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中华口腔医学研究杂志(电子版) ›› 2016, Vol. 10 ›› Issue (05) : 309 -314. doi: 10.3877/cma.j.issn.1674-1366.2016.05.002

所属专题: 文献

基础研究

泡状棘球蚴感染对实验性牙周炎的影响
哈丽娅1, 阿依甫汗·阿汗2, 李泽慧1, 姜涵1, 徐隽1, 古丽努尔·阿吾提1,(), 赵今1   
  1. 1. 830000 乌鲁木齐,新疆医科大学第一附属医院牙周黏膜科
    2. 830000 乌鲁木齐,新疆医科大学第一附属医院肝胆包虫科
  • 收稿日期:2016-02-02 出版日期:2016-10-01
  • 通信作者: 古丽努尔·阿吾提
  • 基金资助:
    新疆维吾尔自治区自然科学基金(2014211C063)

Influence of alveolar echinococcosis on the experimental periodontitis

Haliya1, Ayifuhan Ahan2, Zehui Li1, Han Jiang1, Jun Xu1, Gulinuer Auwuti1,(), Jin Zhao1   

  1. 1. Department of Periodontal and Mucosal Disease, The First Affiliated Hospital, Xinjiang Medical University, Urumqi 830000, China
    2. Department of Hepatobiliary and Hydatid Disease, The First Affiliated Hospital, Xinjiang Medical University, Urumqi 830000, China
  • Received:2016-02-02 Published:2016-10-01
  • Corresponding author: Gulinuer Auwuti
  • About author:
    Corresponding author: Auwuti Gulinuer, Email:
引用本文:

哈丽娅, 阿依甫汗·阿汗, 李泽慧, 姜涵, 徐隽, 古丽努尔·阿吾提, 赵今. 泡状棘球蚴感染对实验性牙周炎的影响[J]. 中华口腔医学研究杂志(电子版), 2016, 10(05): 309-314.

Haliya, Ayifuhan Ahan, Zehui Li, Han Jiang, Jun Xu, Gulinuer Auwuti, Jin Zhao. Influence of alveolar echinococcosis on the experimental periodontitis[J]. Chinese Journal of Stomatological Research(Electronic Edition), 2016, 10(05): 309-314.

目的

探讨泡状棘球蚴感染对大鼠牙周炎的影响及其机制。

方法

30只Wistar大鼠采用随机数字表法分为A组(泡状棘球蚴感染+牙周炎造模组)、B组(牙周炎造模组)、C组(正常对照组),每组各10只。A组为用结扎线结扎第2磨牙颈部,在丝线上涂抹细菌混悬液,建立牙周炎模型,同时经皮肝脏穿刺注射泡状棘球蚴原头节感染泡状棘球蚴,B组为牙周炎组,建模方法同上。观察体重及牙周指标变化,留取标本进行细胞因子等指标测定。采用LSD-t检验及方差分进行统计学分析。

结果

在泡状棘球蚴感染6个月后,A组和B组大鼠牙周探诊深度(PD)及临床附着丧失(CAL)明显重于正常对照组,而A组大鼠的PD和CAL与B大鼠比较明显改善[PDA =(3.53 ± 0.54)mm,PDB=(5.68 ± 0.47)mm;CALA=(3.47 ± 0.48)mm,CALB=(5.78 ± 0.45)mm],差异有统计学意义(tPD= 9.497,PPD<0.001;tCAL= 11.102,PCAL<0.001);在泡状棘球蚴感染6个月后,A组大鼠血清及龈沟液白细胞介素(IL)-10、IL-4含量高于B组,差异有统计学意义(血清tIL-10= 6.267,PIL-10<0.001;tIL-4= 2.942,PIL-4= 0.004;龈沟液tIL-10=2.220,PIL-10=0.019;tIL-4= 5.458,PIL-4<0.001),而B组低于C组,差异有统计学意义(血清tIL-10= 9.507,PIL-10<0.001;tIL-4= 6.465,PIL-4<0.001;龈沟液tIL-10= 8.378,PIL-10<0.001;tIL-4= 7.444,PIL-4<0.001);A组大鼠血清及龈沟液IL-2、干扰素γ(IFN-γ)含量低于B组,差异有统计学意义(血清tIL-2= 1.906,PIL-2= 0.036;tINF= 2.844,PINF= 0.005;龈沟液tIL-2= 2.815,PIL-2= 0.005;tINF= 2.575,PINF= 0.009),而B组高于C组,差异有统计学意义(血清tIL-2= 3.271,PIL-2= 0.002;tINF= 7.095,PINF<0.001;龈沟液tIL-2= 5.919,PIL-2<0.001;tINF= 7.020,PINF<0.001)。

结论

泡状棘球蚴感染对牙周炎具有拮抗作用,其机制可能与Th1/Th2免疫偏移有关。

Objective

To investigate the effect of alveolar echinococcosis on the experimental periodontitis.

Methods

Thirty male Wistar rats were randomly divided into 3 groups: alveolar echinococcosis + periodontitis group (group A, n= 10) , periodontitis group (group B, n= 10) , control group (group C, n= 10) . Each rat of group A was received silk ligatures around their upper mandible second molars followed by an application of a periodontal pathogen, P.g, H.a, F.n and P.i, to induce periodontitis and injected by Echinococcus multilocularis at the same time. Periodontitis was induced in group B by silk ligatures as group A but without injection. The changes of body weight and periodontal index of each group were recorded dynamically. At the end of 6 months post-infection, rats were executed. Sera and gingival crevicular fluid were collected, and periodontal tissue was removed for HE staining. The IFN-γ, IL-2, IL-10 and IL-4 levels in scrum and gingival crevicular fluid were measured by ELISA. LSD-t test and variance analysis were used for statistical analysis.

Results

After 6 months, PPD and CAL of A group and B group were significantly heavier than the control group. PPD and CAL in A group were significantly improved than that in group B (3.53 ± 0.54 vs. 5.68 ± 0.47, 3.47 ± 0.48 vs. 5.78 ± 0.45; tPD= 9.497, PPD<0.001; tCAL= 11.102, PCAL<0.001) . Compared with group B, the pathological changes, such as gingival swelling, bleeding, periodontal pocket formation and alveolar bone resorption were significantly improved, in which the number of osteoclasts was decreased, in group A. After 6 months of experiment IL-10 and IL-4 levels in group A were significantly higher than that in group B (serum: 207 ± 35 vs. 124 ± 23, tIL-10= 6.267, PIL-10<0.001; 209 ± 71 vs. 126 ± 54, tIL-4= 2.942, PIL-4= 0.004; gingival crevicular fluid: 143 ± 56 vs. 97 ± 34, tIL-10= 2.220, PIL-10= 0.019; 178 ± 56 vs. 64 ± 35, tIL-4= 5.458, PIL-4<0.001) , and IL-10 and IL-4 levels in group C were significantly higher than that in group B (serum: 320 ± 61 vs. 124 ± 23, tIL-10= 9.507, PIL-10<0.001; 353 ± 97 vs. 126 ± 54, tIL-4= 6.465, PIL-4<0.001; gingival crevicular fluid: 293 ± 76 vs. 97 ± 34, tIL-10= 8.378, PIL-10<0.001; 310 ± 86 vs. 64 ± 35, tIL-4= 7.444, PIL-4<0.001) . IL-2 and IFN-γ levels in group A were significantly lower than that in group B (serum: 140 ± 48 vs. 184 ± 55, tIL-2= 1.906, PIL-2= 0.036; 185 ± 53 vs. 257 ± 60, tINF= 2.844, PINF= 0.005; gingival crevicular fluid: 131 ± 35 vs. 179 ± 41, tIL-2= 2.815, PIL-2= 0.005; 166 ± 45 vs. 222 ± 52, tINF= 2.575, PINF= 0.009) , and IL-2 and IFN-γ levels in group B were significantly lower than that in group C (serum: 116 ± 36 vs. 184 ± 55, tIL-2= 3.271, PIL-2= 0.002; 112 ± 24 vs. 257 ± 60, tINF= 7.095, PINF<0.001; gingival crevicular fluid: 91 ± 23 vs. 179 ± 41, tIL-2= 5.919, PIL-2<0.001; 103 ± 13 vs. 222 ± 52, tINF = 7.020, PINF<0.001) .

Conclusions

The protective immunity of periodontitis is a kind of Th2 immune response with IL-10 and IL-4, and the regulating of Th1/Th2 response is beneficial to improve the process of periodontitis. Echinococcus multilocularis infection had a significant influence on the Th1/Th2 balance of periodontitis in rats, with regulating the balance to Th2 predominant reaction, which had an antagonistic effect on periodontitis.

表1 实验后6个月各组大鼠的体重情况(±s
表2 各组大鼠实验前后牙周指标的变化(mm,±s
表3 实验后6个月大鼠龈沟液中IL-2、IFN-γ、IL-4和IL-10 ELISA检测(ng/ml,±s
表4 实验后6个月大鼠血清中IL-2、IFN-γ、IL-4和IL-10 ELISA检测(ng/ml,±s
图3 B组(牙周炎组)大鼠实验前后牙周组织改变(苏木精-伊红 × 400;图3A为实验后;图3B为实验前)
[1]
郭伟.口腔临床免疫学[M].上海:复旦大学出版社,2003:49-57.
[2]
Alayan J, Ivanovski S, Farah CS. Alveolar bone loss in T helper 1/T helper 2 cytokine-deficient mice[J]. J Periodontal Res,2007,42(2):97-103.
[3]
Gemmell E, Marshall RI, Seymour GJ. Cytokines and prostaglandins in immune homeostasis and tissue destruction in periodontal disease[J]. Periodontol 2000,1997,14(1):112-143.
[4]
Teng YT. Mixed periodontal Th1-Th2 cytokine profile in Actinobacillus actinomycetemcomitans-specific osteoprotegerin ligand(or RANK-L)-mediated alveolar bone destruction in vivo[J]. Infect Immun,2002,70(9):5269-5273.
[5]
Moqi M, Otoqoto J, Ota N,et al. Interleukin 1 beta,interleukin 6,beta 2-microglobulin,and transforming growth factor-alpha in gingival crevicular fluid from human periodontal disease[J]. Arch Oral Biol,1999,44(6):535-539.
[6]
O′Brien-Simpson NM, Pathirana RD, Paolini RA,et al. An immune response directed to proteinase and adhesin functional epitopes protects against Porphyromonas gingivalis-induced periodontal bone loss[J]. J Immunol,2005,175(6):3980-3989.
[7]
买合皮热提汗·艾尔肯,王云海,赵晋明,等.泡状棘球蚴感染诱导免疫耐受的研究[J].中华实验外科杂志,2011,28(10):1749-1752.
[8]
Spahr A, Klein E, Khuseyinova N,et al. Periodontal infections and coronary heart disease:role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease(CORODONT)study[J]. Arch Intern Med,2006,166(5):554-559.
[9]
Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for atherosclerosis,cardiovascular disease,and stroke. A systematic review[J]. Ann Periodontol,2003,8(1):38-53.
[10]
Seymour GJ, Ford PJ, Cullinan MP,et al. Relationship between periodontal infections and systemic disease[J]. Clin Microbiol Infect,2007,13(Suppl 4):3-10.
[11]
Perrino MA. Diabetes and periodontal disease:an example of an oral/systemic relationship[J]. N Y State Dent J,2007,73(5):38-41.
[12]
Gomes-Filho IS, da Cruz SS, Rezende EJ,et al. Periodontal status as predictor of prematurity and low birth weight[J]. J Public Health Dent,2006,66(4):295-298.
[13]
Sánchez AR, Bagniewski S, Weaver AL,et al. Correlations between maternal periodontal conditions and preterm low birth weight infants[J]. J Int Acad Periodontol,2007,9(2):34-41.
[14]
DeStefano F, Anda RF, Kahn HS,et al. Dental disease and risk of coronary heart disease and mortality[J]. BMJ,1993,306(6879):688-691.
[15]
Offenbacher S, Katz V, Fertik G,et al. Periodontal infection as a possible risk factor for preterm low birth weight[J]. J Periodontol,1996,67(10 Suppl):1103-1113.
[16]
Iacopino AM. Periodontitis and diabetes interrelationships:role of inflammation[J]. Ann Periodontol,2001,6(1):125-137.
[17]
Gemmell E, Bird PS, Ford PJ,et al. Modulation of the antibody response by Porphyromonas gingivalis and Fusobacterium nucleatum in a mouse model[J]. Oral Microbiol Immunol,2004,19(4):247-251.
[18]
Li CH, Amar S. Morphometric,histomorphometric,and microcomputed tomographic analysis of periodontal inflammatory lesions in a murine model[J]. J Periodontol,2007,78(6):1120-1128.
[19]
Boubaker G, Hemphill A, Huber CO,et al. Prevention and immunotherapy of secondary murine alveolar echinococcosis employing recombinant EmP29 antigen[J]. PLoS Negl Trop Dis,2015,9(6):e0003795.
[20]
Wang J, Vuitton DA, Müller N,et al. Deletion of fibrinogen-like protein 2(FGL-2),a novel CD4+ CD25+ treg effector molecule,leads to improved control of echinococcus multilocularis infection in mice[J]. PLoS Negl Trop Dis,2015,9(5):e0003755.
[21]
Dai WJ, Hemphill A, Waldvogel A,et al. Major carbohydrate antigen of Echinococcus multilocularis induces an immunoglobulin G response independent of alphabeta CD4+ cells[J]. Infect Immun,2001,69(10):6074-6083.
[22]
李富荣,石佑思,史大中,等.泡状棘球蚴病宿主淋巴细胞的变化及意义[J].中国人兽共患病杂志,2003,19(3):91-94.
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