| Systemic inflammatory responses in progressing periodontitis during pregnancy in a baboon model. | |
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MedLine Citation:
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PMID: 21070210 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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This study tested the hypothesis that pregnant female baboons exhibit increased levels of various inflammatory mediators in serum resulting from ligature-induced periodontitis, and that these profiles would relate to periodontal disease severity/extent in the animals. The animals were sampled at baseline (B), mid-pregnancy (MP; two quadrants ligated) and at delivery (D; four quadrants ligated). All baboons developed increased plaque, gingival inflammation and bleeding, pocket depths and attachment loss following placement of the ligatures. By MP, both prostaglandin E(2) (PGE(2)) and bactericidal permeability inducing factor (BPI) were greater than baseline, while increased levels of interleukin (IL)-6 occurred in the experimental animals by the time of delivery. IL-8, MCP-1 and LBP all decreased from baseline through the ligation phase of the study. Stratification of the animals by baseline clinical presentation demonstrated that PGE(2), LBP, IL-8 and MCP-1 levels were altered throughout the ligation interval, irrespective of baseline clinical values. IL-6, IL-8 and LBP were significantly lower in the subset of animals that demonstrated the least clinical response to ligation, indicative of progressing periodontal disease. PGE(2), macrophage chemotactic protein (MCP)-1, regulated upon activation, normal T cell expressed and secreted (RANTES) and LBP were decreased in the most diseased subset of animals at delivery. Systemic antibody responses to Fusobacterium nucleatum, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Campylobacter rectus were associated most frequently with variations in inflammatory mediator levels. These results provide a profile of systemic inflammatory mediators during ligature-induced periodontitis in pregnant baboons. The relationship of the oral clinical parameters to systemic inflammatory responses is consistent with a contribution to adverse pregnancy outcomes in a subset of the animals. |
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Authors:
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J L Ebersole; M J Steffen; S C Holt; L Kesavalu; L Chu; D Cappelli |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Clinical and experimental immunology Volume: 162 ISSN: 1365-2249 ISO Abbreviation: Clin. Exp. Immunol. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-12 Completed Date: 2011-03-08 Revised Date: 2011-12-21 |
Medline Journal Info:
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Nlm Unique ID: 0057202 Medline TA: Clin Exp Immunol Country: England |
Other Details:
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Languages: eng Pagination: 550-9 Citation Subset: IM |
Copyright Information:
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© 2010 Authors. Clinical and Experimental Immunology © 2010 British Society for Immunology. |
Affiliation:
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Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY 40536, USA. jleber2@uky.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acute-Phase Proteins Animals Antibodies, Bacterial / blood Antimicrobial Cationic Peptides / blood Blood Proteins Carrier Proteins / blood Cytokines / blood Dinoprostone / blood Disease Models, Animal Disease Progression Female Gingivitis Immunoglobulin G / blood Inflammation Mediators / blood* Ligation / adverse effects Membrane Glycoproteins / blood Papio Periodontal Index Periodontitis / blood, etiology, immunology*, physiopathology Pregnancy Pregnancy Complications / blood, etiology, immunology*, physiopathology |
| Grant Support | |
ID/Acronym/Agency:
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13986//PHS HHS; DE13958/DE/NIDCR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Acute-Phase Proteins; 0/Antibodies, Bacterial; 0/Antimicrobial Cationic Peptides; 0/Blood Proteins; 0/Carrier Proteins; 0/Cytokines; 0/Immunoglobulin G; 0/Inflammation Mediators; 0/Membrane Glycoproteins; 0/bactericidal permeability increasing protein; 0/lipopolysaccharide-binding protein; 363-24-6/Dinoprostone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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