Higashi Yukihito, Goto Chikara, Jitsuiki Daisuke, Umemura Takashi, Nishioka Kenji, Hidaka Takayuki, Takemoto Hiroaki, Nakamura Shuji, Soga Junko, Chayama Kazuaki, Yoshizumi Masao, Taguchi Akira
Department of Cardiovascular Physiology and Medicine, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Hypertension. 2008 Feb;51(2):446-53. doi: 10.1161/HYPERTENSIONAHA.107.101535. Epub 2007 Nov 26.
The purpose of this study was to evaluate endothelial function in patients with periodontitis. We evaluated forearm blood flow responses to acetylcholine and sodium nitroprusside in patients with periodontitis who had no other cardiovascular risk factors (32 men; 25+/-3 years of age), in a normal control group (20 men; 26+/-3 years of age), and in hypertensive patients with periodontitis (28 men and 10 women; 56+/-12 years of age) and without periodontitis (control group; 18 men and 6 women; 54+/-13 years of age). Forearm blood flow was measured using strain-gauge plethysmography. Circulating levels of C-reactive protein and interleukin-6 were significantly higher in the periodontitis group than in the control group. Both in healthy and hypertensive subjects, forearm blood flow responses to acetylcholine were significantly smaller in the periodontitis group than in the control group. Sodium nitroprusside-stimulated vasodilation was similar in the 2 groups. Periodontal therapy reduced serum concentrations of C-reactive protein and interleukin-6 and augmented acetylcholine-induced vasodilation in periodontitis patients with and without hypertension. After administration of N(G)-monomethyl-L-arginine, an NO synthase inhibitor, forearm blood flow response to acetylcholine was similar before and after treatment. These findings suggest that periodontitis is associated with endothelial dysfunction in subjects without cardiovascular risk factors, as well as hypertensive patients, through a decrease in NO bioavailability and that systemic inflammation may be, at least in part, a cause of endothelial dysfunction, leading to cardiovascular diseases.
本研究的目的是评估牙周炎患者的内皮功能。我们评估了无其他心血管危险因素的牙周炎患者(32名男性,年龄25±3岁)、正常对照组(20名男性,年龄26±3岁)、患有牙周炎的高血压患者(28名男性和10名女性,年龄56±12岁)以及无牙周炎的高血压患者(对照组,18名男性和6名女性,年龄54±13岁)对乙酰胆碱和硝普钠的前臂血流反应。使用应变片体积描记法测量前臂血流。牙周炎组循环中的C反应蛋白和白细胞介素-6水平显著高于对照组。在健康和高血压受试者中,牙周炎组对乙酰胆碱的前臂血流反应均显著小于对照组。两组对硝普钠刺激的血管舒张反应相似。牙周治疗降低了有或无高血压的牙周炎患者血清C反应蛋白和白细胞介素-6的浓度,并增强了乙酰胆碱诱导的血管舒张。给予一氧化氮合酶抑制剂N(G)-单甲基-L-精氨酸后,治疗前后对乙酰胆碱的前臂血流反应相似。这些发现表明,牙周炎通过一氧化氮生物利用度降低与无心血管危险因素的受试者以及高血压患者的内皮功能障碍有关,并且全身炎症可能至少部分是内皮功能障碍的原因,进而导致心血管疾病。