Ekuni D, Tomofuji T, Sanbe T, Irie K, Azuma T, Maruyama T, Tamaki N, Murakami J, Kokeguchi S, Yamamoto T
Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
J Periodontal Res. 2009 Aug;44(4):434-42. doi: 10.1111/j.1600-0765.2008.01122.x. Epub 2009 Feb 6.
Periodontitis is a risk factor for the development of atherosclerosis. Recent studies indicate that oxidative mechanisms, including lipid peroxidation, are involved not only in periodontitis but also in atherosclerosis. Lipid peroxidation may play an important role in the pathogenesis of atherosclerosis, particularly during its earliest stages. The purpose of this study was to investigate the relationship between lipid peroxidation induced by periodontitis and the initiation of atherosclerosis.
Sixteen rats were randomly divided into two groups of eight rats each. Periodontitis was ligature-induced for 4 wk in the experimental group, whereas the control group was left untreated. After the experimental period, the mandibular first molar regions were resected and then subjected to histological analysis and measurement of hexanoyl-lysine expression as an indicator of lipid peroxidation. Descending aorta was used for measuring the levels of hexanoyl-lysine, reactive oxygen species and lipid deposits, and for real-time polymerase chain reaction microarray analysis. The level of hexanoyl-lysine was also measured in serum.
In the experimental group, the levels of hexanoyl-lysine in periodontal tissue and serum increased. Only aorta samples in the experimental group showed lipid accumulation, with increased expression of hexanoyl-lysine, reactive oxygen species and oxidative stress-related genes (including nitric oxide synthases 2 and 3), whereas the superoxide dismutase 1 gene level was down-regulated.
In a ligature-induced periodontitis rat model, increased lipid peroxidation was found in serum and aorta as well as in periodontal tissue. Atherosclerosis-related gene expression and histological changes were also stimulated. Periodontitis-induced lipid peroxidation in the aorta may be involved in the early stage of atherosclerosis.
牙周炎是动脉粥样硬化发生发展的一个危险因素。近期研究表明，包括脂质过氧化在内的氧化机制不仅参与牙周炎，也参与动脉粥样硬化。脂质过氧化可能在动脉粥样硬化的发病机制中起重要作用，尤其是在其早期阶段。本研究的目的是探讨牙周炎诱导的脂质过氧化与动脉粥样硬化起始之间的关系。
16只大鼠随机分为两组，每组8只。实验组通过结扎诱导牙周炎4周，而对照组不做处理。实验期结束后，切除下颌第一磨牙区域，然后进行组织学分析，并测量己酰赖氨酸表达作为脂质过氧化的指标。降主动脉用于测量己酰赖氨酸、活性氧和脂质沉积水平，并进行实时聚合酶链反应微阵列分析。血清中也测量了己酰赖氨酸水平。
实验组牙周组织和血清中的己酰赖氨酸水平升高。仅实验组的主动脉样本出现脂质蓄积，己酰赖氨酸、活性氧和氧化应激相关基因（包括一氧化氮合酶2和3）的表达增加，而超氧化物歧化酶1基因水平下调。
在结扎诱导的牙周炎大鼠模型中，血清、主动脉以及牙周组织中均发现脂质过氧化增加。动脉粥样硬化相关基因表达和组织学变化也受到刺激。牙周炎诱导的主动脉脂质过氧化可能参与动脉粥样硬化的早期阶段。
