Endodontic Division, Department of Restorative Dentistry, Institute of Science and Technology, São Paulo State University - UNESP, São José dos Campos, São Paulo, Brazil.
Int Endod J. 2021 Aug;54(8):1342-1352. doi: 10.1111/iej.13515. Epub 2021 Apr 8.
To establish an experimental model combining chronic stress and apical periodontitis by assessing the development of periapical lesions in rats in three different time points.
Forty-eight male Wistar rats were randomly assigned into two equal groups: Apical periodontitis (AP) and AP + Stress (AP + S). The animals of the AP group were not exposed to stressful conditions whereas the AP + S group were exposed to a variety of stressors on a daily basis until the end of the experiment. After three weeks of chronic unpredictable stress, apical periodontitis was induced in both groups by exposing the pulpal tissue of the mandibular first molar to the oral environment. Each group was further subdivided into three subgroups according to the euthanasia period: 14, 21 and 28 days after pulp exposure. The animals were weighed, and the blood was collected for corticosterone serum dosage by radioimmunoassay. The mandibles were removed and submitted to histopathological and microtomography analyses to assess the inflammatory response and the progression of periapical lesions. Comparisons between the AP and AP + S groups were performed using Student's t-test and Mann-Whitney U-test for parametric and nonparametric data, respectively. The one-way anova test followed by Tukey's test (parametric data) and Kruskal-Wallis followed by Dunn's test (nonparametric data) were used for comparisons between the three time points within the same group (P < 0.05).
The AP + S group had a significantly lower average percentage of weight gain at 14 days and 21 days after AP induction (P < 0.05). Significantly higher levels of corticosterone were found in the AP + S group at 21 days (P < 0.05). The AP + S group had a significantly greater intensity and extension of inflammatory infiltrate with larger areas of bone loss compared to the AP groups at 21 days (P < 0.05). The volume of the periapical lesions in the AP + S group was significantly larger than that of the AP group 21 days following pulp exposure (P < 0.05).
The chronic unpredictable stress model applied for 6 weeks exacerbated the inflammatory response and increased bone loss associated with AP, especially 21 days after its induction. This model appears to be suitable for investigating the bidirectional relationship between apical periodontitis and chronic stress.
通过评估大鼠根尖周病变的发展,建立一个结合慢性应激和根尖周炎的实验模型,在三个不同的时间点进行。
将 48 只雄性 Wistar 大鼠随机分为两组:根尖周炎(AP)和 AP+应激(AP+S)。AP 组的动物不暴露于应激条件下,而 AP+S 组则每天接受各种应激源的刺激,直至实验结束。在 3 周的慢性不可预测应激后,通过将下颌第一磨牙的牙髓组织暴露于口腔环境中,在两组中均诱导根尖周炎。根据安乐死时间,每组进一步分为 3 个亚组:牙髓暴露后 14、21 和 28 天。称重动物,采集血液通过放射免疫法测定皮质酮血清浓度。取下颌骨进行组织病理学和微断层扫描分析,以评估炎症反应和根尖周病变的进展。使用 Student's t 检验和 Mann-Whitney U 检验分别对 AP 和 AP+S 组进行参数和非参数数据的比较。对于同一组内的三个时间点,使用单向方差分析(参数数据)和 Kruskal-Wallis 检验(非参数数据) followed by Dunn's test(非参数数据)进行比较(P<0.05)。
AP+S 组在 AP 诱导后 14 天和 21 天的平均体重增长率显著降低(P<0.05)。AP+S 组在 21 天时皮质酮水平显著升高(P<0.05)。与 AP 组相比,AP+S 组在 21 天时炎症浸润的强度和范围更大,骨丢失面积更大(P<0.05)。AP+S 组在牙髓暴露后 21 天的根尖周病变体积明显大于 AP 组(P<0.05)。
应用 6 周的慢性不可预测应激模型加重了 AP 相关的炎症反应和骨丢失,特别是在诱导后 21 天。该模型似乎适用于研究根尖周炎和慢性应激之间的双向关系。