Etiology and Therapy of Periodontal Diseases (ETEP) Research Group, University Complutense of Madrid, Madrid, Spain.
Department of Biochemistry and Molecular Biology III, Faculty of Medicine, University Complutense of Madrid.
J Periodontol. 2018 Feb;89(2):176-185. doi: 10.1902/jop.2017.170355. Epub 2018 Feb 16.
Obesity and overweight have been associated with periodontitis. This study aims to evaluate periodontal and systemic effects of this association in a validated experimental model.
Twenty-eight male Wistar rats were randomly divided into four groups: 1) control group (Con) (fed with standard diet); 2) high-fat diet group (HFD) (fed with a diet containing 35.2% fat); 3) control group with induced periodontitis (Con-Perio); and 4) HFD group with induced periodontitis (HFD-Perio). To induce periodontitis, oral gavages with Porphyromonas gingivalis ATCC W83K1 and Fusobacterium nucleatum DMSZ 20482 were used. Periodontal outcomes were evaluated by inflammatory parameters, periodontal probing depth (PD), and modified gingival index (MGI). Systemic effects were evaluated by measuring levels of inflammatory cytokines, insulin, adiponectin, and leptin using multiplex immunoassays and levels of visfatin, resistin, lipid profiles, transaminases, and plasma endotoxin using colorimetric tests and the glucose tolerance test.
Clinical parameters (PD and MGI) were significantly increased (P < 0.05) in the induced periodontitis groups compared with controls. The HFD-Perio group demonstrated significantly higher PD compared with Con-Perio group. Lipid profiles, cytokines, and adipocytokines showed significantly elevated levels in the HFD-Perio group compared with the other groups. Similarly, glucose levels in the HFD-Perio group were significantly higher (P < 0.05) than in the HFD group, and hepatic damage parameters demonstrated a tendency toward higher levels in the HFD-Perio group.
Obesity and periodontitis demonstrated a comorbidity effect on both systemic inflammatory and metabolic dysregulation biomarkers, with increased glucose, dyslipidemia and hepatic damage.
肥胖和超重与牙周炎有关。本研究旨在验证实验模型中这种关联的牙周和全身效应。
将 28 只雄性 Wistar 大鼠随机分为四组:1)对照组(Con)(喂食标准饮食);2)高脂肪饮食组(HFD)(喂食含 35.2%脂肪的饮食);3)诱导牙周炎的对照组(Con-Perio);和 4)诱导牙周炎的 HFD 组(HFD-Perio)。使用牙龈卟啉单胞菌 ATCC W83K1 和核梭杆菌 DMSZ 20482 的口服灌胃来诱导牙周炎。通过炎症参数、牙周探诊深度(PD)和改良牙龈指数(MGI)评估牙周病结局。通过使用多重免疫分析测量炎症细胞因子、胰岛素、脂联素和瘦素的水平,以及使用比色法测量内脏脂肪素、抵抗素、脂质谱、转氨酶和血浆内毒素的水平和葡萄糖耐量试验来评估全身效应。
与对照组相比,诱导牙周炎组的临床参数(PD 和 MGI)显著升高(P<0.05)。HFD-Perio 组的 PD 明显高于 Con-Perio 组。HFD-Perio 组的脂质谱、细胞因子和脂肪细胞因子水平明显高于其他组。同样,HFD-Perio 组的血糖水平明显高于 HFD 组,HFD-Perio 组的肝损伤参数也表现出较高的趋势。
肥胖和牙周炎对全身炎症和代谢失调生物标志物表现出共病效应,导致血糖升高、血脂异常和肝损伤。