| 1. |
- Chapple, Iain L C, et al.
(author)
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Interaction of lifestyle, behaviour or systemic diseases with dental caries and periodontal diseases: consensus report of group 2 of the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases.
- 2017
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In: Journal of clinical periodontology. - : Wiley. - 1600-051X .- 0303-6979. ; 44:Suppl 18
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Journal article (peer-reviewed)abstract
- Periodontal diseases and dental caries are the most common diseases of humans and the main cause of tooth loss. Both diseases can lead to nutritional compromise and negative impacts upon self-esteem and quality of life. As complex chronic diseases, they share common risk factors, such as a requirement for a pathogenic plaque biofilm, yet they exhibit distinct pathophysiologies. Multiple exposures contribute to their causal pathways, and susceptibility involves risk factors that are inherited (e.g. genetic variants), and those that are acquired (e.g. socio-economic factors, biofilm load or composition, smoking, carbohydrate intake). Identification of these factors is crucial in the prevention of both diseases as well as in their management.To systematically appraise the scientific literature to identify potential risk factors for caries and periodontal diseases.One systematic review (genetic risk factors), one narrative review (role of diet and nutrition) and reference documentation for modifiable acquired risk factors common to both disease groups, formed the basis of the report.There is moderately strong evidence for a genetic contribution to periodontal diseases and caries susceptibility, with an attributable risk estimated to be up to 50%. The genetics literature for periodontal disease is more substantial than for caries and genes associated with chronic periodontitis are the vitamin D receptor (VDR), Fc gamma receptor IIA (Fc-γRIIA) and Interleukin 10 (IL10) genes. For caries, genes involved in enamel formation (AMELX, AMBN, ENAM, TUFT, MMP20, and KLK4), salivary characteristics (AQP5), immune regulation and dietary preferences had the largest impact. No common genetic variants were found. Fermentable carbohydrates (sugars and starches) were the most relevant common dietary risk factor for both diseases, but associated mechanisms differed. In caries, the fermentation process leads to acid production and the generation of biofilm components such as Glucans. In periodontitis, glycaemia drives oxidative stress and advanced glycation end-products may also trigger a hyper inflammatory state. Micronutrient deficiencies, such as for vitamin C, vitamin D or vitamin B12, may be related to the onset and progression of both diseases. Functional foods or probiotics could be helpful in caries prevention and periodontal disease management, although evidence is limited and biological mechanisms not fully elucidated. Hyposalivation, rheumatoid arthritis, smoking/tobacco use, undiagnosed or sub-optimally controlled diabetes and obesity are common acquired risk factors for both caries and periodontal diseases.
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| 2. |
- Clark, Andrew G., et al.
(author)
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Evolution of genes and genomes on the Drosophila phylogeny
- 2007
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In: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 450:7167, s. 203-218
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Journal article (peer-reviewed)abstract
- Comparative analysis of multiple genomes in a phylogenetic framework dramatically improves the precision and sensitivity of evolutionary inference, producing more robust results than single-genome analyses can provide. The genomes of 12 Drosophila species, ten of which are presented here for the first time (sechellia, simulans, yakuba, erecta, ananassae, persimilis, willistoni, mojavensis, virilis and grimshawi), illustrate how rates and patterns of sequence divergence across taxa can illuminate evolutionary processes on a genomic scale. These genome sequences augment the formidable genetic tools that have made Drosophila melanogaster a pre-eminent model for animal genetics, and will further catalyse fundamental research on mechanisms of development, cell biology, genetics, disease, neurobiology, behaviour, physiology and evolution. Despite remarkable similarities among these Drosophila species, we identified many putatively non-neutral changes in protein-coding genes, non-coding RNA genes, and cis-regulatory regions. These may prove to underlie differences in the ecology and behaviour of these diverse species.
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| 3. |
- Dommisch, Henrik, et al.
(author)
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Effect of micronutrient malnutrition on periodontal disease and periodontal therapy
- 2018
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In: Periodontology 2000. - : John Wiley & Sons. - 0906-6713 .- 1600-0757. ; 78:1, s. 129-153
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Research review (peer-reviewed)abstract
- Periodontitis is a complex chronic inflammatory noncommunicable disease, initiated by the development of a dysbiotic microbial plaque biofilm below the gingival margin. Whilst the pathogenic biofilm is a “necessary cause” of periodontitis, it is insufficient on its own to cause the disease, and a destructive immune‐inflammatory response is a key to the translation of risk to destructive events. Other exposures or “component causes” include individual genetic predisposition, lifestyle (including smoking and nutrition), and environmental factors. Dietary nutrients are essential for life as they provide crucial energy sources in the form of macronutrients, as well as important cofactors in the form of micronutrients, which regulate the functionality of enzymes during the regulation of anabolic and catabolic processes in human cells. Moreover, micronutrients can regulate gene transcription factors, such as the proinflammatory nuclear factor kappa B and the anti‐inflammatory nuclear factor (erythroid‐derived 2)‐like 2. This review focuses on the role of vitamins (vitamin A, carotenoids, the vitamin B complex, vitamins C, D, and E, and coenzyme Q10) and minerals (calcium, magnesium, iron, zinc, potassium, copper, manganese, and selenium) in human physiology and the impact of their deficiencies upon periodontal health and disease.
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| 4. |
- Herrera, David, et al.
(author)
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Consensus report of the second European Consensus Workshop on Education in Periodontology
- 2024
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In: JOURNAL OF CLINICAL PERIODONTOLOGY. - 0303-6979 .- 1600-051X.
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Journal article (peer-reviewed)abstract
- BackgroundThe second European Consensus Workshop on Education in Periodontology was commissioned, as a result of the changes in the discipline and the advances in educational methods/technology, to update the 2009 Consensus report of the first European Federation of Periodontology (EFP) Workshop on the same topic that was jointly authored by the Association for Dental Education in Europe.AimTo identify and propose changes necessary in periodontal education at three levels, namely undergraduate, specialist and continuing professional development (CPD), with respect to learning outcomes, competencies and methods of learning/training and evaluation.MethodsFour working groups (WGs) considered education in periodontology at the undergraduate, specialist and CPD levels, and education methods. Four commissioned position papers, one per WG, summarized the relevant information. Workshop participants gathered at an in-person consensus meeting to discuss the individual reviews, and this consensus report summarizes the conclusions.ResultsThe learning outcomes for undergraduate and specialist education in periodontology have been updated, and a proposal for learning outcomes for CPD programmes was made. Learning/teaching/training and evaluation methods were proposed for each level of education, which included face-to-face, virtual and blended learning methods.ConclusionDevelopments in oral/dental medicine and in contemporary educational technologies have been translated into updated learning outcomes and learning/teaching/ training/evaluation methods relevant to education in periodontology.
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| 5. |
- Hirschfeld, Josefine, et al.
(author)
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Effects of Aggregatibacter actinomycetemcomitans leukotoxin on neutrophil migration and extracellular trap formation.
- 2016
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In: Journal of Oral Microbiology. - : Informa UK Limited. - 2000-2297. ; 8
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Journal article (peer-reviewed)abstract
- BACKGROUND: Aggressive periodontitis is associated with the presence of Aggregatibacter actinomycetemcomitans, a leukotoxin (Ltx)-producing periodontal pathogen. Ltx has the ability to lyse white blood cells including neutrophils.OBJECTIVES: This study was aimed at investigating the interactions between neutrophils and Ltx with regard to the chemotactic properties of Ltx and the release of neutrophil extracellular traps (NETs).METHODS: Neutrophils from healthy blood donors were isolated and incubated for 30 min and 3 h with increasing concentrations of Ltx (1, 10, and 100 ng/mL) as well as with A. actinomycetemcomitans strains (NCTC 9710 and HK 1651) producing different levels of Ltx. Formation of NETs and cell lysis were assessed by microscopy, fluorescence-based assays, and measurement of released lactate dehydrogenase. Neutrophil migration in response to different Ltx gradients was monitored by real-time video microscopy, and image analysis was performed using ImageJ software.RESULTS: Although Ltx (10 and 100 ng/mL) and the leukotoxic A. actinomycetemcomitans strain HK 1651 lysed some neutrophils, other cells were still capable of performing NETosis in a concentration-dependent manner. Low doses of Ltx and the weakly leukotoxic strain NCTC 9710 did not lead to neutrophil lysis, but did induce some NETosis. Furthermore, all three concentrations of Ltx enhanced random neutrophil movement; however, low directional accuracy was observed compared with the positive control (fMLP).CONCLUSIONS: The results indicate that Ltx acts both as a neutrophil activator and also causes cell death. In addition, Ltx directly induces NETosis in neutrophils prior to cell lysis. In future studies, the underlying pathways involved in Ltx-meditated neutrophil activation and NETosis need to be investigated further.
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| 6. |
- Sanz, Mariano, et al.
(author)
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Clinical research on peri-implant diseases : consensus report of Working Group 4.
- 2012
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In: Journal of Clinical Periodontology. - 0303-6979 .- 1600-051X. ; 39:Suppl 12, s. 202-6
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Journal article (peer-reviewed)abstract
- BACKGROUND: Two systematic reviews have evaluated the quality of research and reporting of observational studies investigating the prevalence of, the incidence of and the risk factors for peri-implant diseases and of experimental clinical studies evaluating the efficacy of preventive and therapeutic interventions.MATERIALS AND METHODS: For the improvement of the quality of reporting for both observational and experimental studies, the STROBE and the Modified CONSORT recommendations were encouraged.RESULTS: To improve the quality of research in peri-implant diseases, the following were recommended: the use of unequivocal case definitions; the expression of outcomes at the subject rather than the implant level; the implementation of study validation tools; the reporting of potential sources of bias; and the use of appropriate statistical methods.CONCLUSIONS: In observational studies, case definitions for peri-implantitis were agreed. For risk factor determination, the progressive use of cross-sectional and case-control studies (univariate analyses), to prospective cohorts (multilevel modelling for confounding), and ultimately to intervention studies were recommended. For preventive and interventional studies of peri-implant disease management, parallel arm RCTs of at least 6-months were encouraged. For studies of non-surgical and surgical management of peri-implantitis, the use of a composite therapeutic end point was advocated. The development of standard control therapies was deemed essential.
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| 7. |
- Sanz, Mariano, et al.
(author)
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Clinical research on peri-implant diseases : consensus report of Working Group 4.
- 2012
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In: Journal of Clinical Periodontology. - : Blackwell Munksgaard. - 0303-6979 .- 1600-051X. ; 39:Suppl 12, s. 202-6
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Journal article (peer-reviewed)abstract
- BACKGROUND: Two systematic reviews have evaluated the quality of research and reporting of observational studies investigating the prevalence of, the incidence of and the risk factors for peri-implant diseases and of experimental clinical studies evaluating the efficacy of preventive and therapeutic interventions. MATERIALS AND METHODS: For the improvement of the quality of reporting for both observational and experimental studies, the STROBE and the Modified CONSORT recommendations were encouraged. RESULTS: To improve the quality of research in peri-implant diseases, the following were recommended: the use of unequivocal case definitions; the expression of outcomes at the subject rather than the implant level; the implementation of study validation tools; the reporting of potential sources of bias; and the use of appropriate statistical methods. CONCLUSIONS: In observational studies, case definitions for peri-implantitis were agreed. For risk factor determination, the progressive use of cross-sectional and case-control studies (univariate analyses), to prospective cohorts (multilevel modelling for confounding), and ultimately to intervention studies were recommended. For preventive and interventional studies of peri-implant disease management, parallel arm RCTs of at least 6-months were encouraged. For studies of non-surgical and surgical management of peri-implantitis, the use of a composite therapeutic end point was advocated. The development of standard control therapies was deemed essential.
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