like structures of DNA and proteins, being important to kill pathogens extracellularly. We investigated whether eosinophils infiltrating airways in an experimental model of asthma would induce eosinophil extracellular traps (EETs) in bronchoalveolar lavage fluid and lung tissue. We showed that an ovalbumin (OVA) asthma protocol presented a significant increase in eosinophil counts with increased extracellular DNA in bronchoalveolar lavage fluid as well as in lung tissue, confirming the presence of DNA traps colocalized with eosinophil peroxidase. EETs formation was reversed by DNase treatment. With these approaches, we demonstrated for the first time that OVA-challenged mice release extracellular DNA traps, which could aggravate pulmonary dysfunction.