11 research outputs found
Characterization of the nanoscratch, microstructure, and composition in hypoplastic amelogenesis imperfecta
Genetic variation in Ameloblastin is associated with caries in asthmatic children
AIM: Evidence suggests caries experience is higher in children with asthma. In this study, we compared caries experience in asthmatic and non-asthmatic children and defined whether variation in the distribution of caries experience differs between the two groups and is dependent of the presence of genetic variation in enamel formation genes. METHODS: Children with asthma were recruited at the Istanbul University, Faculty of Medicine, Department of Pediatrics, Division of Pediatric Allergy and Pulmonary Diseases, and non-affected children were recruited at the Istanbul University, Faculty of Dentistry, Department of Pedodontics. Cases (N=100) were defined as children between the ages of 6 and 12 years with asthma and controls (N=100) as children without asthma. Cases and controls were matched by sex and age. All study subjects received a complete dental exam, provided demographic and other caries and asthma risk factors data, and a saliva sample for DNA extraction. Caries experience was defined based on DMFT/dmft and DMFS/dmfs scores. Genotypes of 11 SNPs were selected in intronic regions of enamel development genes. PCR with TaqMan chemistry were used for genotyping all selected markers. Association between caries experience (caries free versus caries affected) depending on asthma status and SNPs was tested with PLINK by logistic regression, adjusting by risk, and other preventive measures. P-values below 0.0045 (0.05/11) were considered statistically significant. RESULTS: Logistic regression analysis showed an association between AMBN rs4694075 and caries experience (p=2.525e-007). CONCLUSIONS: Our study provides, for the first time, evidence that ameloblastin is associated with caries in asthmatic children
Role of sortase in Streptococcus mutans under the effect of nicotine
Streptococcus mutans is a common Gram-positive bacterium and plays a significant role in dental caries. Tobacco and/or nicotine have documented effects on S. mutans growth and colonization. Sortase A is used by many Gram-positive bacteria, including S. mutans, to facilitate the insertion of certain cell surface proteins, containing an LPXTGX motif such as antigen I/II. This study examined the effect of nicotine on the function of sortase A to control the physiology and growth of S. mutans using wild-type S. mutans NG8, and its isogenic sortase-defective and -complemented strains. Briefly, the strains were treated with increasing amounts of nicotine in planktonic growth, biofilm metabolism, and sucrose-induced and saliva-induced antigen I/II-dependent biofilm formation assays. The strains exhibited no significant differences with different concentrations of nicotine in planktonic growth assays. However, they had significantly increased (P≤0.05) biofilm metabolic activity (2- to 3-fold increase) as the concentration of nicotine increased. Furthermore, the sortase-defective strain was more sensitive metabolically to nicotine than the wild-type or sortase-complemented strains. All strains had significantly increased sucrose-induced biofilm formation (2- to 3-fold increase) as a result of increasing concentrations of nicotine. However, the sortase-defective strain was not able to make as much sucrose- and saliva-induced biofilm as the wild-type NG8 did with increasing nicotine concentrations. These results indicated that nicotine increased metabolic activity and sucrose-induced biofilm formation. The saliva-induced biofilm formation assay and qPCR data suggested that antigen I/II was upregulated with nicotine but biofilm was not able to be formed as much as wild-type NG8 without functional sortase A
