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

我们报道了牙龈卟啉单胞菌(P.gigivalis)诱导人血小板聚集。在外周动脉疾病患者和正常志愿者之间进行了全血血小板聚集试验。PAD患者的血小板聚集率明显高于正常对照组，Fontaine III/IV组高于Fontaine II组，且PAD患者PAD患者的血小板聚集率明显高于Fontaine II组，且PAD患者的血小板聚集率明显高于Fontaine II组，FcrRIIa/IIIb(CD32)抗体预处理可使PAD患者出现PG诱导的血小板聚集完全消失、部分抑制和完全反应三种类型。当CD32抗体预处理(>5欧姆)后充分诱导血小板聚集时，PG不能诱导额外的血小板聚集。反之，在轻度上调时(<1-3欧姆)，PG诱导的血小板聚集不受抑制，提示CD32抗体和PG竞争诱导血小板聚集。重度牙周炎患者刷牙后可诱导血小板聚集。提示牙龈假单胞菌通过激活血小板参与了PAD的加重。

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.