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Diet-induced Generalized Periodontitis in Lewis Rats

机译:Lewis大鼠饮食诱导的广义牙周炎

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Periodontitis is an important public health concern worldwide. Because rodents from the genus Rattus are resistant to spontaneous periodontitis, experimental periodontitis must be initiated by mechanical procedures and interventions. Due to their exacerbated Th1 response and imbalanced Th17 regulatory T-cell responses, Lewis rats are highly susceptible to inducible inflammatory and autoimmune diseases. We hypothesized that feeding Lewis rats a diet high in sucrose and casein (HSC) would alter the oral microenvironment and induce inflammation and the development of periodontitis lesions without mechanical intervention. A baseline group (BSL, n = 8) was euthanized at age 6 wk. Beginning at 6 wk of age, 2 groups of Lewis rats were fed standard (STD, n = 12) or HSC (n = 20) chow and euthanized at 29 wk of age. We evaluated the degree of periodontitis through histology and mu CT of maxillae and mandibles. The HSC-induced inflammatory response of periodontal tissues was assessed by using immunohistochemistry. Gene expression analysis of inflammatory cytokines associated with Th1 and Th17 responses, innate immunity cytokines, and tissue damage in response to bacteria were assessed also. The potential systemic effects of HSC diet were evaluated by assessing body composition and bone densitometry endpoints; serum leptin and insulin concentrations; and gene expression of inflammatory cytokines in the liver. Placing Lewis rats on HSC diet for 24 wk induced a host Th1-immune response in periodontal tissues and mild to moderate, generalized periodontitis characterized by inflammatory cell infiltration (predominantly T cells and macrophages), osteoclast resorption of alveolar bone, and hyperplasia and migration of the gingival epithelium. HSC-fed Lewis rats developed periodontitis without mechanical intervention in the oral cavity and in the absence of any noteworthy metabolic abnormalities. Consequently, the rat model we described here may be a promising approach for modeling mild to moderate periodontitis that is similar in presentation to the human disease.
机译:牙周炎是全世界重要的公共卫生问题。由于来自rattus属的啮齿动物对自发牙周炎具有抗性,因此必须通过机械程序和干预来启动实验牙周炎。由于其加剧的Th1反应和妊娠Th17调节T细胞应答,Lewis大鼠对诱导型炎症和自身免疫疾病高度影响。我们假设饲喂Lewis大鼠蔗糖和酪蛋白(HSC)的饮食将改变口腔微环境并诱导炎症和牙周炎病变的发展,而不会机械干预。基线组(BSL,N = 8)在6周内安乐死。从6周期开始,2组Lewis大鼠被喂食标准(STD,N = 12)或HSC(n = 20)种,并在29%的年龄下安乐死。我们通过Maxillae和颌骨的组织学和MU CT评估了牙周炎的程度。通过使用免疫组织化学评估牙周组织的HSC诱导的炎症反应。还评估了与Th1和Th17反应,先天免疫细胞因子相关的炎性细胞因子的基因表达分析,并评估了对细菌的反应响应细菌的组织损伤。通过评估体组成和骨密度终点来评估HSC饮食的潜在全身效应;血清瘦素和胰岛素浓度;肝脏炎性细胞因子的基因表达。将Lewis大鼠在HSC饮食上诱导牙周组织中的宿主Th1免疫应答,以炎症细胞浸润(主要是T细胞和巨噬细胞),肺泡骨的破骨细胞吸收和迁移,以及迁移的增量牙龈上皮。 HSC喂养的Lewis大鼠在口腔中没有机械干预的情况下发育牙周炎,并且在没有任何值得注意的代谢异常的情况下。因此,我们在此描述的大鼠模型可能是用于模拟轻度至中度牙周炎的有希望的方法,其类似于呈现给人类疾病。

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