Journal of clinical periodontology · 2007
Acute effects of periodontal therapy on bio-markers of vascular health.
Клиническое исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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D'Aiuto Francesco, Parkar M, Tonetti Maurizio S
Аннотация
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)-1beta, tumour necrosis factor-alpha], 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-1beta (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.
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)-1beta, tumour necrosis factor-alpha], 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-1beta (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.