An association between peripheral artery disease and periodontal pathogen relating with platelet aggregation

点击翻译按钮获取中文摘要

We reported that Porphyromonas gingivalis (P. gingivalis) induced human platelet aggregation. Platelet aggregation using whole blood was assessed between patients with peripheral artery disease and normal volunteers. P. gingivalis induced platelet aggregation increased in PAD patients than normal control, which showed higher in patients with Fontaine III/IV compared with Fontaine II, and exhibited positive correlation with IgG titer for P. gingivalis. FcrRIIa/IIIb(CD32) antibody pretreatment resulted PAD patients in three categories including complete abolishment, partial suppression, and full reaction of Pg induced platelet aggregation. When platelet aggregation was induced sufficiently after CD32 antibody pretreatment (more than 5 ohm), Pg did not induce additionalplatelet aggregation. In contrast, Pg induced platelet aggregation was not suppressed when slight upregulation was shown (less than 1-3 ohm), suggesting that CD32 antibody and Pg induced platelet aggregation competitively. Platelet aggregation was induced after tooth brushing in patients with severe periodontitis. It was suggested that P. gingivalis involved in PAD aggravation by platelet activation.