Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions
JournalJournal of Clinical Periodontology
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AbstractBackground: A variety of systemic diseases and conditions can affect the course of periodontitis or have a negative impact on the periodontal attachment apparatus. Gingival recessions are highly prevalent and often associated with hypersensitivity, the development of caries and non-carious cervical lesions on the exposed root surface and impaired esthetics. Occlusal forces can result in injury of teeth and periodontal attachment apparatus. Several developmental or acquired conditions associated with teeth or prostheses may predispose to diseases of the periodontium. The aim of this working group was to review and update the 1999 classification with regard to these diseases and conditions, and to develop case definitions and diagnostic considerations. Methods: Discussions were informed by four reviews on 1) periodontal manifestions of systemic diseases and conditions; 2) mucogingival conditions around natural teeth; 3) traumatic occlusal forces and occlusal trauma; and 4) dental prostheses and tooth related factors. This consensus report is based on the results of these reviews and on expert opinion of the participants. Results: Key findings included the following: 1) there are mainly rare systemic conditions (such as Papillon-Lefevre Syndrome, leucocyte adhesion deficiency, and others) with a major effect on the course of periodontitis and more common conditions (such as diabetes mellitus) with variable effects, as well as conditions affecting the periodontal apparatus independently of dental plaque biofilm-induced inflammation (such as neoplastic diseases); 2) diabetes-associated periodontitis should not be regarded as a distinct diagnosis, but diabetes should be recognized as an important modifying factor and included in a clinical diagnosis of periodontitis as a descriptor; 3) likewise, tobacco smoking - now considered a dependence to nicotine and a chronic relapsing medical disorder with major adverse effects on the periodontal supporting tissues - is an important modifier to be included in a clinical diagnosis of periodontitis as a descriptor; 4) the importance of the gingival phenotype, encompassing gingival thickness and width in the context of mucogingival conditions, is recognized and a novel classification for gingival recessions is introduced; 5) there is no evidence that traumatic occlusal forces lead to periodontal attachment loss, non-carious cervical lesions, or gingival recessions; 6) traumatic occlusal forces lead to adaptive mobility in teeth with normal support, whereas they lead to progressive mobility in teeth with reduced support, usually requiring splinting; 7) the term biologic width is replaced by supracrestal tissue attachment consisting of junctional epithelium and supracrestal connective tissue; 8) infringement of restorative margins within the supracrestal connective tissue attachment is associated with inflammation and/or loss of periodontal supporting tissue. However, it is not evident whether the negative effects on the periodontium are caused by dental plaque biofilm, trauma, toxicity of dental materials or a combination of these factors; 9) tooth anatomical factors are related to dental plaque biofilm-induced gingival inflammation and loss of periodontal supporting tissues. Conclusion: An updated classification of the periodontal manifestations and conditions affecting the course of periodontitis and the periodontal attachment apparatus, as well as of developmental and acquired conditions, is introduced. Case definitions and diagnostic considerations are also presented. Copyright 2018 American Academy of Periodontology and European Federation of Periodontology
plastic periodontal surgery
Identifier to cite or link to this itemhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85048836248&doi=10.1111%2fjcpe.12951&partnerID=40&md5=db6d9385c397c0d81065508cfe887cd5; http://hdl.handle.net/10713/9754
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Periodontal, metabolic, and cardiovascular disease: Exploring the role of inflammation and mental healthPostolache, T.T.; Makkar, H.; Wadhawan, A. (De Gruyter, 2018)Previous evidence connects periodontal disease, a modifiable condition affecting a majority of Americans, with metabolic and cardiovascular morbidity and mortality. This review focuses on the likely mediation of these associations by immune activation and their potential interactions with mental illness. Future longitudinal, and ideally interventional studies, should focus on reciprocal interactions and cascading effects, as well as points for effective preventative and therapeutic interventions across diagnostic domains to reduce morbidity, mortality and improve quality of life. Copyright 2018 Hina Makkar et al.
Inhibition of CCL2 by bindarit alleviates diabetes-associated periodontitis by suppressing inflammatory monocyte infiltration and altering macrophage propertiesShen, Zongshan; Kuang, Shuhong; Zhang, Min; Huang, Xin; Chen, Jiayao; Guan, Meiliang; Qin, Wei; Xu, Hockin H. K.; Lin, Zhengmei (Springer Science and Business Media LLC, 2020-07-16)Diabetes-associated periodontitis (DP) aggravates diabetic complications and increases mortality from diabetes. DP is caused by diabetes-enhanced host immune-inflammatory responses to bacterial insult. In this study, we found that persistently elevated CCL2 levels in combination with proinflammatory monocyte infiltration of periodontal tissues were closely related to DP. Moreover, inhibition of CCL2 by oral administration of bindarit reduced alveolar bone loss and increased periodontal epithelial thickness by suppressing periodontal inflammation. Furthermore, bindarit suppressed the infiltration of proinflammatory monocytes and altered the inflammatory properties of macrophages in the diabetic periodontium. This finding provides a basis for the development of an effective therapeutic approach for treating DP.
In vitro production of human antibodies reactive with periodontal pathogens, using Epstein-Barr virus immortalization of B lymphocytes derived from peripheral blood of periodontal patients, with an emphasis on the production of a human monoclonal antibody reactive with the heat-modifiable outer membrane protein of Actinobacillus actinomycetemcomitansRaulin, Leslie A.; Falkler, William A., Ph.D. (1995)The purpose of this research was to develop cell line(s) that produce a human monoclonal antibody (huMAb) specific to an oral pathogenic microorganism using Epstein-Barr virus (EBV) transformation of B cells isolated from the gingiva and the peripheral blood of periodontal patients with active disease. The resulting huMAB was then characterized. Excised gingival tissue was obtained from 6 patients and peripheral blood was obtained from 3 of the same patients. To release cells, the gingival tissue was digested with collagenase. Gingival mononuclear cells (GMC) and peripheral blood mononuclear cells (PBMC) were then separated from the gingival extracts, patient peripheral blood, and leukophoresed blood from an anonymous donor by Ficoll centrifugation. The resulting cells were infected with EBV, cultured in 96-well plates, and observed for foci of transformation. Using a dot-immunobinding assay (DIB), the cell culture supernatant fluids (CCS) of transformation-positive wells were tested for Ab reactivity to a panel of 11 microorganisms. Continuously positive cultures were expanded and cloned by limiting dilution. Using an ELISA, clone CCS was tested for Ab reactivity to the microorganism to which the originating culture had exhibited reactivity (target organism). Positive responders were expanded and retested with the ELISA. Continuously producing clones were expanded further, CCS was collected, and excess cells were cryopreserved. The class of Ab in each CCS was determined with a DIB, IgG subclasses and concentration were determined with a commercial ELISA, and the light chain type was determined with a fixed cell indirect immunofluorescence assay (IFA). Using representative strains of the target microorganism, Western blots were performed (separation of bacterial proteins by SDS-PAGE, electroblotting onto nitrocellulose, and probing with concentrated CCS) to determine the MW of the band(s) to which the human antibodies (huAbs) bound. To exclude the possibility of non-specific Ig binding by the target organism, a Western blot was performed with a huMAb of the same IgG subclass and light chain type but with specificity toward a viral protein.;GMC did not transform. Of 517 wells receiving PBMC, 503 wells (97%) had foci of transformation. CCS from 71 of the 517 (14%) wells initially tested positive for Ab activity, most commonly to Eikenella corrodens, Actinobacillus actinomycetemcomitans (Aa), Bacteroides fragilis, Peptostreptococcus micros, and Campylobacter rectus, in order of decreasing frequency. Subsequent DIB during expansion of the cells demonstrated 28, 12, 7, 3, and finally 1 culture with Ab activity (II-24P, reactive with Aa ATCC 43718).;A similar (pilot) experiment was performed with PBMC from 2 healthy control volunteers and from leukophoresed blood. Although initial Ab-producing cultures were obtained, none of the clones produced significant amounts of Ab. (Abstract shortened by UMI).