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Journal of Lipid Research, Vol. 45, 139-147, January 2004
Copyright © 2004 by American Society for Biochemistry and Molecular Biology
* Institute of Dentistry, University of Helsinki, and Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Helsinki, Finland
Department of Molecular Medicine, National Public Health Institute, Helsinki, Finland
Department of Health and Functional Ability, National Public Health Institute, Helsinki, Finland
** Adhesion Center/Oral Microbiology, Department of Medicine and Odontology, Umeå University, Umeå, Sweden
1 To whom correspondence should be addressed. e-mail: pirkko.pussinen{at}helsinki.fi
Periodontitis, a consequence of persistent bacterial infection and chronic inflammation, has been suggested to predict coronary heart disease (CHD). The aim of this study was to investigate the impact of periodontitis on HDL structure and antiatherogenic function in cholesterol efflux in vitro. HDL was isolated from 30 patients (age 43.6 ± 6.1 years, mean ± SD) with periodontitis before and after (3.2 ± 1.4 months) periodontal treatment. The capacity of HDL for cholesterol efflux from macrophages (RAW 264.7), HDL composition, and key proteins of HDL metabolism were determined. After periodontal treatment, phospholipid transfer protein (PLTP) activity was 6.2% (P < 0.05) lower, and serum HDL cholesterol concentration, PLTP mass, and cholesteryl ester transfer protein activity were 10.7% (P < 0.001), 7.1% (P = 0.078), and 19.4% (P < 0.001) higher, respectively. The mean HDL2/HDL3 ratio increased from 2.16 ± 0.87 to 3.56 ± 0.48 (P < 0.05). HDL total phospholipid mass and sphingomyelin-phosphatidylcholine ratio were 7.4% (P < 0.05) and 36.8% (P < 0.001) higher, respectively. The HDL-mediated cholesterol efflux tended to be higher after periodontal treatment; interestingly, this increase was significant (P < 0.05) among patients whose C-reactive protein decreased (53.7% reduction, P = 0.015) and who were positive by PCR for Actinobacillus actinomycetemcomitans.
These results suggest that periodontitis causes similar, but milder, changes in HDL metabolism than those that occur during the acute-phase response and that periodontitis may diminish the antiatherogenic potency of HDL, thus increasing the risk for CHD.
Abbreviations: apoA-I, apolipoprotein A-I; CETP, cholesteryl ester transfer protein; CHD, coronary heart disease; CRP, C-reactive protein; HL, hepatic lipase; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PLTP, phospholipid transfer protein; PS, phosphatidylserine; SAA, serum amyloid A; SM, sphingomyelin; TG, triglyceride
Supplementary key words HDL metabolism • atherosclerosis • reverse cholesterol transport • cholesterol efflux • inflammation
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