Department of Physiology and Biophysics, Boston University School of Medicine, 700 Albany Street, W302, Boston, MA, 02118-2526, USA.
Department of Applied Oral Sciences, The Forsyth Institute, 245 First Street, Cambridge, MA, 02142, USA.
Curr Atheroscler Rep. 2017 Nov 6;19(12):57. doi: 10.1007/s11883-017-0696-4.
This review aims to discuss the existing evidence on the link between atherosclerosis and periodontitis by particularly presenting new findings that link the pathology and therapy of these diseases. Acute vascular ischemic events that can lead to stroke or myocardial infarction are initiated by inflammatory processes leading to rupture or erosion of plaques susceptible to thrombosis ("high risk" or "vulnerable"). These are highly inflamed plaques residing in the media and adventitia that may not be detected by angiography measurments of luminal narrowing. Statistically significant excess risk for atherosclerotic cardiovascular disease has been reported in persons with periodontitis independent of established risk factors. We hypothesized that the systemic pathologic links also represent potential therapeutic links.
We recently demonstrated that periodontal inflammation promotes atherosclerotic plaque inflammation and destabilization. As discrete pathological regions, these plaques with a high susceptibility to rupture can be imaged and differentiated from lower risk plaques. In cholesterol-fed rabbits with periodontal disease, circulating inflammatory mediators were also significantly elevated thereby contributing to "vulnerable blood," a systemic characteristic of high risk for cardiovascular events. New studies show that certain lipid mediators, including lipoxins and resolvins, are potent in preventing and possibly treating a number of inflammation-associated diseases, including periodontitis and vascular inflammation. The concept of the vulnerable patient and the pro-resolving approach open new terrain for discovery of paradigm-changing therapies for the prevention and treatment of two of the most common diseases of man. Importantly, lipoxins and resolvins are natural receptor agonists that do not exhibit the same pro-atherogenic side effects attributed to anti-inflammatory medications (e.g., NSAIDs) but rather coordinate resolution of inflammation and a return to homeostasis.
本综述旨在讨论动脉粥样硬化和牙周炎之间的关联，特别提出新的发现，将这些疾病的病理学和治疗联系起来。导致中风或心肌梗死的急性血管缺血性事件是由炎症过程引发的，这些炎症过程导致斑块破裂或侵蚀，容易形成血栓（“高危”或“易损”）。这些高度炎症的斑块位于中膜和外膜，可能无法通过血管造影测量管腔狭窄来检测。有研究报道，牙周炎患者发生动脉粥样硬化性心血管疾病的风险显著增加，且独立于已知的危险因素。我们假设系统性病理联系也代表潜在的治疗联系。
我们最近证明了牙周炎炎症促进了动脉粥样硬化斑块的炎症和不稳定性。这些斑块具有高破裂倾向，可作为离散的病理区域进行成像和区分，与低风险斑块区分开来。在患有牙周病的胆固醇喂养兔中，循环炎症介质也显著升高，从而导致“易损血液”，这是心血管事件高风险的全身性特征。新的研究表明，某些脂质介质，包括脂氧素和 resolvins，在预防和治疗多种炎症相关疾病方面具有强大的作用，包括牙周炎和血管炎症。易损患者的概念和促解决方法为发现预防和治疗两种最常见人类疾病的变革性治疗方法开辟了新的领域。重要的是，脂氧素和 resolvins 是天然的受体激动剂，它们不会表现出与抗炎药物（如 NSAIDs）相同的促动脉粥样硬化副作用，而是协调炎症的解决和恢复到体内平衡。
