Department of Internal and Agricultural Medicine, Jagiellonian University Collegium Medicum, Kraków, Poland.
Department of Periodontology, Oral Pathology and Dental Prophylaxis, Jagiellonian University Collegium Medicum, Kraków, Poland.
Kardiol Pol. 2021;79(11):1206-1214. doi: 10.33963/KP.a2021.0161.
Hypertension and periodontitis are both highly prevalent co-morbidities worldwide, and their occurrence increases with age. Multiple observational epidemiological studies have shown that periodontitis is associated with an increased cardiovascular disease (CVD) occurrence. Large systematic reviews and metanalyses further show that periodontitis increases the risk of hypertension and is associated with increased systolic and diastolic blood pressure. Genetic and clinical evidence, utilizing mendelian randomization and randomized clinical trials, support the causal role of periodontitis in hypertension. The mechanisms of this link remain unclear. Critical components of immune and inflammatory pathogenesis of periodontitis considerably overlap with immune mechanisms of hypertension. Clinical studies support that both C-reactive protein (CRP) levels and white blood cell counts (WBC) mediate the relationship between periodontal disease and high blood pressure. In particular, activation of Th1, Th17, T regulatory cells, and proinflammatory monocytes has been shown to be essential in both conditions. Immunosenescent dysregulated CD28null T cells have been implicated, along with key effector cytokines such as interleukin 6 (IL-6), TNF-alpha (TNF-α), interferon-gamma (IFN-γ), and interleukin 17 (IL-17). A better understanding of the relationships between hypertension and periodontitis is essential not only for possible utilization of this knowledge for a non-pharmacological approach to improving blood pressure control. It may also provide valuable pathogenetic clues linking inflammation and hypertension, which has become particularly relevant in the light of links between hypertension and autoimmune disorders or, more recently, COVID-19.
高血压和牙周炎是全球范围内高度流行的共病，其发生随着年龄的增长而增加。多项观察性流行病学研究表明，牙周炎与心血管疾病（CVD）的发生增加有关。大型系统评价和荟萃分析进一步表明，牙周炎会增加高血压的风险，并与收缩压和舒张压升高有关。利用孟德尔随机化和随机临床试验的遗传和临床证据支持牙周炎在高血压中的因果作用。这种联系的机制尚不清楚。牙周炎的免疫和炎症发病机制的关键组成部分与高血压的免疫机制有很大的重叠。临床研究支持 C 反应蛋白（CRP）水平和白细胞计数（WBC）均介导牙周病与高血压之间的关系。特别是，Th1、Th17、调节性 T 细胞和促炎性单核细胞的激活已被证明在这两种情况下都是必不可少的。免疫衰老失调的 CD28null T 细胞以及关键效应细胞因子（如白细胞介素 6（IL-6）、肿瘤坏死因子-α（TNF-α）、干扰素-γ（IFN-γ）和白细胞介素 17（IL-17））也被牵连其中。更好地理解高血压和牙周炎之间的关系不仅对于利用这方面的知识来改善血压控制的非药物方法至关重要，而且还可能为炎症与高血压之间的致病联系提供有价值的线索，鉴于高血压与自身免疫性疾病或最近与 COVID-19 之间的联系，这一点尤其重要。
