Systemic inflammatory responses in progressing periodontitis during pregnancy in a baboon model.
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.
Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY 40536, USA. jleber2@uky.edu
J L
JL
Ebersole
M J
MJ
Steffen
S C
SC
Holt
L
L
Kesavalu
L
L
Chu
D
D
Cappelli
D000209:Acute-Phase Proteins; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D023181:Antimicrobial Cationic Peptides / Q000097:blood; D001798:Blood Proteins; D002352:Carrier Proteins / Q000097:blood; D016207:Cytokines / Q000097:blood; D015232:Dinoprostone / Q000097:blood; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D005891:Gingivitis; D007074:Immunoglobulin G / Q000097:blood; D018836:Inflammation Mediators / Q000097:blood*; D008026:Ligation / Q000009:adverse effects; D008562:Membrane Glycoproteins / Q000097:blood; D010215:Papio; D010512:Periodontal Index; D010518:Periodontitis / Q000097:blood / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D000099231:Lipopolysaccharide-Binding Protein
D000209:Acute-Phase Proteins; D000907:Antibodies, Bacterial; D023181:Antimicrobial Cationic Peptides; D001798:Blood Proteins; D002352:Carrier Proteins; D016207:Cytokines; D015232:Dinoprostone; D007074:Immunoglobulin G; D018836:Inflammation Mediators; D008562:Membrane Glycoproteins; D000099231:Lipopolysaccharide-Binding Protein; C021623:bactericidal permeability increasing protein