PATHOGENESIS OF INDUCED RAT PERIAPICAL LESIONS
PATHOGENESIS OF INDUCED RAT PERIAPICAL LESIONS
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DOI：
10.1016/0030-4220(94)90044-2
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发表时间：
1994-10-01
影响因子：
--
通讯作者：
YU, SM
中科院分区：
文献类型：
--
作者：
STASHENKO, P;WANG, CY;YU, SM
采用大鼠外科髓暴露模型，对根尖周病变的发病机制进行了研究。在这个模型中，根尖周围病变在0-15天(活动期)发展迅速，之后发展较慢(慢性期)。一种类似于人类的革兰氏阴性厌氧菌很快就建立起来了。皮损中含有混合炎症细胞，由T细胞、中性粒细胞、B细胞、巨噬细胞和浆细胞组成。活动期以辅助性T细胞为主，慢性期以抑制性T细胞为主。根尖周围病变的提取物含有骨吸收活性，当病变活跃扩张时，骨吸收活性最高。根据生化标准和抗体中和研究，大多数骨吸收活动是由细胞因子白介素1α介导的。前列腺素2占吸收活动的10%到15%。通过原位杂交和免疫染色，从暴露后第2天开始在牙髓中鉴定出表达IL-1α的细胞，从第7天开始在根尖周围组织中鉴定出表达IL-1α的细胞。巨噬细胞、成纤维细胞、中性粒细胞和破骨细胞表达IL-1αmRNA和蛋白。表达肿瘤坏死因子α的细胞也被检测到，而表达白细胞介素1β或肿瘤坏死因子β的细胞缺失。最后，白介素1受体拮抗剂对根尖周骨破坏有60%的抑制作用。这些研究确立了白介素1α在大鼠模型根尖周病变发病机制中的关键作用。
Studies of the mechanisms of pathogenesis of periapical lesions were undertaken using a rat model of surgical pulp exposure. In this model, periapical lesions develop rapidly between days 0 and 15 (active phase) and more slowly thereafter (chronic phase). A Gram-negative anaerobic flora, similar to that seen in human beings, are quickly established. Lesions contain a mixed inflammatory cell infiltrate consisting of T cells, neutrophils, B cells, macrophages, and plasma cells. Helper T cells predominate during the active phase, whereas suppressor T cells are more frequent in the chronic phase. Extracts of periapical lesions contain bone-resorbing activity, the highest levels of which are present when lesions are actively expanding. Most bone-resorbing activity is mediated by the cytokine interleukin-1alpha, as determined by biochemical criteria and antibody neutralization studies. Prostaglandin2 accounts for 10% to 15% of resorptive activity. Cells that express interleukin-1alpha were identified in pulp beginning on day 2 after exposure and in periapical tissue beginning on day 7, as determined by in situ hybridization and immunostaining. Macrophages, fibroblasts, neutrophils, and osteoclasts were positive for interleukin-1alpha mRNA and protein. Cells that express tumor necrosis factor alpha were also detected, whereas cells expressing interleukin-1beta or tumor necrosis factor beta were absent. Finally, periapical bone destruction was inhibited by 60% by treatment with interleukin-1 receptor antagonist. These studies establish a key role for interleukin-1alpha in the pathogenesis of periapical lesions in the rat model.