10 research outputs found

    Tooth Color Change Due To Different Etching And Debonding Procedures

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    Objectives: To compare the effects of different etching techniques, 12-, 24-bladed tungsten carbide burs, and polishing discs on tooth color changes during orthodontic treatment. Materials and Methods: 59 individuals (mean age: 15.20 +/- 1.59 years) were divided into four groups: 37% phosphoric acid and adhesive primer was used in Groups I and II whereas self-etch primer was used in Groups III and IV for enamel preparation. After orthodontic treatment, residual adhesives were cleaned with 12-bladed tungsten carbide burs in Groups I and III, while 24-bladed tungsten carbide burs were used in Groups II and IV. All teeth were polished with medium and fine Sof-Lex XT discs (3M ESPE, St Paul, Minnesota). Color measurements were taken from upper incisors and canines at pretreatment (T0), after cleaning with tungsten carbide burs (T1) and polishing with discs (T2). Wilcoxon test was used for evaluation of L*, a*, b* changes and Kruskal-Wallis for intergroup comparison of color changes. Results: L*, a*, b* values, except a* at Groups I, II, IV, and b* at Group III, changed significantly (P < .05). Groups III and IV showed significantly different color alterations from T0 to T1 (P < .05). After polishing, tooth color alterations were not significantly different among the groups. Conclusions: In self-etch bonding groups, a 12-bladed tungsten carbide bur caused less color change than the 24-bladed tungsten carbide bur. Orthodontic treatment resulted with visible and clinically unacceptable tooth color alterations regardless of the enamel preparation and clean-up techniques. Polishing reduced the effect of tungsten carbide burs, but did not affect the total influence of orthodontic treatment on the tooth color.WoSScopu

    Relationship between midpalatal suture maturation and age and maturation of cervical vertebrae: radiographic evaluation

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    Objective: To evaluate the stages of midpalatal suture (MPS) maturation in patients older than 15 years, and to determine the correlation between the stage of MPS maturation and age and cervical vertebral maturation (CVM). Materials and Method: Cone-beam computed tomography (CBCT) scans of 50 patients (29 female and 21 male; mean age, 19.79 ± 4.09 years) were evaluated. Good quality CBCT images from 15–30-year-old patients for evaluation of impacted canines or determination of orthognathic surgery were selected. The CBCT images were evaluated at two different time intervals for determination of the stages of MPS and CVM. The stages of MPS maturation were classified as A, B, C, D, or E using the axial sections by using a method validated previously. The stages of CVM were classified using sagittal sections of the CBCT images. Intra-examiner agreement was assessed using the Kappa test. The correlations between MPS maturation and chronological age and CVM were assessed using Spearman’s rank correlation analysis. Results: The Kappa coefficients for intra-examiner agreement were 0.837 and 0.865 for classification of the stages of MPS maturation and CVM, respectively. No significant correlation was observed between chronological age and maturation of MPS (r = 0.212, p = 0.139) and between the stages of CVM and maturation of MPS (r = 0.030, p = 0.839). Conclusion: The limitation of our study was a small sample size, and, on the basis of our results, neither CVM nor chronological age could be used as a convenient tool to determine the stage of MPS maturation in 15–30-year-old patients

    Cluster analysis of paediatric Behcet's disease: Data from The Pediatric Rheumatology Academy-Research Group

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    Objectives Behcet's disease (BD) is a systemic vasculitis affecting many organ systems, with the involvement of all-sized arteries and veins. The study aims to determine the main characteristics of paediatric BD patients and also analyse the clustering phenotypes. Methods Demographic data, clinical manifestations, laboratory features, treatment schedules, and disease outcomes were achieved from patients' charts retrospectively. A cluster analysis was performed according to the phenotype. Results A total of 225 (109 male/116 female) patients with BD were enrolled in the study. The median ages of disease onset and diagnosis were 131 (36-151) and 156 (36-192) months, respectively. According to cluster analysis, 132 (58.6%) patients belonged to the mucocutaneous-only cluster (C1), while 35 (15.6%) patients fitted to articular type (C2), 25 (11.1%) were in the ocular cluster (C3), 26 (11.6%) were in the vascular cluster (C4), and 7(3.1%) belonged to the gastrointestinal cluster (C5). Ocular and vascular clusters were more common in boys (p < .001), while girls usually presented with the mucocutaneous-only cluster. The disease activity at the diagnosis and the last control was higher in ocular, vascular, and gastrointestinal clusters. Conclusions These identified juvenile BD clusters express different phenotypes with different outcomes Our analysis may help clinicians to identify the disease subtypes accurately and to arrange personalized treatment

    Real-Life Data From the Largest Pediatric Familial Mediterranean Fever Cohort

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    Familial Mediterranean fever (FMF) is the most common monogenic autoinflammatory disease manifesting phenotypic heterogeneity. It is a clinically diagnosed disease supported by MEditerranean FeVer (MEFV) gene mutation analysis. However, the phenotype-genotype correlation is not yet established clearly. We aimed to determine the clinical findings, phenotype-genotype correlation, and treatment outcomes within a large pediatric FMF cohort. The medical charts of children with FMF who were diagnosed and followed up at the eight pediatric rheumatology units were reviewed retrospectively. All patients in the cohort were analyzed for sequence variants in exon 2,3,5 and 10 of the MEFV gene. Patients without any mutations or with polymorphisms including R202Q were excluded. A total of 3,454 children were involved in the study. The mean +/- standard deviation of current age, age at symptom onset, and age at diagnosis were 12.1 +/- 5.2, 5.1 +/- 3.8, and 7.3 +/- 4.0 years, respectively. Of 3,454 patients, 88.2% had abdominal pain, 86.7% had fever, 27.7% had arthritis, 20.2% had chest pain, 23% had myalgia, and 13.1% had erysipelas-like erythema. The most common MEFV mutation patterns were homozygous (32.5%) and heterozygous (29.9%) mutations of exon 10. Homozygous M694V was present in 969 patients (28.1%). Allele frequencies of common mutations were M694V (55.3%), M680I (11.3%), V726A (7.6%), and E148Q (7.2%). Children carrying homozygous or compound heterozygous exon 10 mutations had an earlier age of disease onset (4.6 vs. 5.6 years, p = 0.000) and a higher number of attacks per year (11.1 vs. 9.6, p = 0.001). Although 8% of the patients had a family history of amyloidosis, 0.3% (n = 11) had the presence of amyloidosis. M694V homozygosity was detected in nine patients who developed amyloidosis. Colchicine resistance was present in 4.2% of our patients. In this largest pediatric cohort reviewed and presented to date, patients with exon 10 mutations, particularly the M694V homozygous mutation, have been demonstrated earlier disease onset, annual attack count, and more frequent colchicine-resistant cases. Although E148Q is considered as a polymorphism in some populations, it was identified as a disease-causing mutation in our cohort. Secondary amyloidosis is still happening in adults however, it is extremely rare among children, presumably due to increased awareness, tight control, and the availability of anti-IL1 agents in colchicine-resistant cases

    Differences and similarities of multisystem inflammatory syndrome in children, Kawasaki disease and macrophage activating syndrome due to systemic juvenile idiopathic arthritis: a comparative study

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    To compare the clinical and laboratory findings of multisystem inflammatory syndrome in children (MIS-C), patients with Kawasaki disease (KD) and with macrophage activating syndrome due to systemic juvenile idiopathic arthritis (sJIA-MAS) on real-life data. Patients diagnosed with MIS-C, KD, and sJIA-MAS from 12 different centers in Turkey who were followed for at least 6 months were included in the study. Demographic, clinical, and laboratory findings of all patients were analyzed. A total of 154 MIS-C, 59 KD, and 31 sJIA-MAS patients were included. The median age of patients with MIS-C were higher than those with KD while lower than those with sJIA-MAS (8.2, 3, 12 years, respectively). Myalgia (39.6%), cardiac (50.6%), gastrointestinal (72.7%), and neurological (22.1%) involvements were more common in patients with MIS-C compared to others. MIS-C patients had lower levels of lymphocyte (950 vs 1700 cells/mu l) and thrombocyte (173,000 vs 355,000 cells/mu l) counts and higher pro-BNP (1108 vs 55 pg/ml) levels than KD. Ferritin levels were higher in patients with MIS-C compared to patients with KD while they were lower than patients with sJIA-MAS (440, 170, 10,442 ng/ml, respectively). Patients with MIS-C had a shorter duration of hospitalization than sJIA-MAS (p = 0.02) while they required intensive care unit admission more frequently (55 vs 8 patients, p < 0.001). The median MAS/sJIA score of MIS-C patients was - 1.64 (- 5.23 to 9.68) and the median MAS/sJIA score of sJIA-MAS patients was -2.81 ([- 3.79] to [- 1.27]). MIS-C patients displayed certain differences in clinical and laboratory features when compared to KD and sJIA-MAS. Definition of the differences and similarities between MIS-C and the other intense inflammatory syndromes of childhood such as KD and MAS will help the clinicians while making timely diagnosis

    Inborn errors of OAS–RNase L in SARS-CoV-2–related multisystem inflammatory syndrome in children

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    International audienceMultisystem inflammatory syndrome in children (MIS-C) is a rare and severe condition that follows benign COVID-19. We report autosomal recessive deficiencies of OAS1 , OAS2 , or RNASEL in five unrelated children with MIS-C. The cytosolic double-stranded RNA (dsRNA)–sensing OAS1 and OAS2 generate 2′-5′-linked oligoadenylates (2-5A) that activate the single-stranded RNA–degrading ribonuclease L (RNase L). Monocytic cell lines and primary myeloid cells with OAS1, OAS2, or RNase L deficiencies produce excessive amounts of inflammatory cytokines upon dsRNA or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) stimulation. Exogenous 2-5A suppresses cytokine production in OAS1-deficient but not RNase L–deficient cells. Cytokine production in RNase L–deficient cells is impaired by MDA5 or RIG-I deficiency and abolished by mitochondrial antiviral-signaling protein (MAVS) deficiency. Recessive OAS–RNase L deficiencies in these patients unleash the production of SARS-CoV-2–triggered, MAVS-mediated inflammatory cytokines by mononuclear phagocytes, thereby underlying MIS-C
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