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Lipopolysaccharide associates with pro-atherogenic lipoproteins in periodontitis patients

Institute of Dentistry, University of Helsinki, and Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Helsinki, Finland, elisa.kallio{at}helsinki.fi

Kåre Buhlin

Division of Periodontology, Institute of Odontology, Karolinska Institutet, Huddinge, Sweden

Matti Jauhiainen

Department of Molecular Medicine, National Public Health Institute, Helsinki, Finland

Ritva Keva

Institute of Dentistry, University of Helsinki, and Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Helsinki, Finland

Anita M. Tuomainen

Institute of Dentistry, University of Helsinki, and Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Helsinki, Finland

Björn Klinge

Division of Periodontology, Institute of Odontology, Karolinska Institutet, Huddinge, Sweden

Anders Gustafsson

Division of Periodontology, Institute of Odontology, Karolinska Institutet, Huddinge, Sweden

Pirkko J. Pussinen

Division of Periodontology, Institute of Odontology, Karolinska Institutet, Huddinge, Sweden

Introduction: 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.

Patients and 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.

Key Words: Infection • inflammation • lipoproteins • lipoprotein subclasses • periodontal disease • teeth

Innate Immunity, Vol. 14, No. 4, 247-253 (2008)
DOI: 10.1177/1753425908095130


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