{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362544420073855488.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1111/prd.12104"}},{"identifier":{"@type":"URI","@value":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fprd.12104"}},{"identifier":{"@type":"URI","@value":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/prd.12104"}}],"dc:title":[{"@value":"Molecular aspects of the pathogenesis of periodontitis"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title><jats:p>The past decade of basic research in periodontology has driven radical changes in our understanding and perceptions of the pathogenic processes that drive periodontal tissue destruction. The core elements of the classical model of disease pathogenesis, developed by Page & Kornman in 1997, remain pertinent today; however, our understanding of the dynamic interactions between the various microbial and host factors has changed significantly. The molecular era has unraveled aspects of genetics, epigenetics, lifestyle and environmental factors that, in combination, influence biofilm composition and the host's inflammatory immune response, creating a heterogenic biological phenotype that we label as ‘periodontitis’. In this volume of <jats:italic>Periodontology 2000</jats:italic>, experts in their respective fields discuss these emerging concepts, such as a health‐promoting biofilm being essential for periodontal stability, involving a true symbiosis between resident microbial species and each other and also with the host response to that biofilm. Rather like the gut microbiome, changes in the local environment, which may include inflammatory response mediators or viruses, conspire to drive dysbiosis and create a biofilm that supports pathogenic species capable of propagating disease. The host response is now recognized as the major contributor to periodontal tissue damage in what becomes a dysfunctional, poorly targeted and nonresolving inflammation that only serves to nourish and sustain the dysbiosis. The role of epithelial cells in signaling to the immune system is becoming clearer, as is the role of dendritic cells as transporters of periodontal pathogens to distant sites within the body, namely metastatic infection. The involvement of nontraditional immune cells, such as natural killer cells, is being recognized, and the simple balance between T‐helper 1‐ and T‐helper 2‐type T‐cell populations has become less clear with the emergence of T‐regulatory cells, T‐helper 17 cells and follicular helper cells. The dominance of the neutrophil has emerged, not only as a potential destructor when poorly regulated but as an equally unpredictable effector cell for specific B‐cell immunity. The latter has emerged, in part, from the realization that neutrophils live for 5.4 days in the circulation, rather than for 24 h, and are also schizophrenic in nature, being powerful synthesizers of proinflammatory cytokines but also responding to prostaglandin signals to trigger a switch to a pro‐resolving phenotype that appears capable of regenerating the structure and function of healthy tissue. Key to these outcomes are the molecular signaling pathways that dominate at any one time, but even these are influenced by microRNAs capable of ‘silencing’ certain inflammatory genes. This volume of <jats:italic>Periodontology 2000</jats:italic> tries to draw these complex new learnings into a contemporary model of disease pathogenesis, in which inflammation and dysbiosis impact upon whether the outcome is driven toward acute resolution and stability, chronic resolution and repair, or failed resolution and ongoing periodontal tissue destruction.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382544420073855488","@type":"Researcher","foaf:name":[{"@value":"Joerg Meyle"}]},{"@id":"https://cir.nii.ac.jp/crid/1382544420073855489","@type":"Researcher","foaf:name":[{"@value":"Iain Chapple"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"09066713"},{"@type":"EISSN","@value":"16000757"}],"prism:publicationName":[{"@value":"Periodontology 2000"}],"dc:publisher":[{"@value":"Wiley"}],"prism:publicationDate":"2015-08-07","prism:volume":"69","prism:number":"1","prism:startingPage":"7","prism:endingPage":"17"},"reviewed":"false","dc:rights":["http://onlinelibrary.wiley.com/termsAndConditions#vor"],"url":[{"@id":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fprd.12104"},{"@id":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/prd.12104"}],"createdAt":"2015-08-07","modifiedAt":"2023-09-30","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050858829286257536","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"The Fungal Metabolite (+)-Terrein Abrogates Inflammatory Bone Resorption via the Suppression of TNF-α Production in a Ligature-Induced Periodontitis Mouse Model"}]},{"@id":"https://cir.nii.ac.jp/crid/1360005519223448064","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Integrated hypothesis of dental caries and periodontal diseases"}]},{"@id":"https://cir.nii.ac.jp/crid/1360005519230141184","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Gingival epithelial barrier: regulation by beneficial and harmful microbes"}]},{"@id":"https://cir.nii.ac.jp/crid/1360025430173894144","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Recent findings on metabolomics and the microbiome of oral bacteria involved in dental caries and periodontal disease"}]},{"@id":"https://cir.nii.ac.jp/crid/1360294645800310016","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Association between Type 2 Diabetes and Classification of Periodontal Disease Severity in Japanese Men and Women: A Cross-Sectional Study"}]},{"@id":"https://cir.nii.ac.jp/crid/1360576118686120192","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Improved epithelial cell–cell adhesion using molecular mobility of supramolecular surfaces"}]},{"@id":"https://cir.nii.ac.jp/crid/1364230498311592064","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Mechanism of alveolar bone destruction in periodontitis — Periodontal bacteria and inflammation"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1111/prd.12104"},{"@type":"CROSSREF","@value":"10.1080/20002297.2019.1710953_references_DOI_DxZLUBfWR4UjaxLk3bU12CBfOed"},{"@type":"CROSSREF","@value":"10.1080/21688370.2019.1651158_references_DOI_DxZLUBfWR4UjaxLk3bU12CBfOed"},{"@type":"CROSSREF","@value":"10.1007/s11274-024-04224-3_references_DOI_DxZLUBfWR4UjaxLk3bU12CBfOed"},{"@type":"CROSSREF","@value":"10.3390/jof9030314_references_DOI_DxZLUBfWR4UjaxLk3bU12CBfOed"},{"@type":"CROSSREF","@value":"10.1039/d1bm01356d_references_DOI_DxZLUBfWR4UjaxLk3bU12CBfOed"},{"@type":"CROSSREF","@value":"10.3390/ijerph19138134_references_DOI_DxZLUBfWR4UjaxLk3bU12CBfOed"},{"@type":"CROSSREF","@value":"10.1016/j.jdsr.2021.09.005_references_DOI_DxZLUBfWR4UjaxLk3bU12CBfOed"}]}