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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 , HDL 3 , 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%, HDL 3  13.1 ± 5.2%, LDL 11.5 ± 3.7%, and HDL 2  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.

Lipopolysaccharide associates with pro-atherogenic lipoproteins in periodontitis patients