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Acute effects of periodontal therapy on bio‐markers of vascular health
Author(s) -
D'Aiuto Francesco,
Parkar M.,
Tonetti Maurizio S.
Publication year - 2007
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.2006.01037.x
Subject(s) - von willebrand factor , medicine , periodontitis , d dimer , endothelial activation , inflammation , gastroenterology , fibrinogen , coagulation , bleeding on probing , chronic periodontitis , in vivo , immunology , platelet , microbiology and biotechnology , biology
Abstract Aim: We aimed to study the impact of periodontal therapy on several bio‐markers related to vascular health. Material and Methods: Fifty‐five consecutive subjects (age range 30–64 years) having severe periodontitis received an intensive session of periodontal therapy under local anaesthesia and provided blood samples before and 1 and 7 and 30 days following therapy. High‐sensitivity assays were utilized to quantify serum concentrations of inflammatory markers [interleukin(IL)‐1 β , tumour necrosis factor‐ α ], plasma haemostatic (D‐dimer) and endothelial soluble markers [soluble E‐selectin(s‐Es) and von Willebrand factor antigen (r‐WF:Ag)]. Results: Periodontal therapy elicited a significant activation of the haemostatic system (38% and 68% mean increases of plasma D‐dimer 1 and 7 days after therapy, respectively, p <0.001), together with moderate endothelial dysfunction (10% and 30% mean increases at 24 h in plasma soluble E‐selectin, p <0.05 and von‐Willebrand factor, p <0.01, respectively). D‐Dimer and s‐Es acute changes were significantly correlated with periodontal treatment time ( p <0.05). Cigarette smoking status and body mass index strongly influenced the acute release of IL‐1 β ( p <0.05), D‐dimer ( p <0.01) and s‐Es ( p <0.01). Conclusions: Periodontal therapy represents a novel and reliable non‐drug‐induced model to investigate in vivo the interplay between inflammation, coagulation and endothelial cell activation.