Inflammatory mediators of the terminal dentition in adult and early onset periodontitis
Identifieur interne : 009947 ( Main/Exploration ); précédent : 009946; suivant : 009948Inflammatory mediators of the terminal dentition in adult and early onset periodontitis
Auteurs : G. E. Salvi [États-Unis, Suisse] ; C. E. Brown [États-Unis] ; K. Fujihashi [États-Unis] ; H. Kiyono [États-Unis] ; F. W. Smith [États-Unis] ; J. D. Beck [États-Unis] ; S. Offenbacher [États-Unis]Source :
- Journal of Periodontal Research [ 0022-3484 ] ; 1998-05.
Descripteurs français
- KwdFr :
- ARN messager (génétique), Adulte, Adulte d'âge moyen, Agranulocytes (immunologie), Cytokines (analyse), Denture, Dinoprostone (analyse), Exsudat gingival (immunologie), Facteur de nécrose tumorale alpha (analyse), Femelle, Humains, Interféron gamma (analyse), Interleukine-1 (analyse), Interleukine-2 (analyse), Interleukine-4 (analyse), Interleukine-6 (analyse), Lipopolysaccharides (immunologie), Lymphocytes auxiliaires Th1 (immunologie), Lymphocytes auxiliaires Th2 (immunologie), Monocytes (immunologie), Mâchoire édentée, Mâle, Médiateurs de l'inflammation (analyse), Parodontite (immunologie), Parodontite agressive (immunologie), Perte dentaire (immunologie), Régulation positive, Sujet âgé, Études transversales.
- MESH :
- analyse : Cytokines, Dinoprostone, Facteur de nécrose tumorale alpha, Interféron gamma, Interleukine-1, Interleukine-2, Interleukine-4, Interleukine-6, Médiateurs de l'inflammation.
- génétique : ARN messager.
- immunologie : Agranulocytes, Exsudat gingival, Lipopolysaccharides, Lymphocytes auxiliaires Th1, Lymphocytes auxiliaires Th2, Monocytes, Parodontite, Parodontite agressive, Perte dentaire.
- Pascal (Inist)
- Adulte, Adulte d'âge moyen, Analyse quantitative, Cellule helper, Culture cellulaire, Denture, Edentation, Etiopathogénie, Femelle, Homme, Humains, In vitro, In vivo, Inflammation, Interleukine, Lymphocyte, Monocyte, Mâchoire édentée, Mâle, Parodontite, Prostaglandine, Précoce, Réaction chaîne polymérase, Régulation positive, Sujet âgé, Études transversales.
- Wicri :
- topic : Analyse quantitative, Homme, Médiateur.
English descriptors
- KwdEn :
- Adult, Adult periodontitis, Adult periodontitis group, Adult periodontitis terminal dentition, Adult periodontitis terminal dentition subjects, Aged, Aggressive Periodontitis (immunology), Biopsy, Cell culture, Cetus, Chapel hill, Clin, Clin periodontol, Clinical measurements, Crevicular, Cross-Sectional Studies, Crude estimate, Cytokine, Cytokines (analysis), Dentition, Dinoprostone (analysis), Disease progression, Early, Early onset periodontitis terminal dentition subjects, Edentulousness, Etiopathogenesis, Female, Fujihashi, Gingival, Gingival Crevicular Fluid (immunology), Gingival crevicular fluid, Gingival tissue biopsies, Helper cell, High levels, Human, Human monocytes, Humans, Immunol, Immunol today, In vitro, In vivo, Inflamed, Inflammation, Inflammation Mediators (analysis), Inflammatory, Inflammatory mediators, Interferon-gamma (analysis), Interleukin, Interleukin-1 (analysis), Interleukin-2 (analysis), Interleukin-4 (analysis), Interleukin-6 (analysis), Intermediate tier, Jaw, Edentulous, Leukocytes, Mononuclear (immunology), Lipopolysaccharides (immunology), Lymphocyte, Male, Maximum expression, Mediator, Middle Aged, Mild expression, Moderate expression, Monocyte, Monocyte isolation, Monocytes (immunology), Monocytic, Monocytic secretion, Mononuclear, Mononuclear cells, Mrna, Multiple extractions, Norwalk, Offenbacher, Onset periodontitis, Onset periodontitis terminal dentition, Ordinal scale, Periodont, Periodontal, Periodontal disease, Periodontal diseases, Periodontal status, Periodontal surgery, Periodontitis, Periodontitis (immunology), Periodontitis patients, Periodontol, Peripheral blood monocytes, Perkin, Perkin elmer cetus, Plasma cells, Pocket depth, Polymerase chain reaction, Previous reports, Prostaglandin, Prosthodontic literature, Quadrant, Quantitative analysis, RNA, Messenger (genetics), Salvi, Secretion, Terminal, Terminal dentition, Terminal dentition periodontitis, Th1 Cells (immunology), Th2 Cells (immunology), Tier, Tnfa, Tooth Loss (immunology), Tooth loss, Tumor Necrosis Factor-alpha (analysis), Up-Regulation.
- MESH :
- chemical , analysis : Cytokines, Dinoprostone, Inflammation Mediators, Interferon-gamma, Interleukin-1, Interleukin-2, Interleukin-4, Interleukin-6, Tumor Necrosis Factor-alpha.
- chemical , genetics : RNA, Messenger.
- immunology : Aggressive Periodontitis, Gingival Crevicular Fluid, Leukocytes, Mononuclear, Lipopolysaccharides, Monocytes, Periodontitis, Th1 Cells, Th2 Cells, Tooth Loss.
- Adult, Aged, Cross-Sectional Studies, Dentition, Female, Humans, Jaw, Edentulous, Male, Middle Aged, Up-Regulation.
- Teeft :
- Adult periodontitis, Adult periodontitis group, Adult periodontitis terminal dentition, Adult periodontitis terminal dentition subjects, Biopsy, Cetus, Chapel hill, Clin, Clin periodontol, Clinical measurements, Crevicular, Crude estimate, Cytokine, Dentition, Disease progression, Early onset periodontitis terminal dentition subjects, Fujihashi, Gingival, Gingival crevicular fluid, Gingival tissue biopsies, High levels, Human monocytes, Immunol, Immunol today, Inflamed, Inflammatory, Inflammatory mediators, Intermediate tier, Maximum expression, Mediator, Mild expression, Moderate expression, Monocyte, Monocyte isolation, Monocytic, Monocytic secretion, Mononuclear, Mononuclear cells, Mrna, Multiple extractions, Norwalk, Offenbacher, Onset periodontitis, Onset periodontitis terminal dentition, Ordinal scale, Periodont, Periodontal, Periodontal disease, Periodontal diseases, Periodontal status, Periodontal surgery, Periodontitis, Periodontitis patients, Periodontol, Peripheral blood monocytes, Perkin, Perkin elmer cetus, Plasma cells, Pocket depth, Previous reports, Prostaglandin, Prosthodontic literature, Quadrant, Salvi, Secretion, Terminal, Terminal dentition, Terminal dentition periodontitis, Tier, Tnfa, Tooth loss.
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‐1β (IL‐1β) and interleukin‐2 (IL‐2), the intermediate tier included tumor necrosis factor alpha (TNFα) and interferon gamma (IFN‐γ) and at the lowest concentration level were interleukin‐4 (IL‐4) and interleukin‐6 (IL‐6). Thus, the GCF analysis dearly indicated that in both AP‐TD and EOP‐TD groups the monocytic, i.e. IL‐1β and PGE2 and Th1, i.e. IL‐2 and IFN‐γ, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL‐4 and IL‐6. LPS‐stimulated monocytic release of IL‐1β, PGE2 and TNFα 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.
Url:
- https://api.istex.fr/document/6E4B84ABF19D74D1145A48C60DC417F46AA140FF/fulltext/pdf
- https://api.istex.fr/document/A7E0606E0544949E58DA354FCFC70C6F96B0940D/fulltext/pdf
DOI: 10.1111/j.1600-0765.1998.tb02193.x
Affiliations:
- Suisse, États-Unis
- Alabama, Canton de Berne, Caroline du Nord
- Berne, Chapel Hill (Caroline du Nord)
- Université de Caroline du Nord à Chapel Hill
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Le document en format XML
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Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-05">1998-05</date></imprint><idno type="ISSN">0022-3484</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3484</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Adult periodontitis</term><term>Adult periodontitis group</term><term>Adult periodontitis terminal dentition</term><term>Adult periodontitis terminal dentition subjects</term><term>Aged</term><term>Aggressive Periodontitis (immunology)</term><term>Biopsy</term><term>Cell culture</term><term>Cetus</term><term>Chapel hill</term><term>Clin</term><term>Clin periodontol</term><term>Clinical measurements</term><term>Crevicular</term><term>Cross-Sectional Studies</term><term>Crude estimate</term><term>Cytokine</term><term>Cytokines (analysis)</term><term>Dentition</term><term>Dinoprostone (analysis)</term><term>Disease progression</term><term>Early</term><term>Early onset periodontitis terminal dentition subjects</term><term>Edentulousness</term><term>Etiopathogenesis</term><term>Female</term><term>Fujihashi</term><term>Gingival</term><term>Gingival Crevicular Fluid (immunology)</term><term>Gingival crevicular fluid</term><term>Gingival tissue biopsies</term><term>Helper cell</term><term>High levels</term><term>Human</term><term>Human monocytes</term><term>Humans</term><term>Immunol</term><term>Immunol today</term><term>In vitro</term><term>In vivo</term><term>Inflamed</term><term>Inflammation</term><term>Inflammation Mediators (analysis)</term><term>Inflammatory</term><term>Inflammatory mediators</term><term>Interferon-gamma (analysis)</term><term>Interleukin</term><term>Interleukin-1 (analysis)</term><term>Interleukin-2 (analysis)</term><term>Interleukin-4 (analysis)</term><term>Interleukin-6 (analysis)</term><term>Intermediate tier</term><term>Jaw, Edentulous</term><term>Leukocytes, Mononuclear 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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><term>Perte dentaire (immunologie)</term><term>Régulation positive</term><term>Sujet âgé</term><term>Études transversales</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Cytokines</term><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></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><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><term>Interleukine-6</term><term>Médiateurs de l'inflammation</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Agranulocytes</term><term>Exsudat gingival</term><term>Lipopolysaccharides</term><term>Lymphocytes auxiliaires Th1</term><term>Lymphocytes auxiliaires Th2</term><term>Monocytes</term><term>Parodontite</term><term>Parodontite agressive</term><term>Perte dentaire</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Aggressive Periodontitis</term><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></keywords><keywords scheme="MESH" xml:lang="en"><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><term>Up-Regulation</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Adulte</term><term>Adulte d'âge moyen</term><term>Analyse quantitative</term><term>Cellule helper</term><term>Culture cellulaire</term><term>Denture</term><term>Edentation</term><term>Etiopathogénie</term><term>Femelle</term><term>Homme</term><term>Humains</term><term>In vitro</term><term>In vivo</term><term>Inflammation</term><term>Interleukine</term><term>Lymphocyte</term><term>Monocyte</term><term>Mâchoire édentée</term><term>Mâle</term><term>Parodontite</term><term>Prostaglandine</term><term>Précoce</term><term>Réaction chaîne polymérase</term><term>Régulation positive</term><term>Sujet âgé</term><term>Études transversales</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Adult periodontitis</term><term>Adult periodontitis group</term><term>Adult periodontitis terminal dentition</term><term>Adult periodontitis terminal dentition subjects</term><term>Biopsy</term><term>Cetus</term><term>Chapel hill</term><term>Clin</term><term>Clin periodontol</term><term>Clinical measurements</term><term>Crevicular</term><term>Crude estimate</term><term>Cytokine</term><term>Dentition</term><term>Disease progression</term><term>Early onset periodontitis terminal dentition subjects</term><term>Fujihashi</term><term>Gingival</term><term>Gingival crevicular fluid</term><term>Gingival tissue biopsies</term><term>High levels</term><term>Human monocytes</term><term>Immunol</term><term>Immunol today</term><term>Inflamed</term><term>Inflammatory</term><term>Inflammatory mediators</term><term>Intermediate tier</term><term>Maximum expression</term><term>Mediator</term><term>Mild expression</term><term>Moderate expression</term><term>Monocyte</term><term>Monocyte isolation</term><term>Monocytic</term><term>Monocytic secretion</term><term>Mononuclear</term><term>Mononuclear cells</term><term>Mrna</term><term>Multiple extractions</term><term>Norwalk</term><term>Offenbacher</term><term>Onset periodontitis</term><term>Onset periodontitis terminal dentition</term><term>Ordinal scale</term><term>Periodont</term><term>Periodontal</term><term>Periodontal disease</term><term>Periodontal diseases</term><term>Periodontal status</term><term>Periodontal surgery</term><term>Periodontitis</term><term>Periodontitis patients</term><term>Periodontol</term><term>Peripheral blood monocytes</term><term>Perkin</term><term>Perkin elmer cetus</term><term>Plasma cells</term><term>Pocket depth</term><term>Previous reports</term><term>Prostaglandin</term><term>Prosthodontic literature</term><term>Quadrant</term><term>Salvi</term><term>Secretion</term><term>Terminal</term><term>Terminal dentition</term><term>Terminal dentition periodontitis</term><term>Tier</term><term>Tnfa</term><term>Tooth loss</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Analyse quantitative</term><term>Homme</term><term>Médiateur</term></keywords></textClass></profileDesc></teiHeader><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‐1β (IL‐1β) and interleukin‐2 (IL‐2), the intermediate tier included tumor necrosis factor alpha (TNFα) and interferon gamma (IFN‐γ) and at the lowest concentration level were interleukin‐4 (IL‐4) and interleukin‐6 (IL‐6). Thus, the GCF analysis dearly indicated that in both AP‐TD and EOP‐TD groups the monocytic, i.e. IL‐1β and PGE2 and Th1, i.e. IL‐2 and IFN‐γ, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL‐4 and IL‐6. LPS‐stimulated monocytic release of IL‐1β, PGE2 and TNFα 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></front></TEI><affiliations><list><country><li>Suisse</li><li>États-Unis</li></country><region><li>Alabama</li><li>Canton de Berne</li><li>Caroline du Nord</li></region><settlement><li>Berne</li><li>Chapel Hill (Caroline du Nord)</li></settlement><orgName><li>Université de Caroline du Nord à Chapel Hill</li></orgName></list><tree><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Salvi, G E" sort="Salvi, G E" uniqKey="Salvi G" first="G. E." last="Salvi">G. E. Salvi</name></region><name sortKey="Beck, J D" sort="Beck, J D" uniqKey="Beck J" first="J. D." last="Beck">J. D. Beck</name><name sortKey="Brown, C E" sort="Brown, C E" uniqKey="Brown C" first="C. E." last="Brown">C. E. Brown</name><name sortKey="Fujihashi, K" sort="Fujihashi, K" uniqKey="Fujihashi K" first="K." last="Fujihashi">K. Fujihashi</name><name sortKey="Kiyono, H" sort="Kiyono, H" uniqKey="Kiyono H" first="H." last="Kiyono">H. Kiyono</name><name sortKey="Offenbacher, S" sort="Offenbacher, S" uniqKey="Offenbacher S" first="S." last="Offenbacher">S. Offenbacher</name><name sortKey="Smith, F W" sort="Smith, F W" uniqKey="Smith F" first="F. W." last="Smith">F. W. Smith</name></country><country name="Suisse"><region name="Canton de Berne"><name sortKey="Salvi, G E" sort="Salvi, G E" uniqKey="Salvi G" first="G. E." last="Salvi">G. E. Salvi</name></region><name sortKey="Salvi, G E" sort="Salvi, G E" uniqKey="Salvi G" first="G. E." last="Salvi">G. E. Salvi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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