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
中科院分区:
文献类型:
--
作者:
Liang S;Hosur KB;Domon H;Hajishengallis G
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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影响因子:
3.4
作者:
Hajishengallis, George;Tapping, Richard I.;Yoshimura, Fuminobu
通讯作者:
Yoshimura, Fuminobu
影响因子:
4.4
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Saftig, Paul
影响因子:
5.8
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Hajishengallis G
影响因子:
5.4
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通讯作者:
Hajishengallis, G
影响因子:
4.3
作者:
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通讯作者:
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