Maruyama Kosuke, Sato Soh
Field of Advanced Conservative Dentistry and Periodontology, periodontology, Course of Clinical Science, The Nippon Dental University Graduate School of Life Dentistry at Niigata, 1-8 Hamaura-cho, chuo-ku, Niigata City, Niigata, 951-8580, Japan.
Department of Periodontology, The Nippon Dental University School of Life Dentistry at Niigata, 1-8 Hamaura-cho, chuo-ku, Niigata City, Niigata, 951-8580, Japan.
Odontology. 2017 Jan;105(1):76-83. doi: 10.1007/s10266-016-0235-8. Epub 2016 Apr 12.
Endothelial cells participate in key aspects of vascular biology, such as maintenance of capillary permeability and regulation of inflammation. According to previous reports, endothelial cells have revealed highly specific characteristics depending on the organs and tissues. In particular, periodontal endothelial cells have a higher permeability than vascular endothelial cells of other types of tissue. Periodontal disease is not only a chronic disease in oral, but also affect the entire body. Diabetes and periodontal disease are closely related, with periodontal disease even been referred to as the sixth complication of disease. However, no reports have investigated the pathophysiology of microvascular in periodontal tissue once diabetes has developed. Therefore, the aim of the present study is to investigate changes in the properties of human periodontal endothelial cells (HPDLECs) that were cultured under high-glucose conditions. We isolated HPDLECs from human periodontal ligament cells. HPDLECs were cultured under high-glucose (5.5, 11.0, 22.0 mM) and investigated proliferation, apoptosis, tube formation and the expression of cell adhesion molecules. A 5.5 mM (100 mg/dl) control was used in this study. HPDLECs stimulated with high glucose concentration exhibited suppression of cell proliferation and an increased percentage of apoptosis-positive cells. This results suggested that apoptosis was caused by TNF-α expression. The expression levels cell adhesion molecules increased. These results suggest that when HPDLECs are stimulated with a high glucose concentrations, PKC in the intracellular cell substrate is activated, increasing the expression of intercellular and vascular adhesion molecules. Thus, the results of this study demonstrate that diabetes exacerbates periodontal disease.
内皮细胞参与血管生物学的关键环节,如维持毛细血管通透性和调节炎症反应。根据以往报道,内皮细胞根据器官和组织的不同呈现出高度特异性的特征。特别是,牙周内皮细胞比其他类型组织的血管内皮细胞具有更高的通透性。牙周病不仅是一种口腔慢性病,还会影响全身。糖尿病与牙周病密切相关,牙周病甚至被称为糖尿病的第六大并发症。然而,尚无报道研究糖尿病发生后牙周组织微血管的病理生理学。因此,本研究的目的是调查在高糖条件下培养的人牙周内皮细胞(HPDLEC)特性的变化。我们从人牙周膜细胞中分离出HPDLEC。将HPDLEC在高糖(5.5、11.0、22.0 mM)条件下培养,并研究其增殖、凋亡、管形成及细胞黏附分子的表达。本研究采用5.5 mM(100 mg/dl)的对照组。高糖浓度刺激的HPDLEC表现出细胞增殖受抑制,凋亡阳性细胞百分比增加。该结果提示凋亡是由TNF-α表达引起的。细胞黏附分子的表达水平升高。这些结果表明,当HPDLEC受到高糖浓度刺激时,细胞内底物中的PKC被激活,增加细胞间和血管黏附分子的表达。因此,本研究结果表明糖尿病会加重牙周病。