METHODS: Forty male Wistar rats were distributed across four groups (n = 10) based on the induction of RA and AP: Control, RA, AP, and RA + AP. RA was induced through two immunisations with type II collagen emulsified in incomplete Freund\'s adjuvant, followed by one immunisation with complete Freund\'s adjuvant. After 21 days of RA induction, AP was induced by exposing the pulp of four molars. Animals were euthanized after 28 days of pulp exposure. Through the experiment, visual and behavioural assessments tracked RA development and the knees and hind paw joints were measured. Micro-computed tomography scans of knees and hind paws, as well as mandibles and maxillae, were conducted to evaluate RA severity and the presence of AP, respectively. Serum samples were collected to analyse proinflammatory cytokines (IL-1β, IL-2, IL-17, and TNF-α). Non-parametric data were analysed using the Kruskal-Wallis test followed by Student-Newman-Keuls test, while one-way anova followed by Tukey\'s test was performed for parametric data. A significance level of 5% was employed.
RESULTS: All molars submitted to access cavity developed AP. All joints subjected to arthritis induction developed the disease, with AP + RA demonstrating a higher arthritis severity when compared to the RA group (p < .05). RA + AP group displayed a significantly larger hind paw and knee circumference compared to the RA group (p < .05). Micro-CT images of RA and RA + AP groups revealed joints with erosions and bone deformities, with a significantly lower bone surface density, lower trabecular number and higher trabecular separation in the hind paw and a significantly lower percent bone volume and higher trabecular separation in the knees of RA + AP group compared to RA group (p < .05). RA + AP group exhibited a significantly higher level of TNF-α and a lower level of IL-2 compared to all other groups (p < .05). Both RA and RA + AP groups had significantly higher IL-17 levels (p < .05), while there was no significant difference in IL-1β levels among the groups (p > .05).
CONCLUSIONS: The findings from this study underscore a possible relationship between apical periodontitis and the exacerbation of rheumatoid arthritis.
方法:根据RA和AP的诱导,将40只雄性Wistar大鼠分为四组(n=10):对照组,RA,AP,RA+AP。RA是通过用不完全弗氏佐剂乳化的II型胶原蛋白进行两次免疫诱导的,然后用完全弗氏佐剂进行一次免疫。RA诱导21天后,AP是通过暴露四个磨牙的牙髓诱导的。在28天的牙髓暴露后使动物安乐死。通过实验,视觉和行为评估追踪RA的发展,并测量膝关节和后爪关节.膝盖和后爪的显微计算机断层扫描扫描,以及下颌骨和上颌骨,进行评估RA的严重程度和AP的存在,分别。收集血清样本以分析促炎细胞因子(IL-1β,IL-2、IL-17和TNF-α)。非参数数据使用Kruskal-Wallis检验和Student-Newman-Keuls检验进行分析。而对参数数据进行单向方差分析,然后进行Tukey检验。采用5%的显著性水平。
结果:所有进入腔发育的磨牙。所有遭受关节炎诱导的关节都患上了这种疾病,与RA组相比,AP+RA显示更高的关节炎严重程度(p<0.05)。与RA组相比,RA+AP组显示显著更大的后爪和膝围(p<.05)。RA和RA+AP组的显微CT图像显示关节侵蚀和骨畸形,骨骼表面密度明显降低,与RA组相比,RAAP组的后爪骨小梁数量减少,后爪骨小梁分离增加,膝关节骨量百分比降低,骨小梁分离增加(p<0.05)。与所有其他组相比,RA+AP组表现出显著较高水平的TNF-α和较低水平的IL-2(p<.05)。RA和RA+AP组的IL-17水平均显著升高(p<0.05),而各组间IL-1β水平无显著差异(p>.05)。
结论:这项研究的结果强调了根尖周炎与类风湿关节炎恶化之间的可能关系。