Lipoprotein-associated phospholipase A2 and plasma lipids in patients with destructive periodontal disease

Objectives: Periodontitis is believed to be an independent risk factor of cardiovascular disease (CVD) and to be associated with a moderate systemic inflammatory reaction and hyperlipidaemia. Lipoprotein‐associated phospholipase A2 (Lp‐PLA2) is an enzyme that has been shown to be a risk factor of CVD and that is involved in the degradation of the phospholipid mediator platelet‐activating factor (PAF), a potent mediator of inflammation. Material and Methods: In the present study, we measured concentrations of plasma lipids and plasma activity of Lp‐PLA2 in 32 patients (mean age 43±11 years) with moderate‐to‐severe periodontitis before and 3 months after local treatment. Results: Periodontal therapy resulted in a significant reduction of local inflammation and tissue destruction as reflected in reduced pocket depths and reduced bleeding indices. Pre‐ and post‐treatment plasma lipid levels were (median and range, mmol/l): total cholesterol (C) 5.01 (3.94–7.15) and 4.91 (3.32–8.01); low‐density lipoprotein‐cholesterol (LDL‐C) 3.14 (2.40–4.84) and 2.96 (1.39–5.04); HDL‐C 1.27 (0.73–2.17) and 1.25 (0.74–2.55); triglycerides 1.37 (0.48–5.11) and 1.14 (0.38–792). Using the Wilcoxon's rank test, neither parameter showed a significant change. In contrast to the lacking response of plasma lipids, we observed a significant reduction in the activity of Lp‐PLA2. Local treatment lowered the enzyme activity by about 10% from 3.61±0.99 to 3.29±0.94 μmol/ml/h (mean±SD; p