title: Lipopolysaccharide associates with pro-atherogenic lipoproteins in periodontitis patients.
abstract: BACKGROUND
  Periodontitis patients are known to suffer from endotoxemia, which may be among the major risk factors for atherosclerosis. In health, lipopolysaccharide (LPS) is mainly carried with high density lipoprotein (HDL) particles. Shift of LPS toward lipoproteins with lower densities may result in less effective endotoxin scavenging. Our aim was to determine plasma LPS activity and lipoprotein-distribution before and after treatment in periodontitis patients.
  
  
  METHODS
  Very low and intermediate density (VLDL-IDL), low density (LDL), HDL 2, HDL3, and lipoprotein-deficient plasma (LPDP) were isolated by sequential ultracentrifugation. Patients included 34 subjects aged 53.5 +/- 8.3 years, before and 6 months after periodontal treatment.
  
  
  RESULTS
  The mean LPS distribution decreased among lipoprotein classes as follows: VLDL-IDL 41.3 +/- 12.1%, LPDP 25.0 +/- 7.0%, HDL3 13.1 +/- 5.2%, LDL 11.5 +/- 3.7%, and HDL2 9.2 +/- 2.8%. Plasma and VLDL-IDL-associated LPS correlated positively, and LDL- and HDL-associated LPS negatively with clinical periodontal parameters and plasma cytokine concentrations. Mean plasma LPS activity increased after periodontal treatment from 44.0 +/- 17.0 to 55.7 +/- 24.2 EU/ml (P = 0.006). No significant changes were found in LPS lipoprotein distribution and lipoprotein compositions after the treatment.
  
  
  CONCLUSIONS
  Endotoxemia increases with severity of periodontitis. In periodontitis, LPS associates preferentially with the pro-atherogenic VLDL-IDL fraction. Periodontal treatment has only minor effects on plasma LPS activity or distribution, which reflects persistence of the disease.
authors.affiliation: Institute of Dentistry, University of Helsinki, and Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Helsinki, Finland. elisa.kallio@helsinki.fi
authors.forename: K A Elisa
authors.initials: KA
authors.lastname: Kallio
authors.forename: Kåre
authors.initials: K
authors.lastname: Buhlin
authors.forename: Matti
authors.initials: M
authors.lastname: Jauhiainen
authors.forename: Ritva
authors.initials: R
authors.lastname: Keva
authors.forename: Anita M
authors.initials: AM
authors.lastname: Tuomainen
authors.forename: Björn
authors.initials: B
authors.lastname: Klinge
authors.forename: Anders
authors.initials: A
authors.lastname: Gustafsson
authors.forename: Pirkko J
authors.initials: PJ
authors.lastname: Pussinen
mesh_terms: D050197:Atherosclerosis / Q000097:blood / Q000209:etiology / Q000276:immunology; D001693:Biological Transport, Active; D004705:Endocytosis / Q000276:immunology; D019446:Endotoxemia / Q000097:blood / Q000276:immunology; D005260:Female; D006801:Humans; D008070:Lipopolysaccharides / Q000097:blood* / Q000276:immunology; D008074:Lipoproteins / Q000097:blood* / Q000737:chemistry / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010518:Periodontitis / Q000097:blood* / Q000188:drug therapy / Q000276:immunology; D011485:Protein Binding; D012720:Severity of Illness Index
chemical_list: D008070:Lipopolysaccharides; D008074:Lipoproteins