Intraplaque hemorrhage, a potential consequence of periodontal bacteria gathering in human carotid atherothrombosis.

Adrian Brun, Hélène Rangé, Bastien Prouvost, Olivier Meilhac, Mikael Mazighi, Pierre Amarenco, Guy Lesèche, Philippe Bouchard, Jean-Baptiste Michel
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Abstract

Periodontal diseases are multifactorial inflammatory diseases, caused by a bacterial biofilm involving both innate and adaptative immunity, characterized by the destruction of tooth-supporting tissues. In the context of periodontitis, the spread of weak pathogenic bacteria into the bloodstream has been described. These bacteria will preferentially localize to existing clot within the circulation. Atherothrombosis of the carotid arteries is a local pathology and a common cause of cerebral infarction. Intraplaque hemorrhages render the lesion more prone to clinical complications such as stroke. The main objective of this study is to explore the biological relationship between carotid intraplaque hemorrhage and periodontal diseases. This study included consecutive patients with symptomatic or asymptomatic carotid stenosis, admitted for endarterectomy surgical procedure (n=41). In conditioned media of the carotid samples collected, markers of neutrophil activation (myeloperoxidase or MPO, DNA-MPO complexes) and hemoglobin were quantified. To investigate the presence of DNA from periodontal bacteria in atherosclerotic plaque, PCR analysis using specific primers was performed. Our preliminary results indicate an association between neutrophil activation and intraplaque hemorrhages, reflected by the release of MPO (p<0,01) and MPO-DNA complexes (p<0,05). Presence of DNA from periodontitis-associated bacteria was found in 32/41 (78%) atheromatous plaque samples. More specifically, DNA from Pg, Tf, Pi, Aa was found in 46%, 24%, 34% and 68% of the samples, respectively. Hemoglobin levels were higher in conditioned media in carotid samples where the bacteria were found, but this was not statistically significant. Our data confirm the relationship between intraplaque hemorrhage and neutrophil activation. In addition, the presence of periodontal bacteria DNA in carotid atheromatous plaque, may contribute to this activation. Further analysis is needed to fully explore the raw data and specimens.

斑块内出血,一个潜在的后果牙周细菌聚集在人颈动脉粥样硬化血栓。
牙周病是一种多因素炎症性疾病,由细菌生物膜引起,涉及先天免疫和适应性免疫,以破坏牙齿支持组织为特征。在牙周炎的情况下,已经描述了弱致病菌进入血液的传播。这些细菌会优先定位于循环中的现有凝块。颈动脉粥样硬化是一种局部病理,也是脑梗死的常见原因。斑块内出血使病变更容易发生临床并发症,如中风。本研究的主要目的是探讨颈动脉斑块内出血与牙周病的生物学关系。本研究纳入了连续接受动脉内膜切除术的有症状或无症状颈动脉狭窄患者(n=41)。在采集的颈动脉样本的条件培养基中,对中性粒细胞活化标志物(髓过氧化物酶或MPO, DNA-MPO复合物)和血红蛋白进行定量。为了研究动脉粥样硬化斑块中牙周细菌DNA的存在,采用特异性引物进行了PCR分析。我们的初步结果表明,中性粒细胞活化与斑块内出血之间存在关联,这可以通过MPO (p< 0.01)和MPO- dna复合物(p< 0.05)的释放来反映。在32/41(78%)的动脉粥样斑块样本中发现了牙周炎相关细菌的DNA。更具体地说,Pg, Tf, Pi, Aa的DNA分别在46%,24%,34%和68%的样本中被发现。在条件培养基中,在发现细菌的颈动脉样本中,血红蛋白水平较高,但这没有统计学意义。我们的数据证实了斑块内出血和中性粒细胞活化之间的关系。此外,颈动脉粥样斑块中牙周细菌DNA的存在可能有助于这种激活。需要进一步分析以充分挖掘原始数据和标本。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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