Atomic force microscopy analysis of the surface alterations of enamel, dentin, composite and ceramic materials exposed to low oral pH in GERD.

Dental erosion is a significant topic in medical literature, both for gastroenterology and dental medicine. Dental structure loss has a psychosocial and functional significance. The pathogenesis of dental erosion in patients diagnosed with gastroesophageal reflux disease (GERD) characterized by the presence of an acidic oral environment after reflux episodes, is not well understood. The present study was designed to observe the effect of low oral pH in time on natural surfaces including enamel and dentine, but also on materials used in treating these dental destructions such as composites and ceramics. The acidic oral environment was estimated in relation to salivary pH. In the dental laboratory, 5-mm2 and 1-mm composite pieces of thick enamel, dentine, Emax Ceramic and Nexco Ivoclar were cut in order to be analyzed using atomic force microscopy (AFM) and to observe the surface alterations. Gastric acid was collected and mixed with saliva until a pH value of 6.0 was obtained, in which the pieces were immersed for 24, 120, 240 h. Roughness of each surface was calculated at a microstructure and nanostructure level. The results showed significant alterations in enamel and dentine exposed to a lower pH level beginning even at a short immersion time, in comparison with composites and ceramics which had no alterations. In conclusion, multidisciplinary attention should be given to detect and manage acidity of the oral cavity caused by GERD, in order to prevent dental erosion.

Interleukin-1A and interleukin-1B gene polymorphisms in gastroesophageal reflux disease.

Inflammation may play contradictory roles in the pathogenesis of gastroesophageal reflux disease (GERD): gastritis decreases gastric output and reduces the risk of esophagitis, while interleukins may favor mucosal inflammation. The inflammation may cause esogastric motility changes and thus increase the risk of esophagitis. Considering the genetic influence of inflammatory response, we looked for the genetic polymorphisms of IL-1 in GERD manifested as reflux esophagitis. This is a prospective study carried out in GERD and healthy controls. We assessed in these groups the following single nucleotide polymorphisms (SNPs): IL-1A (rs1800587), IL-1B (rs16944), IL-1B (rs1143634) and the VNTR for IL-1RN. Both groups were similar according to biographical data. Reflux esophagitis was confirmed by endoscopy and where necessary by pH-impedance monitoring. Reflux esophagitis was associated only with the polymorphism rs16944. No other correlations with the other three genetic polymorphisms were detected. These data suggest that the diverging effects of proinflammatory factors on the upper digestive tract may have deleterious effect on GERD. The IL-1B (rs16944) SNP correlates with reflux esophagitis.