Coating failure of commercial orthodontic magnets and DNA fragmentation of oral mucosa cells.

OBJECTIVE: To investigate possible adverse effects of orthodontic magnets on the oral mucosa. METHODS: Twenty orthodontic patients, between 14 and 20 years of age, were used. All patients consented to participate in the trial, which ran for six months. Following extraction of the first premolars, samarium-cobalt (SmCo5) orthodontic magnets were used to move the upper right canines into the extraction spaces. The contralateral canines were retracted with elastomeric chain. The orthodontic appliance consisted of direct-bonded standard edgewise fibreglass brackets and molar tubes, and teflon-coated preformed archwires. At regular scheduled visits the following were recorded: the condition of the protective magnet coating; weight loss by the magnets; levels of nickel, iron and chromium ions in unstimulated saliva; viability of recovered oral mucosa cells with trypan blue. DNA fragmentation of the oral mucosa cells was analysed at the start of the trial, after one week, one month, three months and six months with the single cell gel electrophoresis assay (Comet assay). The elemental compositions of five magnets were assessed with energy dispersive X-ray microanalysis. RESULTS: By the third month the magnets had lost their protective resin coats. At six months the magnets had lost 3 per cent of their initial weights. Significant weight loss and raised saliva levels of nickel, iron and chromium ions occurred from the first week. The number of oral mucosa cells with DNA fragmentation increased steadily on both sides of the mouth from the first week. More DNA fragmented cells occurred on the Magnet side than on the Non-magnet side. The trial was discontinued when half of the subjects showed DNA damaged mucosal cells. CONCLUSIONS: Because the protective coating failed after a few weeks, orthodontic magnets are unsuitable for long-term intra-oral use. It is uncertain if the greater cell damage on the Magnet side was due to the corrosion products, proximity to the static magnetic field or both factors.

Prevalence of celiac disease, Helicobacter pylori and gastroesophageal reflux in patients with refractory iron deficiency anemia.

OBJECTIVE: The aim of this article is to determine the prevalence of celiac disease (CD), Helicobacter pylori (H. pylori) and gastroesophageal reflux (GER) in patients with resistant iron deficiency anemia (IDA). PATIENTS: The study included 25 patients <18 years of age with refractory IDA (not responding to iron therapy for 3 months in a dose of 6 mg elemental iron/kg/day). METHODS: All patients included in the study were subjected to careful history taking and thorough clinical examination. Blood sample was taken for analysis of antibodies for CD including: antigliadin antibody (AGA), antiendomysial antibody (EMA), antireticulin antibody (ARA) and antitissue Transglutaminase (tTg) IgG antibody. Anti-H. pylori IgG antibodies and a (13)C-urea breath test (UBT) was done to all patients to diagnose H. pylori. Upper gastrointestinal tract endoscopy was done for all patients to evaluate for the presence of some etiologies of intractable anemia as chronic blood loss. These included: CD, H. pylori infection and GER. The upper gastrointestinal tract endoscopy was also done to evaluate the presence of bleeding spots, ulcers or angiomatous malformations. In addition, gastric antral biopsies were taken for diagnosis of H. pylori infection by the following tests: rapid urease test, histopathological examination and culture. RESULTS: CD was positive in 11 out of 25 patients (44%), H. pylori infection in 12 out of 25 patients (48%), while GER was diagnosed in 11 out of 25 patients (44%). Patients with CD had age of presentation < or =2 years in two patients (18.2%) while the remaining nine patients (81.8%) had age of presentation >2 years and it was statistically significant (p = 0.05*). Also patients with H. pylori had age of presentation < or =4 years in five patients (41.7%) and the remaining seven patients (81.8%) had age of presentation >4 years and it was statistically significant (p = 0.03*). Logistic regression analysis demonstrated that the risk factors for severity of anemia were age of patients and duration of anemia. On the other hand, other parameters have no significant influence on the severity of anemia. Also risk factors of short stature were age of presentation of anemia, degree of anemia and H. pylori infection. AGA had the highest sensitivity (100%) followed by antiendomysium antibody (81.8%) while the tTG antibody had the highest specificity (85.7%) for diagnosis of CD. UBT and histopathology had the highest sensitivity (100%) for diagnosis of H. pylori while rapid urease test, culture, H. pylori stool antigen and anti-H. pylori IgG antibody had the highest specificity (100%). In conclusion, refractory IDA may be due to clinically unapparent H. pylori gastritis and CD. CD is one of the most common causes of intestinal malabsorption during childhood which leads to impairment of iron absorption. Apart from offering them gluten-free diet rich in iron, early detection and treatment of IDA and prophylactic iron and folic acid supplementation will go a long way to optimize their mental and psychological functions. Eradication of H. pylori infection with concomitant iron therapy should correct the anemia.