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J. Lipid Res.
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A more recent version of this article appeared on January 1, 2004

Papers In Press, published online ahead of print September 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300250-JLR200
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Submitted on June 11, 2003
Revised on August 27, 2003
Accepted on September 10, 2003

Periodontitis decreases the antiatherogenic potency of high density lipoprotein (HDL)

Pirkko J. Pussinen, Matti Jauhiainen, Tiina Vilkuna-Rautiainen, Jouko Sundvall, Marja Vesanen, Kimmo Mattila, Timo Palosuo, Georg Alfthan, and Sirkka Asikainen

University of Helsinki, Institute of Dentistry, Helsinki FIN-00014

Corresponding Author: 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 (RAW264.7), 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 (CETP) activity 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/phosphatidyl choline –ratio was 7.4% (p<0.05) and 36.8% (p<0.001) higher. The HDL-mediated cholesterol efflux tended to be higher after periodontal treatment; interestingly this increase was significant (p<0.05) among patients whose CRP decreased (53.7%, p=0.015) and who were PCR-positive for Actinobacillus actinomycetemcomitans. The results suggest that periodontitis causes similar, but milder changes in HDL metabolism than those during acute-phase response, and that periodontitis may diminish the antiatherogenic potency of HDL, thus increasing the risk for CHD.


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