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Lipoprotein‐associated phospholipase A 2 and plasma lipids in patients with destructive periodontal disease
Author(s) -
Lösche W.,
Marshal G. J.,
Krause S.,
Kocher T.,
Kinane D. F.
Publication year - 2005
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.2005.00725.x
Subject(s) - medicine , periodontitis , simvastatin , cholesterol , inflammation , endocrinology , phospholipid , lipoprotein , risk factor , phospholipase a2 , chemistry , enzyme , biochemistry , membrane
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 μmol/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.