In addition, HGF and c-Met are expressed in the atherosclerotic vessel wall and in plaque [4] and [20]. There is an emerging interest in the link between oral health and systemic diseases, such as CAD. Indeed, periodontal disease is more p38 MAPK inhibitor prevalent among patients with CAD than among healthy people [21] and [22]. Porphyromonas gingivalis

(P. gingivalis) is an etiological agent strongly associated with periodontal disease [23] and correlates with numerous inflammatory disorders, such as cardiovascular and rheumatic disease. P. gingivalis has been detected in human atheromatous carotid plaques [24], and serum antibodies to P. gingivalis have been shown to predict myocardial infarction [25]. Furthermore, periodontal pockets with a high number of periodontally pathogenic bacteria are a risk

Selleck AUY-922 factor for acute coronary syndrome [26]. Chronically inflamed periodontal pockets may serve as a reservoir for inflammatory stimuli, and by entering the circulation, oral bacteria and their components activate neutrophils and platelets, thereby inducing production of reactive oxygen species [27], and triggering the inflammatory process in the carotid vessels. P. gingivalis contributes to periodontal disease via virulence factors such as cysteine proteinases (gingipains), fimbriae, and LPS, and an infection may lead to chronic inflammation in which hyper-responsive neutrophils contribute to host-mediated tissue destruction. In periodontitis, HGF concentrations,

in gingival Edoxaban crevicular fluid and in saliva, increase proportionally with the progression of periodontal disease [28], and P. gingivalis stimulates HGF synthesis in human gingival fibroblasts [29]. While ELISA is a reliable, sensitive method for protein detection, this method does not differentiate between biologically active and inactive HGF [14]. The binding of HGF to HSPG has previously been shown to be important for the biological activity of HGF and for the induction of cellular responses [30] and [31]. Surface plasmon resonance (SPR) is an optical technique that can determine the affinity of a protein for several ligands or epitopes [32] and [33]. SPR-based assessment of the binding profile of HGF to HSPG may rapidly and sensitively distinguish HGF variants with different biological activities. Appropriate for clinical studies, this method can be used for evaluation of the quality of endogenous HGF [30]. The aim of the present study was to investigate the concentration and the biological activity of HGF with ELISA and SPR, respectively, in patients with confirmed CAD, and to examine the relationship with periodontal disease and the presence of P. gingivalis in periodontal pockets. Thirty six (mean age 59.