5 results on '"Madianos, P. N."'
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2. Porphyromonas gingivalis infection of oral epithelium inhibits neutrophil transepithelial migration
- Author
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Madianos, P N, primary, Papapanou, P N, additional, and Sandros, J, additional
- Published
- 1997
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3. Porphyromonas gingivalis FDC381 multiplies and persists within human oral epithelial cells in vitro
- Author
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Madianos, P N, primary, Papapanou, P N, additional, Nannmark, U, additional, Dahlén, G, additional, and Sandros, J, additional
- Published
- 1996
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4. The synthetic chemoattractant Trp-Lys-Tyr-Met-Val-DMet activates neutrophils preferentially through the lipoxin A4receptor
- Author
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Dahlgren, Claes, Christophe, Thierry, Boulay, Francois, Madianos, Phoebus N., Rabiet, Marie J., and Karlsson, Anna
- Abstract
A D-methionine–containing peptide, Trp-Lys-Tyr-Met-Val-D-Met-NH2(WKYMVm), featuring a unique receptor specificity was investigated with respect to its ability to activate neutrophil effector functions. The peptide was found to be more potent than the N-formylated peptide N-formyl-Met-Leu-Phe (fMLF) at inducing neutrophil chemotaxis, mobilization of neutrophil complement receptor 3 (CR3), and activation of the neutrophil NADPH-oxidase. The fact that binding of fML[3H]F was inhibited by both fMLF and WKYMVm suggests that N-formyl peptide receptor (FPR) is shared by these peptides. However, the neutrophil response induced by the WKYMVm peptide was insensitive to the fMLF antagonists, cyclosporin H, and Boc-FLFLF that specifically block the function of the FPR. These results suggest that even though WKYMVm may bind FPR the cells are activated preferentially through a receptor distinct from the FPR. Using transfected HL-60 cells expressing either the FPR or its neutrophil homologue FPRL1, also referred to as LXA4R because it has been shown to bind lipoxin A4, we show that WKYMVm is about 300-fold more active at mobilizing intracellular calcium through FPRL1 than through FPR. The WKYMVm activates FPRL1-expressing cells in a cyclosporin H-independent manner with an EC50of around 75 pmol/L, whereas it activates FPR-expressing cells with an EC50of around 25 nmol/L. The observation that exudated cells are primed in their response to WKYMVm suggests that FPRL1/LXA4R like FPR is stored in mobilizable organelles.
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- 2000
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5. 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
- Author
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Jasim M. Albandar, Carlo Ercoli, Kazuhisa Yamazaki, Korkud Demirel, Evanthia Lalla, Pierpaolo Cortellini, Michael P. Mills, Michael K. McGuire, Lijian Jin, Søren Jepsen, Anton Sculean, Philip M. Preshaw, Nicola X West, Francis J. Hughes, Jack G. Caton, Nicolaas C. Geurs, Mark A. Reynolds, Phoebus N. Madianos, Cristiano Susin, Philippe Bouchard, Debora C Matthews, Jingyuan Fan, Nabil F. Bissada, Massimo de Sanctis, Alpdogan Kantarci, Jepsen, S., Caton, J. G., Albandar, J. M., Bissada, N. F., Bouchard, P., Cortellini, P., Demirel, K., de Sanctis, M., Ercoli, C., Fan, J., Geurs, N. C., Hughes, F. J., Jin, L., Kantarci, A., Lalla, E., Madianos, P. N., Matthews, D., Mcguire, M. K., Mills, M. P., Preshaw, P. M., Reynolds, M. A., Sculean, A., Susin, C., West, N. X., Yamazaki, K., Jepsen, Søren, Caton, Jack G., Albandar, Jasim M., Bissada, Nabil F., Bouchard, Philippe, Cortellini, Pierpaolo, Demirel, Korkud, de Sanctis, Massimo, Ercoli, Carlo, Fan, Jingyuan, Geurs, Nicolaas C., Hughes, Francis J., Jin, Lijian, Kantarci, Alpdogan, Lalla, Evanthia, Madianos, Phoebus N., Matthews, Debora, Mcguire, Michael K., Mills, Michael P., Preshaw, Philip M., Reynolds, Mark A., Sculean, Anton, Susin, Cristiano, West, Nicola X., and Yamazaki, Kazuhisa
- Subjects
0301 basic medicine ,gingival inflammation ,diagnosis ,gingival thickness ,Peri ,Junctional epithelium ,periodontal disease ,Dentistry ,systemic disease ,Esthetics, Dental ,Gingivitis ,0302 clinical medicine ,periodontiti ,dental restorations ,tooth ,610 Medicine & health ,gingiviti ,dental prostheses ,gingival recession ,diagnosi ,classification ,mucogingival surgery ,Periodontics ,medicine.symptom ,Occlusal trauma ,attachment loss ,medicine.medical_specialty ,anatomy ,Consensus ,Dental Plaque ,Dental plaque ,03 medical and health sciences ,genetic disease ,medicine ,plastic periodontal surgery ,Humans ,dental prosthese ,gingival thickne ,Workgroup ,attachment lo ,Intensive care medicine ,Periodontitis ,Gingival recession ,Periodontal Diseases ,bruxism ,dental restoration ,business.industry ,occlusal trauma ,030206 dentistry ,Periodontium ,medicine.disease ,Peri-Implantitis ,stomatognathic diseases ,030104 developmental biology ,Clinical attachment loss ,Implant ,business - Abstract
Background: 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.
- Published
- 2018
- Full Text
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