Periodontal inflammation and bone loss in aged mice.

Periodontal inflammation and bone loss in aged mice.
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DOI:
10.1111/j.1600-0765.2009.01245.x
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发表时间:
2010-08
影响因子:
3.5
通讯作者:
Hajishengallis G
Hajishengallis G
中科院分区:
医学3区
文献类型:
--
作者:
Liang S;Hosur KB;Domon H;Hajishengallis G

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年轻的小鼠不会出现可测量的牙周骨丢失,除非严重感染了人类牙周病原体。然而,免疫系统发生遗传改变的小鼠无法控制自己的口腔植物群,并在生命早期患上牙周炎。基于固有口腔微生物群引起牙周炎的潜力,我们假设正常小鼠可能最终发展为炎性牙周骨丢失,即,as a function函数of age年龄.如果得到证实,这可以作为慢性牙周炎的衰老模型。在幼龄(8-10周龄)、老龄(≥ 18月龄)和中龄小鼠中,测量牙周膜骨水平,即牙骨质-釉质连接(CEJ)至牙槽骨嵴(ABC)的距离。通过实时定量PCR测定年轻和老年小鼠牙龈炎性介质的差异表达。与年轻小鼠相比,老年小鼠表现出显著的(P < 0.05)牙周骨丢失增加,同时伴有促炎细胞因子表达升高(白细胞介素-1 β、肿瘤坏死因子-α和白细胞介素-17 A)和参与炎症诱导或扩增的先天免疫受体(Toll样受体2、CD 14、CD 11b、CD 18、补体C5 a受体和髓样细胞上表达的触发受体-3)。小鼠发展自然诱导的牙周骨丢失作为年龄的函数。这种牙周炎的老化模型代表了一种真正的慢性模型,以研究牙周组织破坏的机制。
Young mice do not develop measurable periodontal bone loss, unless heavily infected with human periodontal pathogens. However, mice with genetically altered immune system are unable to control their own oral flora and develop periodontitis early in life. Based on the potential of the indigenous oral microbiota to cause periodontitis, we hypothesized that normal mice may ultimately develop inflammatory periodontal bone loss, i.e., as a function of age. If confirmed, this could serve as an aging model of chronic periodontitis. Periodontal bone levels were measured as the distance from the cementoenamel junction (CEJ) to the alveolar bone crest (ABC), in young (8-10 weeks of age), old (≥ 18 months of age), and mice of intermediate ages. Differential expression of inflammatory mediators in the gingivae of young and old mice was determined by quantitative real-time PCR. In comparison to young mice, old mice displayed significantly (p < 0.05) increased periodontal bone loss, accompanied by elevated expression of proinflammatory cytokines (interleukin-1β, tumor necrosis factor-α, and interleukin-17A) and innate immune receptors involved in the induction or amplification of inflammation (Toll-like receptor 2, CD14, CD11b, CD18, complement C5a receptor, and triggering receptor expressed on myeloid cells-3). Mice develop naturally-induced periodontal bone loss as a function of age. This aging model of periodontitis represents a genuinely chronic model to study mechanisms of periodontal tissue destruction.
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