Periodontal Infection and Endothelial Dysfunction

• Brachial Artery Flow-mediated Dilation [ Time Frame: Baseline; 24 hours post periodontal therapy; 12 weeks post periodontal therapy ]
  All the assessments of vascular function were performed in the morning, in a temperature controlled room, with participants required to fast for at least 8 hours. Flow-mediated, endothelium dependent vasodilatation of the brachial artery (FMD) was measured using the technique described by Celermajer et al. using the guidelines reported by Coretti et al. FMD was calculated as the percentage of change in the diameter of brachial artery measured 45-60 s after cuff release in relation to the baseline measure (FMD%).
  
  

• High-sensitivity C-Reactive Protein [ Time Frame: Baseline; 24 hours post periodontal therapy; 12 weeks post periodontal therapy ]
  The fasting plasma hs-CRP concentrations was evaluated using a quantitative solid-phase, chemiluminescent immunometric assay (Immulite 1000, Siemens).
  
  
• Total Cholesterol [ Time Frame: Baseline; 24 hours post periodontal therapy; 12 weeks post periodontal therapy ]
  
• White Blood Cell Count [ Time Frame: Baseline; 24 hours post periodontal therapy; 12 weeks post periodontal therapy ]
  
• Subgingival Microbiota [ Time Frame: 12 weeks post-periodontal therapy ]
  Polymerase chain reaction (PCR) was used for detection of the three red-complex periodontal pathogens in periodontal pockets: Porphyromonas gingivalis (Pg), Treponema denticola (Td) and Tannerella forsythia (Tf).
  
  
• LDL Cholesterol [ Time Frame: Baseline; 24 hours post periodontal therapy; 12 weeks post periodontal therapy ]
  
• Endothelial Leukocyte Adhesion Molecule-1 (E-Selectin) [ Time Frame: 12 weeks post periodontal therapy ]

  Multiplexed immuno-cytometric assay for the simultaneous measurement of MMP-9, MPO, tPAI-1, E-Selectin, ICAM-1, and VCAM-1 in serum samples (Milliplex® MAP kit, Human Cardiovascular Disease Panel 1, Millipore®).

  Luminex® 200™ IS Total System and xPONENT software were used for data acquisition and analysis.

  
  
• Intercellular Adhesion Molecule 1 (ICAM-1) [ Time Frame: 12 weeks post periodontal therapy ]
  
• Vascular Cell Adhesion Molecule 1 (VCAM-1) [ Time Frame: 12 weeks post periodontal therapy ]
  
• Myeloperoxidase (MPO) [ Time Frame: 12 weeks post periodontal therapy ]
  
• Matrix Metalloproteinase-9 (MMP-9) [ Time Frame: 12 weeks post periodontal therapy ]
  
• Tissue Plasminogen Activator Inhibitor-1 (tPAI-1) [ Time Frame: 12 weeks post periodontal therapy ]
  

Periodontitis is one of the most prevalent chronic diseases and a frequent cause of tooth loss. Accumulation of subgingival dental biofilm in susceptible individuals is associated with an inflammatory host response characterized by the production of Matrix Metalloproteinases, reduction in collagen synthesis, increase in cytokine gene expression, and apoptosis of gingival fibroblasts. Finally, inflammation leads to destruction of periodontal ligament, alveolar bone resorption, and chronic periodontitis.

Periodontitis is associated with increased serum levels of inflammatory cytokines and acute phase reactants. Multiple case-control and cohort studies have suggested that periodontitis is an independent risk factor for cardiovascular events, diabetic end-organ damage, pregnancy complications and respiratory diseases. Recent interventional studies have found that periodontal therapy could increase endothelium-dependent brachial artery flow-mediated dilation.

The purpose of this controlled clinical trial is to determine the effect of periodontal therapy on endothelial function in subjects with moderate to severe chronic periodontitis. Furthermore, the relationship between putative periodontal pathogens and endothelial function will be also evaluated.