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  • 1
    In: Journal of Clinical Microbiology, American Society for Microbiology, Vol. 44, No. 9 ( 2006-09), p. 3078-3085
    Abstract: The etiologic role of oral treponemes in human periodontitis is still under debate. Although seen by dark-field microscopy in large numbers, their possible role is still unclear since they comprise some 60 different phylotypes, most of which are still uncultured. To determine their status as mere commensals or opportunistic pathogens, molecular epidemiological studies are required that include both cultured and as-yet-uncultured organisms. Here we present such data, comparing treponemal populations from chronic periodontitis (CP) or generalized aggressive periodontitis (GAP) patients. As a periodontitis-resistant (PR) control group, we included elderly volunteers with more than 20 natural teeth and no history of periodontal treatment and no or minimal clinical signs of periodontitis. Almost every treponemal phylotype was present in all three groups. For most treponemes, the proportion of subjects positive for a certain species or phylotype was higher in both periodontitis groups than in the PR group. This difference was pronounced for treponemes of the phylogenetic groups II and IV and for Treponema socranskii and Treponema lecithinolyticum . Between the periodontitis groups the only significant differences were seen for T. socranskii and T. lecithinolyticum , which were found more often in periodontal pockets of GAP patients than of CP patients. In contrast, no difference was found for Treponema denticola . Our findings, however, strengthen the hypothesis of treponemes being opportunistic pathogens. It appears that T. socranskii , T. lecithinolyticum and group II and IV treponemes may represent good indicators for periodontitis and suggest the value of the respective probes for microbiological diagnosis in periodontitis subjects.
    Type of Medium: Online Resource
    ISSN: 0095-1137 , 1098-660X
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2006
    detail.hit.zdb_id: 1498353-9
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2021
    In:  Clinical Oral Investigations Vol. 25, No. 8 ( 2021-08), p. 5109-5112
    In: Clinical Oral Investigations, Springer Science and Business Media LLC, Vol. 25, No. 8 ( 2021-08), p. 5109-5112
    Abstract: Observational research suggests that periodontitis affects pulmonary function; however, observational studies are subject to confounding and reverse causation, making causal inference and the direction of these associations difficult. We used Mendelian randomization (MR) to assess the potential causal association between genetic liability to periodontitis and pulmonary function. Materials and methods We used six single-nucleotide polymorphisms (SNPs) associated with periodontitis ( P   〈  5 × 10 −6 ) from a genome-wide association study (GWAS) of 17,353 European descent periodontitis cases and 28,210 controls from the GeneLifestyle Interactions in Dental Endpoints consortium and the UK Biobank, and related these to SNPs from a lung function GWAS including 79,055 study participants of the SpiroMeta Consortium. Results MR analysis suggested no effect of periodontitis on the ratio of forced expiratory volume in one second to lower forced vital capacity (standard deviation increment in outcome per doubling of the odds of the exposure (95% confidence interval) =  − 0.004 (− 0.028; 0.020)). Replication analysis using genetic instruments from two different GWAS and sensitivity analyses to address potential pleiotropy led to no substantial changes in estimates. Conclusions Collectively, these findings do not support a relationship between genetic liability for periodontitis and pulmonary function. Clinical relevance Periodontitis does not seem to be a risk factor for worsening of pulmonary function.
    Type of Medium: Online Resource
    ISSN: 1432-6981 , 1436-3771
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 1472578-2
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  • 3
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2018
    In:  Clinical Oral Investigations Vol. 22, No. 7 ( 2018-9), p. 2669-2673
    In: Clinical Oral Investigations, Springer Science and Business Media LLC, Vol. 22, No. 7 ( 2018-9), p. 2669-2673
    Type of Medium: Online Resource
    ISSN: 1432-6981 , 1436-3771
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 1472578-2
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  • 4
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2023
    In:  Clinical Oral Investigations Vol. 27, No. 8 ( 2023-06-13), p. 4803-4808
    In: Clinical Oral Investigations, Springer Science and Business Media LLC, Vol. 27, No. 8 ( 2023-06-13), p. 4803-4808
    Abstract: Observational studies suggested an inverse association between physical activity and periodontitis. However, observational studies might be subject to unobserved confounding and reverse causation bias. We conducted an instrumental variable study to strengthen the evidence on the relationship between physical activity and periodontitis. Materials and methods We used genetic variants associated with self-reported and accelerometer-assessed physical activity in 377,234 and 91,084 UK Biobank participants, respectively, as instruments. For these instruments, genetic associations with periodontitis were obtained from 17,353 cases and 28,210 controls in the GeneLifestyle Interactions in Dental Endpoints consortium. Results We found no evidence for effects of self-reported moderate-to-vigorous physical activity, self-reported vigorous physical activity, accelerometry “average accelerations,” and “fraction of accelerations  〉  425 milli-gravities” on periodontitis. For example, the odds ratio for self-reported moderate-to-vigorous physical activity was 1.07 (95% credible interval: 0.87; 1.34) in Causal Analysis using Summary Effect Estimates. We conducted sensitivity analyses to rule out weak instrument bias and correlated horizontal pleiotropy. Conclusions The study does not support an effect of physical activity on the risk of periodontitis. Clinical relevance This study provides little evidence that recommending physical activity would help prevent periodontitis.
    Type of Medium: Online Resource
    ISSN: 1436-3771
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 1472578-2
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  • 5
    In: Journal of Periodontology, Wiley, Vol. 92, No. 11 ( 2021-11), p. 1536-1545
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0022-3492 , 1943-3670
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2040047-0
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  • 6
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 14 ( 2023-6-5)
    Abstract: Interleukin 6 (IL-6) is considered to play a role in the dysbiotic host response in the development of periodontitis. While the inhibition of the IL-6 receptor using monoclonal antibodies is a well-established therapy for some diseases, so far, its potential benefit in patients with periodontitis has not been examined. We tested the association of genetically proxied downregulation of IL-6 signaling with periodontitis to explore whether downregulation of IL-6 signaling could represent a viable treatment target for periodontitis, Materials and methods As proxies for IL-6 signaling downregulation, we selected 52 genetic variants in close vicinity of the gene encoding IL-6 receptor that were associated with lower circulating C-reactive protein (CRP) levels in a genome-wide association study (GWAS) of 575 531 participants of European ancestry from the UK Biobank and the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium. Associations with periodontitis were tested with inverse-variance weighted Mendelian randomization in a study of 17 353 cases and 28 210 controls of European descent in the Gene-Lifestyle Interactions in Dental Endpoints (GLIDE) consortium. In addition, the effect of CRP reduction independent of the IL-6 pathway was assessed. Results Genetically proxied downregulation of IL-6 signaling was associated with lower odds of periodontitis (odds ratio (OR) = 0.81 per 1-unit decrement in log-CRP levels; 95% confidence interval (CI): [0.66;0.99]; P = 0.0497). Genetically proxied reduction of CRP independent of the IL-6 pathway had a similar effect (OR = 0.81; 95% CI: [0.68; 0.98] ; P = 0.0296). Conclusion In conclusion, genetically proxied downregulation of IL-6 signaling was associated with lower odds of periodontitis and CRP might be a causal target for the effect of IL-6 on the risk of periodontitis.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606827-8
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  • 7
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 23, No. 13 ( 2022-06-30), p. 7266-
    Abstract: Periodontitis is a multifactorial disease. The aim of this explorative study was to investigate the role of Interleukin-(IL)-1, IL-4, GATA-3 and Cyclooxygenase-(COX)-2 polymorphisms after non-surgical periodontal therapy with adjunctive systemic antibiotics (amoxicillin/metronidazole) and subsequent maintenance in a Caucasian population. Analyses were performed using blood samples from periodontitis patients of a multi-center trial (ClinicalTrials.gov NCT00707369=ABPARO-study). Polymorphisms were analyzed using quantitative real-time PCR. Clinical attachment levels (CAL), percentage of sites showing further attachment loss (PSAL) ≥1.3 mm, bleeding on probing (BOP) and plaque score were assessed. Exploratory statistical analysis was performed. A total of 209 samples were genotyped. Patients carrying heterozygous genotypes and single-nucleotide-polymorphisms (SNP) on the GATA-3-IVS4 +1468 gene locus showed less CAL loss than patients carrying wild type. Heterozygous genotypes and SNPs on the IL-1A-889, IL-1B +3954, IL-4-34, IL-4-590, GATA-3-IVS4 +1468 and COX-2-1195 gene loci did not influence CAL. In multivariate analysis, CAL was lower in patients carrying GATA-3 heterozygous genotypes and SNPs than those carrying wild-types. For the first time, effects of different genotypes were analyzed in periodontitis progression after periodontal therapy and during supportive treatment using systemic antibiotics demonstrating a slight association of GATA-3 gene locus with CAL. This result suggests that GATA-3 genotypes are a contributory but non-essential risk factor for periodontal disease progression.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2019364-6
    SSG: 12
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  • 8
    In: Plant Biotechnology Journal, Wiley, Vol. 15, No. 5 ( 2017-05), p. 605-613
    Abstract: Food supplementation with the conditionally essential amino acid arginine (Arg) has been shown to have nutritional benefits. Degradation of cyanophycin ( CGP ), a peptide polymer used for nitrogen storage by cyanobacteria, requires cyanophycinase ( CGP ase) and results in the release of β‐aspartic acid (Asp)‐Arg dipeptides. The simultaneous production of CGP and CGP ase in plants could be a convenient source of Arg dipeptides. Different variants of the cph B coding region from Thermosynechococcus elongatus BP ‐1 were transiently expressed in Nicotiana benthamiana plants. Translation and enzyme stability were optimized to produce high amounts of active CGP ase. Protein stability was increased by the translational fusion of CGP ase to the green fluorescent protein ( GFP ) or to the transit peptide of the small subunit of RuBis CO for peptide production in the chloroplasts. Studies in mice showed that plant‐expressed CGP fed in combination with plant‐made CGP ase was hydrolysed in the intestine, and high levels of ß‐Asp‐Arg dipeptides were found in plasma, demonstrating dipeptide absorption. However, the lack of an increase in Asp and Arg or its metabolite ornithine in plasma suggests that Arg from CGP was not bioavailable in this mouse group. Intestinal degradation of CGP by CGP ase led to low intestinal CGP content 4 h after consumption, but after ingestion of CGP alone, high CGP concentrations remained in the large intestine; this indicated that intact CGP was transported from the small to the large intestine and that CGP was resistant to colonic microbes.
    Type of Medium: Online Resource
    ISSN: 1467-7644 , 1467-7652
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2136367-5
    SSG: 12
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  • 9
    In: Journal of Clinical Periodontology, Wiley, Vol. 49, No. 3 ( 2022-03), p. 200-209
    Abstract: Higher educational attainment is associated with a lower risk of periodontitis, but the extent to which this association is causal and mediated by intermediate factors is unclear. Materials and Methods Using summary data from genetic association studies from up to 1.1 million participants of European descent, univariable and multivariable Mendelian randomization analyses were performed to infer the total effect of educational attainment on periodontitis and to estimate the degree to which income, smoking, alcohol consumption, and body mass index mediate the association. Results The odds ratio of periodontitis per 1 standard deviation increment in genetically predicted education was 0.78 (95% CI: 0.68–0.89). The proportions mediated of the total effect of genetically predicted education on periodontitis were 64%, 35%, 15%, and 46% for income, smoking, alcohol consumption, and body mass index, respectively. Conclusions Using a genetic instrumental variable approach, this study triangulated evidence from existing observational epidemiological studies and suggested that higher educational attainment lowers periodontitis risk. Measures to reduce the burden of educational disparities in periodontitis risk may tackle downstream risk factors, particularly income, smoking, and obesity.
    Type of Medium: Online Resource
    ISSN: 0303-6979 , 1600-051X
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2026349-1
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  • 10
    In: Journal of Clinical Periodontology, Wiley, Vol. 49, No. 7 ( 2022-07), p. 633-641
    Abstract: To examine the associations between bone turnover markers and periodontitis in two cross‐sectional population‐based studies. Materials and Methods We used data from two independent adult samples ( N  = 4993), collected within the Study of Health in Pomerania project, to analyse cross‐sectional associations of N‐procollagen type 1 amino‐terminal propeptide (P1NP), C‐terminal cross‐linking telopeptide, osteocalcin, bone‐specific alkaline phosphatase (BAP), fibroblast growth factor 23, wingless‐type mouse mammary tumour virus integration site family member 5a (WNT5A), and sclerostin values with periodontitis. Confounder‐adjusted gamma and fractional response regression models were applied. Results Positive associations were found for P1NP with mean pocket probing depth (PPD; ; 95% confidence interval [CI]: 1.001–1.015), mean clinical attachment loss (mean CAL; ; 95% CI: 1.011–1.044), and proportion of sites with bleeding on probing (%BOP; ; 95% CI: 1.005–1.109). Similar associations were seen for BAP with %BOP (; 95% CI: 1.042–1.205), proportion of sites with PPD ≥4 mm (%PPD4) (; 95% CI: 1.005–1.161), and sclerostin with %BOP (; 95% CI: 1.005–1.704). WNT5A was inversely associated with mean PPD (; 95% CI: 0.920–0.993) and %PPD4 (; 95% CI: 0.642–0.982). Conclusions This study revealed scattered associations of P1NP, BAP, WNT5A, and sclerostin with periodontitis, but the results are contradictory in the overall context. Associations reported in previous studies could not be confirmed.
    Type of Medium: Online Resource
    ISSN: 0303-6979 , 1600-051X
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2026349-1
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