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Gingival vascular functions are altered in type 2 diabetes mellitus model and/or periodontitis model

机译:2型糖尿病模型和/或牙周炎模型中的牙龈血管功能发生改变

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摘要

The association of vascular reactivity between diabetes and periodontal disease has not been clarified. Gingival blood flow was measured by laser Doppler flowmetry for 31 weeks in Wistar rats, Wistar rats orally challenged with Porphyromonas gingivalis (Wistar rats + Porphyromonas gingivalis), Goto-Kakizaki rats, and Goto-Kakizaki rats orally challenged with Porphyromonas gingivalis (Goto-Kakizaki rats + Porphyromonas gingivalis). Effects of alveolar bone resorption on periodontal tissue was enhanced in Wistar rats + Porphyromonas gingivalis, and Goto-Kakizaki rats, with this effect being significantly enhanced by Goto-Kakizaki rats + Porphyromonas gingivalis. Using the L-band electron spin resonance technique, we succeeded in measuring oxidative stress as decay rate constant (K1 and K2) of 3-carbamoyl-2,2,5,5-tetramethylpyrrolidin-1-yloxy in the oral and maxillofacial region of the animal models. The decay rate constant (K1) of 3-carbamoyl-2,2,5,5-tetramethylpyrrolidin-1-yloxy was significantly greater in the oral and maxillofacial region of Goto-Kakizaki rats + Porphyromonas gingivalis compared to Wistar rats, Wistar rats + Porphyromonas gingivalis and Goto-Kakizaki rats groups. Gingival reactive hyperemia was attenuated by periodontal disease, and this effect was also remarkable in the diabetes mellitus model. Taken together, we found that vascular endothelial function was decreased in diabetes mellitus and/or periodontal disease animal models due to increasing oxidative stress in the gingival circulation.
机译:糖尿病与牙周疾病之间血管反应性的关联尚不清楚。通过激光多普勒血流仪测量Wistar大鼠,口服牙龈卟啉单胞菌(Wistar大鼠+牙龈卟啉单胞菌),Wito-Kakizaki大鼠和Goto-Kakizaki大鼠口服齿龈卟啉单胞菌(Goto-Kakizaki)的齿龈血流31周大鼠+牙龈卟啉单胞菌)。 Wistar大鼠+牙龈卟啉单胞菌和Goto-Kakizaki大鼠的牙槽骨吸收对牙周组织的影响增强,而Goto-Kakizaki大鼠+牙龈卟啉单胞菌明显增强了这种影响。使用L带电子自旋共振技术,我们成功地测量了口腔内和颌面部3-氨基甲酰基-2,2,5,5-四甲基吡咯烷-1-基氧基的衰变速率常数(K1和K2)的氧化应激。动物模型。与Wistar大鼠,Wistar大鼠+牙龈卟啉单胞菌和后藤崎崎大鼠组。牙周疾病减轻了牙龈反应性充血,这种作用在糖尿病模型中也很明显。两者合计,我们发现由于增加牙龈循环中的氧化应激,在糖尿病和/或牙周疾病动物模型中血管内皮功能降低。

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