摘要
目的利用牙周炎与类风湿关节炎小鼠模型研究牙龈卟啉单胞菌感染对类风湿关节炎的影响。方法实验小鼠被分为单纯类风湿关节炎组与牙周炎合并类风湿关节炎组。实验中通过口腔涂抹牙龈卟啉单胞菌构建牙周炎模型,利用牛Ⅱ型胶原诱导小鼠类风湿关节炎模型的建立。通过比较牙龈卟啉单胞菌感染与否对类风湿关节炎严重程度的影响来探讨牙龈卟啉单胞菌感染是否会促进类风湿关节炎的发生及发展。实验中通过类风湿关节炎评分评估类风湿关节炎的严重程度;利用酶联免疫分析试剂盒检测血浆中类风湿关节炎相关因子的水平。结果牙龈卟啉单胞菌感染合并胶原诱导类风湿关节炎组的类风湿关节炎症状出现时间较单纯胶原诱导类风湿关节炎组明显缩短,并且在牙龈卟啉单胞菌感染情况下的类风湿关节炎的症状及类风湿关节炎相关炎症因子如TNF-α、IL-1、IL-6、IL-17的水平也明显升高。结论牙龈卟啉单胞菌感染能促进类风湿关节炎的发生并加重类风湿关节炎症状。
Objective To study the effect of Porphyromonas gingivalis infection on the rheumatoid arthritis using periodontitis and rheumatoid arthritis mice models.Methods The mice were divided into rheumatoid arthritis(CIA)group and periodontitis combined with rheumatoid arthritis(CIA+P.g)group.Periodontitis models were constructed by oral inoculation of Porphyromonas gingivalis,and the rheumatoid arthritis model was induced by bovineⅡcollagen.To determine whether Porphynomonas gingivalis infection will promote the occurrence and development of rheumatoid arthritis,the effect of Porphynomonas gingivalis infection on the severity of rheumatoid arthritis was compared.The severity of rheumatoid arthritis was assessed by rheumatoid arthritis score.The level of rheumatoid factor in plasma was detected by enzyme linked immunoassay kit.Results The onset of rheumatoid arthritis in the CIA+P.g group was significantly shorter than that of the CIA group,and the symptoms were more serious.The inflammatory factors related to rheumatoid arthritis such as TNF-α,IL-1,IL-6 and IL-17 were also significantly higher in CIA+P.g group.Conclusion The infection of Porphyromonas gingivalis can promote the occurrence of rheumatoid arthritis and aggravate its symptoms.
作者
宋亮
陈慧娟
胡凤玲
刘柳慧
郑义彩
刘阳
徐斌
SONG Liang;CHEN Huijuan;HU Fengling;LIU Liuhui;ZHENG Yicai;LIU Yang;XU Bin(Department of Stomatology,The Fifth People’s Hospital of Shanghai,Fudan University,Shanghai 200240,China;不详)
出处
《口腔医学》
CAS
2019年第7期587-591,共5页
Stomatology
基金
上海市闵行区科委课题(2014MHZ050)
复旦大学附属上海市第五人民医院菁英人才培养项目(2017WYRCJY02)
关键词
牙周炎
类风湿关节炎
牙龈卟啉单胞菌
炎症因子
periodontitis
rheumatoid arthritis
Porphyromonas gingivalis
inflammatory factor