Document Detail


Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.
MedLine Citation:
PMID:  9689617     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
G E Salvi; C E Brown; K Fujihashi; H Kiyono; F W Smith; J D Beck; S Offenbacher
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of periodontal research     Volume:  33     ISSN:  0022-3484     ISO Abbreviation:  J. Periodont. Res.     Publication Date:  1998 May 
Date Detail:
Created Date:  1998-10-05     Completed Date:  1998-10-05     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0055107     Medline TA:  J Periodontal Res     Country:  DENMARK    
Other Details:
Languages:  eng     Pagination:  212-25     Citation Subset:  D; IM; X    
Affiliation:
University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Aggressive Periodontitis / immunology*
Cross-Sectional Studies
Cytokines / analysis
Dentition
Dinoprostone / analysis
Female
Gingival Crevicular Fluid / immunology
Humans
Inflammation Mediators / analysis*
Interferon-gamma / analysis
Interleukin-1 / analysis
Interleukin-2 / analysis
Interleukin-4 / analysis
Interleukin-6 / analysis
Jaw, Edentulous
Leukocytes, Mononuclear / immunology
Lipopolysaccharides / immunology
Male
Middle Aged
Monocytes / immunology
Periodontitis / immunology*
RNA, Messenger / genetics
Th1 Cells / immunology
Th2 Cells / immunology
Tooth Loss / immunology*
Tumor Necrosis Factor-alpha / analysis
Up-Regulation
Grant Support
ID/Acronym/Agency:
DE 10519/DE/NIDCR NIH HHS; DE 12453/DE/NIDCR NIH HHS; DE08228/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/Inflammation Mediators; 0/Interleukin-1; 0/Interleukin-2; 0/Interleukin-6; 0/Lipopolysaccharides; 0/RNA, Messenger; 0/Tumor Necrosis Factor-alpha; 207137-56-2/Interleukin-4; 363-24-6/Dinoprostone; 82115-62-6/Interferon-gamma

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