State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
J Periodontal Res. 2013 Oct;48(5):582-90. doi: 10.1111/jre.12041. Epub 2013 Jan 14.
Diabetes mellitus is believed to increase the risk and severity of periodontitis. However, less evidence is available on the converse effects of periodontitis on diabetes. The objective of the study was to investigate to what degree experimental periodontitis induced by Porphyromonas gingivalis might influence the onset and severity of diabetes in different mouse models.
Twenty-eight male Tallyho/JngJ mice (type 2 diabetes), 20 male streptozotocin-induced diabetes C57BL/6J mice (type 1 diabetes) and 20 male C57BL/6J mice at 4 wks of age were evenly divided into two groups: periodontal infection and sham infection. Periodontitis was induced by Porphyromonas gingivalis W50 (P. gingivalis) oral inoculation before the development of diabetes. Sham-infected mice received vehicle as control. P. gingivalis in the oral cavity were identified by quantitative polymerase chain reaction. Fasting glucose, body weight and food intake levels were monitored and glucose tolerance tests were performed to assess glucose homeostasis for the onset and progression of diabetes. The level of alveolar bone loss and tumor necrosis factor-alpha were determined in week 20 when mice were killed.
Mice in the infection groups developed more alveolar bone loss than those in sham-infection groups (Tallyho p = 0.021; C57-STZ p = 0.014; C57 p = 0.035). Hyperglycemic mice exhibited significantly more bone loss compared to those normal glucose mice (Tallyho vs. C57 p = 0.029; C57-STZ vs. C57 p = 0.024). The level of tumor necrosis factor-alpha was consistent with that of periodontal bone loss and hyperglycemia. There was no significant effect of mouse species on the amount of bone loss at the same level of blood glucose. No statistically significant difference or trend in glucose metabolism was found between the infection and sham-infection group.
Diabetes enhanced the risk for periodontal disease induced by P. gingivalis. However, no converse impact was found between this periodontal infection and onset and severity of diabetes in both type 1 and 2 diabetes mice.
糖尿病被认为会增加牙周炎的风险和严重程度。然而，牙周炎对糖尿病的反作用的证据较少。本研究的目的是调查牙龈卟啉单胞菌（Porphyromonas gingivalis）引起的实验性牙周炎在不同的小鼠模型中对糖尿病的发病和严重程度的影响程度。
28 只雄性 Tallyho/JngJ 小鼠（2 型糖尿病）、20 只雄性链脲佐菌素诱导的糖尿病 C57BL/6J 小鼠（1 型糖尿病）和 20 只 4 周龄雄性 C57BL/6J 小鼠被平均分为两组：牙周感染组和假感染组。在糖尿病发生之前，通过牙龈卟啉单胞菌（P. gingivalis）口腔接种诱导牙周炎。假感染组给予载体作为对照。通过定量聚合酶链反应鉴定口腔中的牙龈卟啉单胞菌。监测空腹血糖、体重和食物摄入量水平，并进行葡萄糖耐量试验以评估糖尿病发病和进展时的葡萄糖稳态。当小鼠在第 20 周处死时，确定牙槽骨丧失的水平和肿瘤坏死因子-α的水平。
感染组的小鼠比假感染组的小鼠发生更多的牙槽骨丧失（Tallyho p = 0.021；C57-STZ p = 0.014；C57 p = 0.035）。高血糖小鼠与正常血糖小鼠相比，骨丢失明显更多（Tallyho 与 C57 p = 0.029；C57-STZ 与 C57 p = 0.024）。肿瘤坏死因子-α的水平与牙周骨丢失和高血糖一致。在相同血糖水平下，小鼠种类对骨丢失量没有显著影响。在感染组和假感染组之间，葡萄糖代谢没有显著差异或趋势。
糖尿病增加了牙龈卟啉单胞菌引起的牙周病的风险。然而，在 1 型和 2 型糖尿病小鼠中，这种牙周感染与糖尿病的发病和严重程度之间没有发现相反的影响。
