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Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.

Identifieur interne : 009B66 ( Main/Merge ); précédent : 009B65; suivant : 009B67

Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.

Auteurs : G E Salvi [États-Unis] ; C E Brown ; K. Fujihashi ; H. Kiyono ; F W Smith ; J D Beck ; S. Offenbacher

Source :

RBID : pubmed:9689617

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Abstract

Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN-gamma) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 beta and PGE2 and Th1, i.e. IL-2 and IFN-gamma, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Th1 and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Th1 cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.

PubMed: 9689617

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<nlm:affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, USA.</nlm:affiliation>
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<orgName type="university">Université de Caroline du Nord à Chapel Hill</orgName>
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<title level="j">Journal of periodontal research</title>
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<term>Adult</term>
<term>Aged</term>
<term>Aggressive Periodontitis (immunology)</term>
<term>Cross-Sectional Studies</term>
<term>Cytokines (analysis)</term>
<term>Dentition</term>
<term>Dinoprostone (analysis)</term>
<term>Female</term>
<term>Gingival Crevicular Fluid (immunology)</term>
<term>Humans</term>
<term>Inflammation Mediators (analysis)</term>
<term>Interferon-gamma (analysis)</term>
<term>Interleukin-1 (analysis)</term>
<term>Interleukin-2 (analysis)</term>
<term>Interleukin-4 (analysis)</term>
<term>Interleukin-6 (analysis)</term>
<term>Jaw, Edentulous</term>
<term>Leukocytes, Mononuclear (immunology)</term>
<term>Lipopolysaccharides (immunology)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Monocytes (immunology)</term>
<term>Periodontitis (immunology)</term>
<term>RNA, Messenger (genetics)</term>
<term>Th1 Cells (immunology)</term>
<term>Th2 Cells (immunology)</term>
<term>Tooth Loss (immunology)</term>
<term>Tumor Necrosis Factor-alpha (analysis)</term>
<term>Up-Regulation</term>
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<term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Agranulocytes (immunologie)</term>
<term>Cytokines (analyse)</term>
<term>Denture</term>
<term>Dinoprostone (analyse)</term>
<term>Exsudat gingival (immunologie)</term>
<term>Facteur de nécrose tumorale alpha (analyse)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Interféron gamma (analyse)</term>
<term>Interleukine-1 (analyse)</term>
<term>Interleukine-2 (analyse)</term>
<term>Interleukine-4 (analyse)</term>
<term>Interleukine-6 (analyse)</term>
<term>Lipopolysaccharides (immunologie)</term>
<term>Lymphocytes auxiliaires Th1 (immunologie)</term>
<term>Lymphocytes auxiliaires Th2 (immunologie)</term>
<term>Monocytes (immunologie)</term>
<term>Mâchoire édentée</term>
<term>Mâle</term>
<term>Médiateurs de l'inflammation (analyse)</term>
<term>Parodontite (immunologie)</term>
<term>Parodontite agressive (immunologie)</term>
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<term>Régulation positive</term>
<term>Sujet âgé</term>
<term>Études transversales</term>
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<term>Dinoprostone</term>
<term>Inflammation Mediators</term>
<term>Interferon-gamma</term>
<term>Interleukin-1</term>
<term>Interleukin-2</term>
<term>Interleukin-4</term>
<term>Interleukin-6</term>
<term>Tumor Necrosis Factor-alpha</term>
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<term>Cytokines</term>
<term>Dinoprostone</term>
<term>Facteur de nécrose tumorale alpha</term>
<term>Interféron gamma</term>
<term>Interleukine-1</term>
<term>Interleukine-2</term>
<term>Interleukine-4</term>
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<term>Médiateurs de l'inflammation</term>
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<term>ARN messager</term>
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<term>Agranulocytes</term>
<term>Exsudat gingival</term>
<term>Lipopolysaccharides</term>
<term>Lymphocytes auxiliaires Th1</term>
<term>Lymphocytes auxiliaires Th2</term>
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<term>Parodontite agressive</term>
<term>Perte dentaire</term>
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<term>Gingival Crevicular Fluid</term>
<term>Leukocytes, Mononuclear</term>
<term>Lipopolysaccharides</term>
<term>Monocytes</term>
<term>Periodontitis</term>
<term>Th1 Cells</term>
<term>Th2 Cells</term>
<term>Tooth Loss</term>
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<term>Adult</term>
<term>Aged</term>
<term>Cross-Sectional Studies</term>
<term>Dentition</term>
<term>Female</term>
<term>Humans</term>
<term>Jaw, Edentulous</term>
<term>Male</term>
<term>Middle Aged</term>
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<term>Femelle</term>
<term>Humains</term>
<term>Mâchoire édentée</term>
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<front>
<div type="abstract" xml:lang="en">Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN-gamma) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 beta and PGE2 and Th1, i.e. IL-2 and IFN-gamma, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Th1 and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Th1 cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.</div>
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