title: Systemic manifestations of periodontitis in the non-human primate.
abstract: This report describes our findings regarding the potential contribution of periodontitis to atherosclerotic processes using a nonhuman primate model. The goal of the investigations was to target general mechanisms which could describe the association of these disease processes, including: (i) systemic translocation of bacteria/products during periodontitis; (ii) alterations in systemic inflammatory biomarkers during periodontitis; and (iii) the relationship of periodontitis to serum lipids/lipoproteins. Increases in serum endotoxin (e.g. LPS) during ligature-induced periodontitis were observed in these animals. We determined serum levels of various acute phase reactants and chemokines (e.g. CRP, alpha 1-antitrypsin, haptoglobin, fibrinogen, IL-8). A number of these host factors were significantly increased during gingivitis and/or periodontitis. Finally, we observed specific changes in serum lipid levels (cholesterol, triglycerides, HDL, LDL) and lipoproteins (apoA-I) during periodontitis, which were exacerbated by exposure of the animals to a diet with elevated fat content. Thus, we have described systemic manifestations of periodontitis that include detection of bacterial products, inflammatory biomarkers, and dyslipoproteinemia consistent with an increased atherogenic risk.
authors.affiliation: Department of Periodontics, School of Dentistry, University of Texas Health Science Center, San Antonio 78284, USA. ebersole@uthscsa.edu
authors.forename: J L
authors.initials: JL
authors.lastname: Ebersole
authors.forename: D
authors.initials: D
authors.lastname: Cappelli
authors.forename: G
authors.initials: G
authors.lastname: Mott
authors.forename: L
authors.initials: L
authors.lastname: Kesavalu
authors.forename: S C
authors.initials: SC
authors.lastname: Holt
authors.forename: R E
authors.initials: RE
authors.lastname: Singer
mesh_terms: D000818:Animals; D016632:Apolipoprotein A-I / Q000097:blood; D001161:Arteriosclerosis / Q000209:etiology*; D018988:Bacterial Translocation / Q000502:physiology; D015415:Biomarkers; D002097:C-Reactive Protein / Q000032:analysis; D018925:Chemokines / Q000097:blood; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004195:Disease Models, Animal; D004731:Endotoxins / Q000502:physiology; D005340:Fibrinogen / Q000032:analysis; D005891:Gingivitis / Q000097:blood / Q000276:immunology / Q000382:microbiology; D006242:Haptoglobins / Q000032:analysis; D006951:Hyperlipoproteinemias / Q000150:complications; D018836:Inflammation Mediators / Q000502:physiology; D016209:Interleukin-8 / Q000097:blood; D008070:Lipopolysaccharides / Q000494:pharmacology; D008252:Macaca fascicularis; D010518:Periodontitis / Q000097:blood / Q000150:complications* / Q000276:immunology / Q000382:microbiology; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D000515:alpha 1-Antitrypsin / Q000032:analysis
chemical_list: D016632:Apolipoprotein A-I; D015415:Biomarkers; D018925:Chemokines; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004731:Endotoxins; D006242:Haptoglobins; D018836:Inflammation Mediators; D016209:Interleukin-8; D008070:Lipopolysaccharides; D014280:Triglycerides; D000515:alpha 1-Antitrypsin; D005340:Fibrinogen; D002097:C-Reactive Protein; D002784:Cholesterol