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Background and Objectives In the oral cavity, the epithelial surface is constantly exposed to a number of different microorganisms that are organized in a well-structured biofilm. The aim of this study was to monitor gingival expression of antimicrobial peptides ( AMPs) and interleukin-8 ( IL-8) in an early gingivitis model. Material and Methods Experimental gingivitis was allowed to develop in healthy volunteers ( n = 17). Bleeding on probing ( BOP%) and gingival crevicular fluid volume ( GCF) were assessed at baseline and day 1, 3, 5, 7 and 14. Expression of AMPs (human beta-defensin-2, hBD-2; CC-chemokine ligand 20, CCL20; psoriasin, pso/ S100 A7) and IL-8 was analyzed by immunohistochemistry in gingival biopsies. In addition, hBD-2 and IL-8 protein expression was monitored in GCF using the ELISA technology. Results Experimental gingivitis gradually developed with an increase in BOP scores and GCF volume over time. In GCF, elevated concentrations of hBD-2 and IL-8 were monitored at day 1, 5 and 7 ( p ≤ 0.0002). Immunohistochemical analysis of gingival sections demonstrated increased staining for hBD-2 at day 3, whereas the CCL20, pso/ S100 A7, and IL-8 expression was increased at later time points ( p < 0.05). Conclusion For the first time, this study showed the time-dependent regulation of AMPs, following clinical signs of experimentally induced gingival inflammation. Differential temporal expression for AMPs may ensure a constant antimicrobial activity against changes in the bacterial composition of the growing dental biofilm. [ABSTRACT FROM AUTHOR]

Introduction: The aim of the study was to examine the effect of an elaborate feedback and an audience response system (ARS) on learning success., Methods: Students of the 1st clinical semester were randomly assigned to a study and a control group. The randomization was carried out considering the factors of age, gender and power spectrum during preliminary dental examination. Within 10 lectures 5 multiple-choice questions were asked about the learning objectives and answered by the students using an ARS. Only the study group received an immediate comprehensive feedback on the results. A final exam at the end was carried out in order to evaluate whether the elaborate feedback leads to a successful learning. Furthermore the effect of the ARS on the lecture atmosphere was investigated., Result: The results of the final exams showed no significant difference between the study and the control group regarding the learning success., Conclusion: Although no significant effect on learning success was found, the ARS creates a more interactive, positive learning environment.

Aim: Many studies investigated the role of genetic variants in periodontitis, but few were established as risk factors. We aimed to validate the associations of recent candidate genes in aggressive periodontitis (AgP)., Material and Methods: We analysed 23 genes in 600 German AgP patients and 1441 controls on the Illumina custom genotyping array Immunochip. We tested a suggestive association in a Dutch and German/Austrian AgP case-control sample, and a German chronic periodontitis (CP) case-control sample using Sequenom iPlex assays. We additionally tested the common known risk variant rs1333048 of the gene ANRIL for its association in a Turkish and Italian population., Results: None of the analysed genes gave statistical evidence for association. Upon covariate adjustment for smoking and gender, in the pooled German-Austrian AgP sample, IL10 SNP rs6667202 was associated with p = 0.016, OR = 0.77 (95% CI = 0.6-0.95), and in the Dutch AgP sample, adjacent IL10 SNP rs61815643 was associated with p = 0.0009, OR = 2.31 (95% CI = 1.4-3.8). At rs61815643, binding of the transcription factor PPARG was predicted. ANRIL rs1333048 was associated in the Turkish sample (pallelic = 0.026, OR = 1.67 [95% CI = 1.11-2.60])., Conclusions: Previous candidate genes carry no susceptibility factors for AgP. Association of IL-10 rs61815643 with AgP is suggested. ANRIL is associated with periodontitis across different populations., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)