In the author’s earlier in vitro investigation, a combination of 0.25 mg/ml green tea and 7.82 mg/ml Salvadora persica L. aqueous extracts was found to exhibit significant synergistic anti-bacterial and anti-adherence effects against primary plaque colonizers biofilm. A clinical trial was needed to support these preliminary in vitro results and to investigate its efficacy as a mouthwash in the control of dental plaque. A 24 h plaque re-growth, double-blinded, randomized crossover trial was carried out. Participants (n = 14) randomly rinsed with test formulation, 0.12% chlorhexidine (control) and placebo mouthwashes for 24 h. A week before the trial, all participants received scaling, polishing and oral hygiene education. On the trial day, the participants received polishing at baseline and rinsed with 15 ml of randomly allocated mouthwash twice daily without oral hygiene measures. After 24 h, plaque index was scored and then the participants entered a 6-days washout period with regular oral hygiene measures. The same protocol was repeated for the next 2 mouthwashes. The results were expressed as mean (±SD) plaque index. The test mouthwash (0.931 ± 0.372) significantly reduced plaque accumulation when compared with placebo (1.440 ± 0.498, p < 0.0167) and chlorhexidine (1.317 ± 0.344, p < 0.0167) mouthwashes. No significant difference was found between chlorhexidine and placebo (p > 0.0167). The test mouthwash has an anti-plaque effect for a 24 h period. Longer-term clinical studies are highly encouraged to investigate its anti-plaque effect for longer periods. This study was registered in ClinicalTrials.gov as NCT02624336 in December 3, 2015.
26 February 2020 in International Journal of Dental Hygiene
Background: To determine the prevalence and severity of periodontitis in an Iraqi population using the 2017 classification. Methods: Data on the periodontal status of patients were retrospectively collected from healthcare records. The information included demographics, clinical parameters including bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment loss (CAL). Descriptive and inferential statistical analyses were performed using SPSS (version 26, IBM, USA) software. Results: Out of 1578 records, the periodontal health, gingivitis, and periodontitis represented 26.4%, 37.1%, and 36.5%, respectively with males more affected by periodontal disease compared with females. Periodontitis cases were dominated by stage 3 and 4 which combined accounted for 77.3%, followed by stage 2 (21.3%), and stage 1 (1.4%). When looking at disease grade and levels of stability, localized pattern, Grade C, and unstable status were the most prevalent domains. Regression analysis suggested age, BOP, male, and positive family history as predictors for increasing extent and severity of CAL both in periodontal health and disease. Conclusion: The prevalence of periodontal disease (periodontitis, and gingivitis) was almost equally expressed. Severe periodontitis was the most dominant group whilst milder forms of disease were least prevalent. The data indicated that demographic variables and clinical parameters could predict severity of attachment loss.
Background: In literature, the levels of miRNA-146a and miRNA-155 are increased in periodontitis. Limited data are available regarding the expression of miRNA-146a and miR-NA-155 in diseased human peri-implant tissue. Therefore, the objective of this study was to explore the expression of miRNA-146a and miRNA-155 in human gingival peri-implant tissue affected by peri-implantitis. Methods: After recording the clinical parameters, human peri-implant pocket tissues were harvested from sites diagnosed with peri-implantitis (n = 15 cases) in addition to healthy peri-implant sulcus tissues (n = 15 controls). The levels of miRNA-146a and miRNA-155 were assessed using real-time qPCR. Results: Cases exhibited a significantly higher mean expression of miRNA-155 (5.2-fold increase) and miRNA-146a (2.8-fold increase) than controls. MiRNA-155 and miRNA-146a demonstrated an appropriate sensitivity (87.5% and 87.5%, respectively) and specificity (73.3% and 66.7%, respectively) in discriminating cases from controls. A moderate correlation (r = 0.544, p = 0.029) was found between miRNA-155 and miRNA-146a levels in the case group. Conclusions: The expressions of miRNA-146a and miR-NA-155 are different between healthy and peri-implantitis affected tissues. Both miRNAs might potentially able to discriminate healthy from peri-implantitis affected tissues.
Inflammation of periodontal tissues is the consequence of interaction between periodontal pathogens and immune system. This is associated with increased expression of inflammatory cytokines, which may exert destructive effect to the periodontal tissues when released over long period. The aim of this study was to chronologically track the homeostasis of oral keratinocytes following removal of periodontal pathogens. This was done by investigating expression of selected inflammatory markers and integrity of epithelial monolayers in vitro. Rat oral keratinocytes were stimulated with heat-killed Fusobacterium nucleatum and Porphyromonas gingivalis over 7-days then bacteria were washed away and epithelial cells re-cultured for 3-days. Expression of IL-1β, IL-6, and IL-8 was measured by ELISA while transcription of tissue inhibitor of metalloproteinase-1 (TIMP-1) and matrix metalloproteinase -8 (MMP-8) was measured by polymerase chain reaction before and after removal of bacteria. Integrity of epithelial sheet was investigated by using transepithelial electrical resistance. Data showed general downregulation of IL-1b, IL-6, and IL-8 associated with restoring transcription of TIMP-1 and MMP-8 to normal level following removal of bacteria from epithelial cultures. However, expression of IL-8 and MMP-8 remained significantly higher than unstimulated epithelial cells despite withdrawal of F. nucleatum and P. gingivalis respectively from oral keratinocytes cultures. In addition, integrity of epithelial barrier function remained compromised even after removal of P. gingivalis. Results suggest that even after three days following removal of periodontal pathogens, oral keratinocytes sustained persistent upregulation of certain inflammatory markers that could compromise integrity of epithelial barrier function.