title: Lipoprotein-associated phospholipase A2 and plasma lipids in patients with destructive periodontal disease.
abstract: OBJECTIVE
  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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Clinic for Anaesthesiology and Intensive Care Medicine, University Hospital Jena, Jena, Germany. wolfgang.loesche@med.uni-jena.de
authors.forename: W
authors.initials: W
authors.lastname: Lösche
authors.forename: G J
authors.initials: GJ
authors.lastname: Marshal
authors.forename: D A
authors.initials: DA
authors.lastname: Apatzidou
authors.forename: S
authors.initials: S
authors.lastname: Krause
authors.forename: T
authors.initials: T
authors.lastname: Kocher
authors.forename: D F
authors.initials: DF
authors.lastname: Kinane
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000328:Adult; D000368:Aged; D002318:Cardiovascular Diseases / Q000209:etiology; D012534:Dental Scaling; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010510:Periodontal Diseases / Q000097:blood* / Q000150:complications / Q000628:therapy; D010741:Phospholipases A / Q000097:blood*; D054467:Phospholipases A2; D012307:Risk Factors; D016745:Root Planing; D018709:Statistics, Nonparametric
chemical_list: D010741:Phospholipases A; D054467:Phospholipases A2; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase