牙骨质
牙槽
结缔组织
牙周炎
疾病
基础(医学)
炎症
转基因小鼠
牙周病
上皮
医学
口腔感染
病理
免疫学
生物
转基因
牙科
内科学
基因
生物化学
牙本质
胰岛素
作者
Shanna Dayan,Philip Stashenko,Richard Niederman,Thomas S. Kupper
标识
DOI:10.1177/154405910408301010
摘要
Periodontal disease is a bacterial infection that results in inflammatory destruction of tissues that support the teeth, including connective tissue and bone. In this study, we report that transgenic mice that overexpress the 17-kDa form of IL-1α in the basal layer of oral mucosal epithelium develop a syndrome that possesses all of the cardinal features of periodontal disease, including epithelial proliferation and apical migration, loss of attachment, and destruction of cementum and alveolar bone. In this model, bacterial colonization and infection were not required, since levels of periodontal bacteria were equivalent in transgenic and wild-type mice, and continuous treatment with antibiotics from birth did not ameliorate the disease. Our findings therefore indicate that elevated levels of IL-1α in the oral micro-environment can mediate all of the clinical features of periodontal disease.
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