Impact of the uninstructed use of a herbal, ayurvedic toothpaste on parameters of gingival health in periodontal aftercare patients: A randomized, double-blinded, two-arm parallel-group study.

AIM: The aim of this study was to evaluate the impact of the uninstructed use of a toothpaste containing herbal ayurvedic ingredients on parameters of gingival health in a cohort of periodontal aftercare patients affected by gingival inflammation compared to the use of a standard, non-herbal toothpaste. MATERIALS AND METHODS: The monocentric, randomized, double-blinded, two-arm parallel-group intervention was performed in a cohort of 88 periodontal aftercare patients with clinical signs of gingival inflammation. At baseline, bleeding on probing (BoP), gingival index (GI) and Quigley-Hein plaque index (QHI) were recorded. Subsequently, the study patients were randomly provided with a herbal ayurvedic toothpaste (n = 44) or a conventional, non-ayurvedic control toothpaste (n = 44) and without additional oral hygiene training instructed to use it 2× daily for the next 28 days. On day 28, BoP, GI and QHI were recorded again. RESULTS: At baseline, there were no significant differences between both groups. On day 28, mean GI and BoP scores were significantly lower (p < 0.001) compared to baseline in both groups. Differences between the groups could not be verified. Mean QHI scores did not change significantly between day 0 and day 28 in both groups. CONCLUSIONS: The impact of uninstructed toothbrushing with an ayurvedic toothpaste on the manifestation of gingival inflammation in periodontal aftercare patients is not significantly different to the use of a conventional, non-herbal toothpaste.

Impact of Dietary Nitrate on the Recovery of Therapy-related Vascular Health Impairments Following Standard Periodontal Aftercare Therapy: a Hypothesis-generating Subanalysis.

This follow-up study assessed the impact of a nitrate-rich diet on salivary nitrate/nitrite levels and the recovery of therapy-induced vascular impairments in a cohort of 39 periodontitis patients treated by standard subgingival mechanical plaque removal (PMPR). At baseline, saliva samples for nitrate/nitrite analysis were collected, and peripheral/central blood and augmentation pressure was documented using the Arteriograph recording system. Immediately after, PMPR vascular parameters were reassessed. All study patients received a randomly allocated supply of a lettuce beverage to be consumed for 14 days, containing either a daily dosage of 200 mg nitrate (test group, n = 20) or being void of nitrate (placebo group, n = 19). At day 14, salivary and vascular parameters were reassessed. Initial salivary and vascular parameters did not differ significantly between the groups. PMPR impaired all vascular parameters in both groups with no differences between the groups. At day 14, salivary nitrate/nitrite levels of the test group were significantly elevated compared to baseline. All vascular parameters had significantly recovered from the impairment inflicted by PMPR. In the placebo group, by contrast, salivary parameters did not differ significantly from baseline, and the recovery of impaired vascular parameters was restricted to a significant improvement of diastolic blood pressure. Correlation analysis identified a significant inverse correlation between salivary nitrate/nitrite sum and central/peripheral blood pressure and augmentation pressure. In conclusion, the data of this subanalysis suggest that increasing salivary nitrate/nitrite levels by a diet rich in nitrate may improve recovery of therapy-induced vascular impairments after PMPR.

Impact of a Specific Collagen Peptide Food Supplement on Periodontal Inflammation in Aftercare Patients-A Randomised Controlled Trial.

Background: This controlled clinical trial evaluated the impact of a specific collagen peptide food supplement on parameters of periodontal inflammation in aftercare patients. Methods: A total of 39 study patients were enrolled. At baseline, bleeding on probing (BoP; primary outcome), gingival index (GI), plaque control record (PCR), recession (REC) and probing pocket depth (PPD) for the calculation of the periodontal inflamed surface area (PISA) were documented. After subsequent professional mechanical plaque removal (PMPR), participants were randomly provided with a supply of sachets containing either a specific collagen peptide preparation (test group; n = 20) or a placebo (placebo group; n = 19) to be consumed dissolved in liquid once daily until reevaluation at day 90. Results: PMPR supplemented with the consumption of the specific collagen peptides resulted in a significantly lower mean percentage of persisting BoP-positive sites than PMPR plus placebo (test: 10.4% baseline vs. 3.0% reevaluation; placebo: 14.2% baseline vs. 9.4% reevaluation; effect size: 0.86). Mean PISA and GI values were also reduced compared to baseline, with a significant difference in favor of the test group (PISA test: 170.6 mm2 baseline vs. 53.7 mm2 reevaluation; PISA placebo: 229.4 mm2 baseline vs. 184.3 mm2 reevaluation; GI test: 0.5 baseline vs. 0.1 reevaluation; GI placebo: 0.4 baseline vs. 0.3 reevaluation). PCR was also significantly decreased in both experimental groups at revaluation, but the difference between the groups did not reach the level of significance. Conclusions: The supplementary intake of specific collagen peptides may further enhance the anti-inflammatory effect of PMPR in periodontal recall patients.

Impact of a two-stage subgingival instrumentation scheme involving air polishing on attachment gain after active periodontal therapy.

BACKGROUND: The aim of this study was to evaluate whether clinical attachment level gain (ΔCAL) in deep untreated periodontal lesions may be improved by a two-stage, subgingival instrumentation scheme involving air polishing. METHODS: This 6-month, randomized, controlled, examiner-masked clinical trial was performed in 44 patients with periodontitis with untreated periodontal lesions ≥6 mm. At baseline, day 28, 84, and 168 CAL, probing depth (PD), bleeding on probing (BOP), and plaque control record (PlaCR) were recorded. After baseline examination control group patients received full-mouth sub- and supragingival instrumentation using scalers and curets. In the test group initial subgingival cleaning was limited to the removal of soft bacterial deposits by air polishing. Subgingival scaling and root planing was performed only after the first re-evaluation at day 28. RESULTS: In deep lesions ≥6 mm a significant reduction of mean CAL scores was observed at day 28 and at day 168 for both experimental groups. Differences between the groups however did not reach the level of significance. Mean PD was also significantly reduced at day 28 and at 168 in both experimental groups, with no significant differences between the groups. Mean BOP scores did not change significantly in both groups during the 168-day observation period. Only in the test group mean PlaCR scores were significantly reduced at day 168 compared with baseline. CONCLUSIONS: Subgingival instrumentation of untreated PD ≥6 mm by air polishing alone results in a significant short-term gain of CAL comparable to conventional scaling and root planing. Its sequential two-step combination with scaling and root planing, however, does not additionally enhance long-term gain of CAL.

Epigenetic adaptations of the masticatory mucosa to periodontal inflammation.

BACKGROUND: In mucosal barrier interfaces, flexible responses of gene expression to long-term environmental changes allow adaptation and fine-tuning for the balance of host defense and uncontrolled not-resolving inflammation. Epigenetic modifications of the chromatin confer plasticity to the genetic information and give insight into how tissues use the genetic information to adapt to environmental factors. The oral mucosa is particularly exposed to environmental stressors such as a variable microbiota. Likewise, persistent oral inflammation is the most important intrinsic risk factor for the oral inflammatory disease periodontitis and has strong potential to alter DNA-methylation patterns. The aim of the current study was to identify epigenetic changes of the oral masticatory mucosa in response to long-term inflammation that resulted in periodontitis. METHODS AND RESULTS: Genome-wide CpG methylation of both inflamed and clinically uninflamed solid gingival tissue biopsies of 60 periodontitis cases was analyzed using the Infinium MethylationEPIC BeadChip. We validated and performed cell-type deconvolution for infiltrated immune cells using the EpiDish algorithm. Effect sizes of DMPs in gingival epithelial and fibroblast cells were estimated and adjusted for confounding factors using our recently developed "intercept-method". In the current EWAS, we identified various genes that showed significantly different methylation between periodontitis-inflamed and uninflamed oral mucosa in periodontitis patients. The strongest differences were observed for genes with roles in wound healing (ROBO2, PTP4A3), cell adhesion (LPXN) and innate immune response (CCL26, DNAJC1, BPI). Enrichment analyses implied a role of epigenetic changes for vesicle trafficking gene sets. CONCLUSIONS: Our results imply specific adaptations of the oral mucosa to a persistent inflammatory environment that involve wound repair, barrier integrity, and innate immune defense.

Sex-specific genetic factors affect the risk of early-onset periodontitis in Europeans.

AIMS: Various studies have reported that young European women are more likely to develop early-onset periodontitis compared to men. A potential explanation for the observed variations in sex and age of disease onset is the natural genetic variation within the autosomal genomes. We hypothesized that genotype-by-sex (G × S) interactions contribute to the increased prevalence and severity. MATERIALS AND METHODS: Using the case-only design, we tested for differences in genetic effects between men and women in 896 North-West European early-onset cases, using imputed genotypes from the OmniExpress genotyping array. Population-representative 6823 controls were used to verify that the interacting variables G and S were uncorrelated in the general population. RESULTS: In total, 20 loci indicated G × S associations (P < 0.0005), 3 of which were previously suggested as risk genes for periodontitis (ABLIM2, CDH13, and NELL1). We also found independent G × S interactions of the related gene paralogs MACROD1/FLRT1 (chr11) and MACROD2/FLRT3 (chr20). G × S-associated SNPs at CPEB4, CDH13, MACROD1, and MECOM were genome-wide-associated with heel bone mineral density (CPEB4, MECOM), waist-to-hip ratio (CPEB4, MACROD1), and blood pressure (CPEB4, CDH13). CONCLUSIONS: Our results indicate that natural genetic variation affects the different heritability of periodontitis among sexes and suggest genes that contribute to inter-sex phenotypic variation in early-onset periodontitis.

The utilization of dental emergency services during COVID-19 pandemic in a German university center: Do we lose vulnerable patients?

OBJECTIVES: The COVID-19 pandemic poses a major challenge to health care worldwide. As a part of the virus containment strategy, health care services were limited to the treatment of essential emergencies. The aim was to evaluate the influence of COVID-19 pandemic on patients' utilization of dental emergency services, focusing on patients vulnerable to severe courses of COVID-19. METHOD AND MATERIALS: Files of 1,299 patients of the Dental School of the University Hospital Wuerzburg between 3 February and 7 June 2020 were retrospectively analyzed. The observation period was divided into pre-lockdown (Pre-L), during lockdown (Dur-L), and post-lockdown (Post-L). Patients' demographics, diagnosis, and medical history including COVID-19 anamnesis were recorded. RESULTS: The number of dental emergency patients decreased by approximately 50% (Pre-L, n = 576; Dur-L, n = 309). Proportions of risk patients among them did not change. Stationary admissions increased by approximately 4% (Pre-L, 12.3% to Dur-L, 16.2%). The most frequent diagnosis was uncontrollable pain (45.6%), originating in 25.2% of endodontic and periodontal diseases. Abscesses (23.0%), dental trauma (16.5%), facial trauma (9.4%), and uncontrollable bleeding (5.5%) followed consecutively. CONCLUSION: Patients with an increased risk for severe courses of COVID-19 infection did not refrain from consulting dental emergency care. Dental emergencies should be treated early to avoid stationary admissions to preserve hospital bed capacities.

Nitrate-rich diet alters the composition of the oral microbiota in periodontal recall patients.

BACKGROUND: This follow-up study evaluated microbiome changes in periodontal recall patients after consuming a nitrate-rich diet that led to a marked decrease of gingival inflammation. METHODS: Subgingival microbial samples of 37 patients suffering from gingival inflammation with reduced periodontium were taken before professional mechanical plaque removal (baseline) and subsequently after 2 weeks of regularly consuming a lettuce juice beverage (day 14) containing a daily dosage of 200 mg of nitrate (test group, n = 18) or being void of nitrate (placebo group, n = 19). Three hundred base pairs paired-end sequencing of the V3-V4 hypervariable region of the 16S rDNA was performed. RESULTS: At baseline, there were no significant differences about the bacterial diversity parameters between the groups (Mann-Whitney U test). After intervention in the test group, Rothia and Neisseria, including species reducing nitrate, increased significantly (negative binomial regression model). Alpha diversity decreased significantly from 115.69 ± 24.30 to 96.42 ± 24.82 aRSVs/sample (P = 0.04, Wilcoxon signed-rank test), accompanied by a significant change in beta diversity (P < 0.001, PERMANOVA). In the control group, however, no genus changed significantly, and alpha-, as well as beta-diversity did not change significantly. CONCLUSIONS: The decrease of gingival inflammation in periodontal recall patients induced by a nitrate-rich diet is accompanied by significant compositional changes within the subgingival microbiome.

Impact of 0.1% octenidine mouthwash on plaque re-growth in healthy adults: a multi-center phase 3 randomized clinical trial.

OBJECTIVES: To investigate plaque inhibition of 0.1% octenidine mouthwash (OCT) vs. placebo over 5 days in the absence of mechanical plaque control. MATERIALS AND METHODS: For this randomized, placebo-controlled, double-blind, parallel group, multi-center phase 3 study, 201 healthy adults were recruited. After baseline recording of plaque index (PI) and gingival index (GI), collection of salivary samples, and dental prophylaxis, subjects were randomly assigned to OCT or placebo mouthwash in a 3:1 ratio. Rinsing was performed twice daily for 30 s. Colony forming units in saliva were determined before and after the first rinse. At day 5, PI, GI, and tooth discoloration index (DI) were assessed. Non-parametric van Elteren tests were applied with a significance level of p < 0.05. RESULTS: Treatment with OCT inhibited plaque formation more than treatment with placebo (PI: 0.36 vs. 1.29; p < 0.0001). OCT reduced GI (0.04 vs. placebo 0.00; p = 0.003) and salivary bacterial counts (2.73 vs. placebo 0.24 lgCFU/ml; p < 0.0001). Tooth discoloration was slightly higher under OCT (DI: 0.25 vs. placebo 0.00; p = 0.0011). Mild tongue staining and dysgeusia occurred. CONCLUSIONS: OCT 0.1% mouthwash inhibits plaque formation over 5 days. It therefore can be recommended when regular oral hygiene is temporarily compromised. CLINICAL RELEVANCE: When individual plaque control is compromised, rinsing with octenidine mouthwash is recommended to maintain healthy oral conditions while side effects are limited.

Consumption of Lactobacillus reuteri-containing lozenges improves periodontal health in navy sailors at sea: A randomized controlled trial.

BACKGROUND: The objective of this trial was to evaluate whether the regular consumption of probiotics may improve the known deterioration of periodontal health in navy sailors during deployments at sea. METHODS: 72 healthy sailors of a naval ship on a practicing mission at sea were recruited and randomly provided with a blinded supply of lozenges to be consumed twice daily for the following 42 days containing either the probiotic strains Lactobacillus reuteri (DSM 17938 and L. reuteri (ATTC PTA 5289) (test n = 36) or no probiotics (placebo n = 36). At baseline, at day 14 and day 42 bleeding on probing (primary outcome), gingival index, plaque control record, probing attachment level, and probing pocket depth were assessed at the Ramfjord teeth. RESULTS: At baseline there were no significant differences between the groups. At day 14 and day 42 test group scores of all assessed parameters were significantly improved (P < 0.001) compared to baseline and to the placebo group which by contrast showed a significant (P < 0.001) deterioration of all parameters at the end of the study. CONCLUSIONS: The consumption of probiotic L. reuteri-lozenges is an efficacious measure to improve and maintain periodontal health in situations with waning efficacy of personal oral hygiene.

Status of periodontal health in German patients suffering from chronic kidney disease-Data from the GCKD study.

AIM: To assess the prevalence and severity of periodontitis in patients with moderate chronic kidney disease (CKD) and comparing the results with the self-reported periodontitis awareness of the study subjects. MATERIAL AND METHODS: The periodontal status of 270 patients with moderate CKD randomly selected from a cohort of 5,217 subjects participating in the prospective observational German Chronic Kidney Disease (GCKD) project was analysed by recording bleeding on probing (BOP), probing pocket depth (PPD) and clinical attachment level (CAL). Furthermore, the awareness of the study subjects of their periodontal conditions was evaluated by a self-reported questionnaire. RESULTS: 24.4% of the CKD study patients showed no or only mild signs of periodontal disease, 47.6% displayed moderate and 27% severe periodontitis. Questionnaire data revealed that 62.3% of the study subjects with severe periodontitis were not aware of the presence of the disease, 44.4% denied having received any systematic periodontal therapy so far, although 50% of them indicated to visit their dentist regularly for professional tooth cleanings. CONCLUSION: While the clinical study data confirm an increased prevalence of periodontitis in CKD patients, their self-reported awareness of periodontitis was low.

A combined epigenome- and transcriptome-wide association study of the oral masticatory mucosa assigns CYP1B1 a central role for epithelial health in smokers.

BACKGROUND: The oral mucosa has an important role in maintaining barrier integrity at the gateway to the gastrointestinal and respiratory tracts. Smoking is a strong environmental risk factor for the common oral inflammatory disease periodontitis and oral cancer. Cigarette smoke affects gene methylation and expression in various tissues. This is the first epigenome-wide association study (EWAS) that aimed to identify biologically active methylation marks of the oral masticatory mucosa that are associated with smoking. RESULTS: Ex vivo biopsies of 18 current smokers and 21 never smokers were analysed with the Infinium Methylation EPICBeadChip and combined with whole transcriptome RNA sequencing (RNA-Seq; 16 mio reads per sample) of the same samples. We analysed the associations of CpG methylation values with cigarette smoking and smoke pack year (SPY) levels in an analysis of covariance (ANCOVA). Nine CpGs were significantly associated with smoking status, with three CpGs mapping to the genetic region of CYP1B1 (cytochrome P450 family 1 subfamily B member 1; best p = 5.5 × 10-8) and two mapping to AHRR (aryl-hydrocarbon receptor repressor; best p = 5.9 × 10-9). In the SPY analysis, 61 CpG sites at 52 loci showed significant associations of the quantity of smoking with changes in methylation values. Here, the most significant association located to the gene CYP1B1, with p = 4.0 × 10-10. RNA-Seq data showed significantly increased expression of CYP1B1 in smokers compared to non-smokers (p = 2.2 × 10-14), together with 13 significantly upregulated transcripts. Six transcripts were significantly downregulated. No differential expression was observed for AHRR. In vitro studies with gingival fibroblasts showed that cigarette smoke extract directly upregulated the expression of CYP1B1. CONCLUSION: This study validated the established role of CYP1B1 and AHRR in xenobiotic metabolism of tobacco smoke and highlights the importance of epigenetic regulation for these genes. For the first time, we give evidence of this role for the oral masticatory mucosa.

No differences in microbiome changes between anti-adhesive and antibacterial ingredients in toothpastes during periodontal therapy.

AIM: This subgroup analysis of a 12-week randomized, double-blind, and two-center trial aimed to evaluate whether two different toothpaste formulations can differentially modulate the dental microbiome. MATERIAL AND METHODS: Forty one mild to moderate periodontitis patients used as an adjunct to periodontal treatment either a toothpaste with anti-adhesive zinc-substituted carbonated hydroxyapatite (HA) or with antimicrobial and anti-adhesive amine fluoride/stannous fluoride (AmF/SnF2 ) during a 12-week period. Plaque samples from buccal/lingual, interproximal, and subgingival sites were taken at baseline, 4 weeks after oral hygiene phase, and 8 weeks after periodontal therapy. Samples were analyzed with paired-end Illumina Miseq 16S rDNA sequencing. The differences and changes on community level (alpha and beta diversity) and on the level of single agglomerated ribosomal sequence variants (aRSV) were calculated with analysis of covariance (ANCOVA) and likelihood ratio test (LRT). RESULTS: Interproximal and subgingival sites harbored predominately Fusobacterium and Prevotella species associated with periodontitis, whereas buccal/lingual sites harbored mainly Streptococcus and Veillonella species associated with periodontal health. Alpha and beta diversity did not change noticeably differently between both toothpaste groups (P > 0.05, ANCOVA). Furthermore, none of the aRSVs showed a noticeably different change between the tested toothpastes during periodontal therapy (Padj . > 0.05, LRT). CONCLUSION: The use of a toothpaste containing anti-adhesive HA did not induce statistically noticeably different changes on microbial composition compared to an antimicrobial and anti-adhesive AmF/SnF2 formulation.

Meta-analysis of genome-wide association studies of aggressive and chronic periodontitis identifies two novel risk loci.

Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. It is classified into the widespread moderate form chronic periodontitis (CP) and the rare early-onset and severe phenotype aggressive periodontitis (AgP). These different disease manifestations are thought to share risk alleles and predisposing environmental factors. To obtain novel insights into the shared genetic etiology and the underlying molecular mechanisms of both forms, we performed a two step-wise meta-analysis approach using genome-wide association studies of both phenotypes. Genotypes from imputed genome-wide association studies (GWAS) of AgP and CP comprising 5,095 cases and 9,908 controls of North-West European genetic background were included. Two loci were associated with periodontitis at a genome-wide significance level. They located within the pseudogene MTND1P5 on chromosome 8 (rs16870060-G, P = 3.69 × 10-9, OR = 1.36, 95% CI = [1.23-1.51]) and intronic of the long intergenic non-coding RNA LOC107984137 on chromosome 16, downstream of the gene SHISA9 (rs729876-T, P = 9.77 × 10-9, OR = 1.24, 95% CI = [1.15-1.34]). This study identified novel risk loci of periodontitis, adding to the genetic basis of AgP and CP.

Genome-wide association meta-analysis of coronary artery disease and periodontitis reveals a novel shared risk locus.

Evidence for a shared genetic basis of association between coronary artery disease (CAD) and periodontitis (PD) exists. To explore the joint genetic basis, we performed a GWAS meta-analysis. In the discovery stage, we used a German aggressive periodontitis sample (AgP-Ger; 680 cases vs 3,973 controls) and the CARDIoGRAMplusC4D CAD meta-analysis dataset (60,801 cases vs 123,504 controls). Two SNPs at the known CAD risk loci ADAMTS7 (rs11634042) and VAMP8 (rs1561198) passed the pre-assigned selection criteria (PAgP-Ger < 0.05; PCAD < 5 × 10-8; concordant effect direction) and were replicated in an independent GWAS meta-analysis dataset of PD (4,415 cases vs 5,935 controls). SNP rs1561198 showed significant association (PD[Replication]: P = 0.008 OR = 1.09, 95% CI = [1.02-1.16]; PD [Discovery + Replication]: P = 0.0002, OR = 1.11, 95% CI = [1.05-1.17]). For the associated haplotype block, allele specific cis-effects on VAMP8 expression were reported. Our data adds to the shared genetic basis of CAD and PD and indicate that the observed association of the two disease conditions cannot be solely explained by shared environmental risk factors. We conclude that the molecular pathway shared by CAD and PD involves VAMP8 function, which has a role in membrane vesicular trafficking, and is manipulated by pathogens to corrupt host immune defense.

Wild-type isolates of Porphyromonas gingivalis derived from periodontitis patients display major variability in platelet activation.

In vitro studies revealed that Porphyromonas gingivalis (Pg), a pathogen intimately associated with the onset and progression of periodontitis, is able to activate platelets, thus linking periodontal inflammation with the endangerment of vascular health. As wild-type Pg strains are characterized by major genetic heterogeneity, the commonness of platelet-activating Pg strains in periodontitis patients is unknown as of yet. Therefore, this study evaluated the platelet activation capacity of wild-type Pg isolates sampled from patients with aggressive periodontitis. METHODS: Extent and velocity of platelet aggregation were determined by light transmission aggregometry. Platelet surface expression of P-selectin was measured by flow cytometry, activation of p38 MAP kinase, and protein kinase C by Western blot using phospho-specific antibodies. RESULTS: Pg isolates displayed high variability regarding extent and velocity of platelet activation, as well as the involved activating pathways. Corresponding results were observed for platelet P-selectin expression, activation of p38 MAP kinase, or protein kinase C. Inhibitors of platelet immune receptor FcγRIIA and protease-activated receptors revealed several, diverging pathways of activation. Some isolates induced platelet aggregation even in the presence of potent therapeutical platelet inhibitors. CONCLUSIONS: Chronic bacteremia involving specific, platelet-activating Pg strains may constitute a substantial hazard for the integrity of cardiovascular health.

Impact of different concentrations of an octenidine dihydrochloride mouthwash on salivary bacterial counts: a randomized, placebo-controlled cross-over trial.

OBJECTIVES: This bi-centric, placebo-controlled, randomized, evaluator-blinded, incomplete cross-over clinical phase II trial was initialized to identify the most appropriate concentration of octenidine dihydrochloride (OCT) in mouth rinses. MATERIALS AND METHODS: Rinses of 0.10, 0.15, and 0.20% OCT were compared to a saline placebo rinse regarding the reduction of salivary bacterial counts (SBCs) in 90 gingivitis patients over 4 days. Changes in plaque (PI) and gingival index (GI), taste perception, and safety issues were evaluated. RESULTS: At baseline, the first OCT (0.10, 0.15, 0.20%) rinse resulted in a decrease of SBC (reduction by 3.63-5.44 log10 colony forming units [CFU]) compared to placebo (p < 0.001). Differences between OCT concentrations were not verified. After 4 days, the last OCT rinse again resulted in a significant SBC decrease (3.69-4.22 log10 CFU) compared to placebo (p < 0.001). Overall, SBC reduction between baseline and day 4 was significantly higher in OCT 0.15 and 0.20% groups compared to OCT 0.10% and placebo. Mean GI/PIs were significantly lower in OCT groups than in the placebo group (p < 0.001). Differences in GI/PI between OCT groups were not verified. Adverse effects increased with increasing OCT concentrations. CONCLUSIONS: Considering antibacterial efficacy, frequency of adverse events, and user acceptance, 0.10% OCT was identified as the preferred concentration to be used in future clinical trials. CLINICAL RELEVANCE: Due to its low toxicity and pronounced antibacterial properties, octenidine dihydrochloride (OCT) is a promising candidate for the use in antiseptic mouth rinses. OCT concentrations of 0.10% are recommended for future clinical trials evaluating the plaque-reducing properties of OCT mouth rinses. ( www.clinicaltrials.gov , NCT022138552).

Impact of anti-infective periodontal therapy on parameters of vascular health.

AIM: This study assessed the impact of anti-infective periodontal therapy on the status of vascular health. MATERIALS AND METHODS: Periodontal and vascular health of 55 patients with severe untreated chronic periodontitis was evaluated before and 12 months after anti-infective periodontal therapy. Observed parameters were bleeding on probing (BoP), pocket probing depth (PPD), periodontal inflamed surface area index (PISA), pulse wave velocity (PWV), augmentation index (AIx), central pulse pressure (PPao) and peripheral systolic pressure (RRsys). RESULTS: ΔPISA (baseline-12 months) correlated with ΔPWV (τ 0.21; p < .03), ΔAIx (τ 0.29; p < .002) and ΔPPao (τ 0.23; p < .02). ΔBoP% (baseline-12 months) correlated with ΔPWV (τ 0.18; p < .05) and ΔAIx (τ 0.25; p < .01), while mean ΔPPD (baseline-12 months) correlated with ΔPWV (τ 0.24; p < .01) and ΔAIx (τ 0.21; p < .03). Grouping patients evenly into three groups based on tertiles of BoP resolution after 12 months revealed a significant decrease in the observed PWV median value by -0.6 m/s (p < .04) in the best response tertile (ΔBoP ≥ 88%). In the worst response tertile (ΔBoP ≤ 66%), by contrast, significant increase in PPao (+10.5 mmHg; p < .02) and AIx (+5.5; p < .02) was observed. CONCLUSION: Efficacious resolution of periodontal inflammation may beneficially impact on vascular health.

A haplotype block downstream of plasminogen is associated with chronic and aggressive periodontitis.

AIM: The intronic variant rs4252120 in the plasminogen gene (PLG) is known to be associated with aggressive periodontitis (AgP) and atherosclerosis. Here, we examined the chromosomal region spanning PLG for associations with both chronic periodontitis (CP) and AgP. MATERIALS AND METHODS: The association of PLG candidate rs4252120 was tested in a German case-control sample of 1,419 CP cases using the genotyping assay hCV11225947 and 4,562 controls, genotyped with HumanOmni BeadChips. The German and Dutch sample of AgP cases (N = 851) and controls (N = 6,836) were genotyped with HumanOmni BeadChips. The North American CP sample (N = 2,681 cases, 1,823 controls) was previously genotyped on the Genome-Wide Human SNP Array 6.0. Genotypes were imputed (software Impute v2), and association tests were performed using an additive genetic model adjusting for sex and smoking. RESULTS: Rs4252120 was not associated with CP. However, a haplotype block downstream of PLG and not in linkage disequilibrium with rs4252120 (r2  = .08) was associated with both AgP (rs1247559; p = .002, odds ratio [OR] = 1.33) and CP (p = .02, OR = 1.15). That locus was also significantly associated with PLG expression in osteoblasts (p = 6.9 × 10-5 ). CONCLUSIONS: Our findings support a role of genetic variants in PLG in the aetiology of periodontitis.