thromboplastin and Periodontitis

The association between periodontal and cardiovascular disease has received considerable attention. Studies have demonstrated a higher incidence of atherosclerotic complications in patients with periodontal disease. Tissue factor (TF) has been known as a key initiator of the coagulation cascade, and the TF pathway is the primary physiological mechanism of initiation of blood coagulation. Recently, it has been shown that the circulating pool of TF in blood is associated with increased blood thrombogenicity in patients with coronary artery disease (CAD). Various tissues and saliva have been known to have TF activity. Consequently, the aim of this study was to investigate plasma TF levels and TF activity of saliva in periodontitis patients with and without diagnosed CAD. Twenty-six patients with a diagnosis of CAD and 26 systemically healthy patients were examined in the dental clinic, and the Community Periodontal Index Treatment Needs (CPITN) scores were recorded. Plasma TF levels were determined using commercially available ELISA kit. Salivary TF activities were determined according to Quick's one-stage method. Plasma TF levels were significantly increased in patients with CAD when compared with the control group. There was no difference in salivary TF activities between the 2 groups, but there was a strong and negative correlation between salivary TF activities and CPITN indexes in both groups. In order to determine the possible role of TF activity as a salivary marker in CAD and periodontitis and to fully understand the negative correlation between salivary TF activities and CPITN, TF activity of gingival crevicular fluid that may also affect saliva can be evaluated.

Topics: Adult; Aged; Aged, 80 and over; Coronary Artery Disease; Female; Humans; Male; Middle Aged; Periodontitis; Saliva; Thromboplastin

Apoptosis provides a mechanism for clearance of unwanted cells in a variety of situations in which programmed or physiological cell death occurs; but the premature death of defensive cells could promote infection, inflammation and concomitant disease. We detected high values of apoptosis in polymorphonuclear cells (PMN) elicited from crevicular sulci of smokers affected by adult periodontitis. To learn more about the effects of nicotine on the periodontal environment, we studied its ability to modulate the apoptosis of two phagocytic lines, PMN and mononuclear cells, which are continuously recruited from gingival vessels to prevent or control plaque extension. Brief exposure of PMN to nicotine concentrations ranging from 0.01 to 0.3% shortened, in a dose-dependent relationship, the lag culture time required to observe at fluorescent microscopy the morphological traces of apoptosis. These observations were confirmed by specific tools of apoptosis: DNA fragmentation on gel electrophoresis and expression of the apoptosis-signaling receptor Fas/Apo-1. The apoptotic effect excited by nicotine on these first line defensive cells may be an important feature of the pathogenesis of periodontal disease. As for mononuclear leukocytes, nicotine was unable to induce apoptotic modifications on cells observed up to 72 h culture time, but the drug inhibited IL-1beta release and procoagulant activity (PCA) expression. The conflicting role played by these lipopolysaccharide (LPS)-induced monocyte functions in the inflammatory process is a further intrigue in the mechanism by which nicotine compromises the oral health.

Topics: Apoptosis; Case-Control Studies; Female; Gingival Crevicular Fluid; Humans; Interleukin-1; Leukocytes, Mononuclear; Lipopolysaccharides; Male; Microscopy, Fluorescence; Middle Aged; Monocytes; Neutrophils; Nicotine; Periodontitis; Thromboplastin