香烟吸入对大鼠实验性根尖周炎免疫炎症特征的影响。

Effects of cigarette smoke inhalation on the immune-inflammatory profile of experimental apical periodontitis in rats.

机构信息

Departamento de Odontologia Preventiva e Restauradora, Faculdade de Odontologia, Universidade Estadual Paulista (UNESP), Araçatuba, Brazil.

Departamento de Ciências Básicas, Faculdade de Odontologia de Araçatuba, Universidade Estadual Paulista (UNESP), São Paulo, Brazil.

出版信息

Int Endod J. 2023 Dec;56(12):1559-1570. doi: 10.1111/iej.13981. Epub 2023 Oct 3.

DOI:10.1111/iej.13981

PMID:37787896

Abstract

OBJECTIVE

To evaluate the effects of cigarette smoke inhalation on the immune-inflammatory profile of experimental apical periodontitis in rats.

METHODOLOGY

In total, 32 male Wistar rats were divided into four groups (n = 8): AP-induced apical periodontitis; S-cigarette smoke inhalation; APS-induced AP and cigarette smoke inhalation; and C (control)-neither AP nor cigarette smoke inhalation. To induce cigarette smoke inhalation, the animals were kept in a chamber filled with tobacco smoke for 8 min thrice a day for 50 days. AP was induced 20 days after inhalation initiation by exposing their coronary pulp to their oral environment for 30 days. After animals were euthanized, their right hemimaxillae were removed for histopathological, semi-quantitative and immunohistochemical (F4/80, CD206 and iNOS) analyses.

RESULTS

Quantitative data showed a moderate number of inflammatory infiltrates in AP and an intense number in APS (p < .05). Comparing F4/80+ cells showed no statistically significant differences among groups, but we found more CD206+ cells in AP than in C and S (p > .05). INOS+ immunostaining showed a significant increase in AP and APS, when compared with C and S (p < .05). APS had more iNOS+ cells than AP (p < .05).

CONCLUSION

Cigarette smoke inhalation worsened AP, leading to a predominantly pro- inflammatory profile in our experimental model.

摘要

目的

评估吸烟对大鼠实验性根尖周炎免疫炎症谱的影响。

方法

共 32 只雄性 Wistar 大鼠分为四组（n=8）：AP 诱导的根尖周炎；S-香烟烟雾吸入；APS 诱导的 AP 和香烟烟雾吸入；C（对照）-既不发生 AP 也不发生香烟烟雾吸入。为了诱导香烟烟雾吸入，动物被置于充满烟草烟雾的室中，每天 3 次，每次 8 分钟，共 50 天。吸入开始后 20 天，通过将其牙冠牙髓暴露于口腔环境中 30 天来诱导 AP。动物安乐死后，取出其右侧上颌骨进行组织病理学、半定量和免疫组织化学（F4/80、CD206 和 iNOS）分析。

结果

定量数据显示 AP 中有中等数量的炎症浸润，APS 中有强烈数量的炎症浸润（p<.05）。比较 F4/80+细胞，各组之间无统计学差异，但我们发现 AP 中 CD206+细胞多于 C 和 S（p>.05）。INOS+免疫染色显示 AP 和 APS 与 C 和 S 相比，显著增加（p<.05）。APS 中的 iNOS+细胞多于 AP（p<.05）。