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 A(2) (Lp-PLA(2)) 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-PLA(2) 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-PLA(2). Local treatment lowered the enzyme activity by about 10% from 3.61+/-0.99 to 3.29+/-0.94 micromol/ml/h (mean+/-SD; p<0.001). The pre-treatment values of Lp-PLA(2) and LDL-C significantly correlated with clinical parameters of inflammation and periodontal destruction.

CONCLUSION

This study indicates that treatment of periodontitis significantly reduces the serum activity of Lp-PLA(2), which is believed to be an independent cardiovascular risk factor.