Host tissue response in chronic periodontal disease. VI. The role of cell-mediated hypersensitivity.
Host tissue response in chronic periodontal disease. VI. The role of cell-mediated hypersensitivity.
复制标题
慢性牙周病的宿主组织反应。
DOI：
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发表时间：
1977
影响因子：
3.5
通讯作者：
R. C. Page
中科院分区：
文献类型：
--
作者：
Greggory Wilde;Marc Cooper;R. C. Page
在人类和一些动物中，菌斑相关的炎症性牙周病的早期阶段表现出迟发性超敏反应的特征。病变出现在斑块聚集后约一周，在浆细胞浸润性病变形成之前。所描述的实验直接是为了了解细胞介导的超敏反应是否是疾病早期阶段的重要组成部分。用二硝基氟苯致敏Fisher 344大鼠和恒河猴，然后在牙龈沟激发。在攻击后48至72小时内，两种动物都出现了具有早期斑块诱导损伤特征的病变。这些特征包括血管炎、致密的单核细胞浸润和结缔组织成分的破坏。在受到攻击的非致敏对照动物中，这种损害没有出现。为了了解是细胞介导的还是体液超敏反应导致了损伤，在大鼠身上进行了转移实验。致敏动物的5×107脾细胞可被非致敏动物激发，而致敏大鼠的血清则不能引起致敏动物的典型损伤。
An early stage of plaque-associated inflammatory periodontal disease in humans and in some animals exhibits features characteristic of a delayed hypersensitivity reaction. This lesion appears about one week following the beginning of plaque accumulation and it precedes the formation of a plasma cell infiltrate. The experiments described were direct toward learning whether or not cell-mediated hypersensitivity is a significant component of the early stage of the disease. Fisher 344 rats and Rhesus monkeys were sensitized using dinitrofluorobenzene and challenged subsequently at the gingival sulcus. Lesions exhibiting features characteristic of the early plaque-induced lesion appeared in both species within 48 to 72 hours following challenge. These features included vasculitis, a dense mononuclear cell infiltrate and destruction of connective tissue constituents. The lesion did not appear in challenged non-sensitized control animals. In order to learn whether cell mediated or humoral hypersensitivity was responsible for the lesion, transfer experiments were done in rats. Typical lesions were induced by challenge of non-sensitized animals previously given an intraperitoneal injection of 5 X 107 spleen cells from sensitized animals, but lesions could not be induced in animals given serum from sensitized rats.