4种白细胞介素在种植体周围炎分期模型中的表达分析

doi:10.19439/j.sjos.2020.02.010

摘要/Abstract

摘要： 目的应用棉线结扎法建立小鼠实验性种植体周围炎模型,通过观测不同时期的大体表现和组织破坏程度,以建立小鼠种植体周围炎分期模型;通过检测疾病不同时期种植体龈沟液中白细胞介素的含量,获得种植体周围炎病程中各白细胞介素的表达变化。方法将40只4周龄(18~22 g)雄性C57BL小鼠随机分为对照组和实验组,拔除小鼠右上颌第一磨牙并即刻植入规格为1.0 mm×1.5 mm的纯钛螺纹种植钉;4周后,实验组小鼠种植钉颈部结扎5-0棉线,建立种植体周围炎模型。每5 d分别对2组种植体进行影像学和大体指标测量,根据测量数据对种植体周围炎进行早、中、晚分期。分别提取实验组小鼠早、中、晚3期种植体龈沟液并检测其IL-1α、IL-1β、IL-6和IL-17A含量。采用SPSS 22.0软件包对数据进行统计学分析。结果棉线结扎建立种植体周围炎模型后10 d,所有实验组小鼠种植体周围牙槽骨吸收达25%,确认为早期;第20天,95%的实验组小鼠牙槽骨吸收达25%~50%,确认为中期;第30天,全部实验组小鼠牙槽骨吸收超过50%,确认为晚期。IL-1α和IL-6在中期组表达水平减少;IL-1α、IL-6和IL-17A在晚期组表达水平减少,差异均有统计学意义(P<0.05)。结论成功使用棉线结扎法在小鼠口内建立种植体周围炎的分期模型,并检测出各白细胞介素在疾病不同时期的表达存在差异,为今后研究小鼠种植体周围炎分期建模和白细胞介素含量与疾病发展的关系提供了依据。

关键词: 棉线结扎, 种植体周围炎, 小鼠分期模型, 白细胞介素

Abstract: PURPOSE: To investigate the gross manifestation and tissue destruction at different inflammatory periods of ligature-induced peri-implantitis in mice model, and to evaluate the changes of interleukins level in the gingival crevicular fluid of implants at different stages. METHODS: Forty 4-week-old male C57BL/6N mice (18-22 g) were used and the maxillary right first molars were extracted, custom-made pure titanium machined screw type implants (1 mm×1.5 mm) were placed immediately, one implant per animal. Four weeks later, the mice were randomly divided into experimental and control group. 5-0 cotton ligatures were applied around implant necks in the experimental group to induce peri-implantitis. Alveolar bone loss and clinical index records of the soft and hard tissue were assessed every 5 days following ligature.According to the measured data, the stages of peri-implantitis were ascertained. The gingival crevicular fluid of implants in the early, middle and late stages in the experimental group was extracted and the expression of IL-1α, IL-1β, IL-6 and IL-17A was detected. SPSS 22.0 software package was used to analyze the data. RESULTS: Alveolar bone absorption of all the mice in the experimental group reached 25% 10 days after ligature. This time point was early stage of peri-implantitis. On day 20, the alveolar bone loss around implant in 95% of mice in the experimental group reached 25%-50%, which was identified as middle stage. The alveolar bone loss of all mice in the experimental group was over 50% 30 days following ligature, which was confirmed as late stage. Compared with the early stage, the expression of IL-1α and IL-6 decreased significantly in the middle stage; while the expression levels of IL-1α, IL-6 and IL-17A decreased significantly in the late stage. CONCLUSIONS: Mice models with peri-implantitis of various stages were successfully established by ligature and the expression of IL-1α, IL-1β, IL-6 and IL-17A in different stages of disease was detected, which provided a basis for further research the relationship between interleukin content and peri-implantitis development.

Key words: Ligature induced, Peri-implantitis, Staged model, Interleukin

中图分类号:

R783.6

冷春涛, 李婷, 高晓蔚. 4种白细胞介素在种植体周围炎分期模型中的表达分析[J]. 上海口腔医学, 2020, 29(2): 162-167.

LENG Chun-tao, LI Ting, GAO Xiao-wei. Study on the expression level of four kinds of interleukins in mice model with peri-implantitis[J]. Shanghai Journal of Stomatology, 2020, 29(2): 162-167.

参考文献

[1] Valente NA, Andreana S.Peri-implant disease: what we know and what we need to know[J]. J. Periodontal Implant Sci, 2016, 46(3): 136-151.
[2] Heitzmayfield LJ.Peri-implant diseases: diagnosis and risk indicators[J]. J Clin Periodontol, 2008, 35(8 Suppl): 292-304.
[3] Atieh MA, Alsabeeha NHM, Faggion CM, et al.The frequency of peri-implant diseases: a systematic review and meta-analysis[J]. J Periodontol, 2013, 84(11): 1586-1598.
[4] Martins O, Ramos JC, Baptista IP, et al.The dog as a model for peri-implantitis: A review[J]. J Invest Surg, 2014, 27(1): 50-56.
[5] von Wilmowsky C, Schlegel KA, Baran C, et al. Peri-implant defect regeneration in the diabetic pig: a preclinical a study[J]. J Craniomaxillofac Surg, 2016, 44(7): 827-834.
[6] Schou S, Holmstrup P, Stoltze K, et al.Probing around implants and teeth with healthy or inflamed peri-implant mucosa/gingiva. A histologic comparison in cynomolgus monkeys (Macacafas cicularis)[J]. Clin Oral Implants Res, 2002, 13(2): 113-126.
[7] Battula S, Lee JW, Wen HB, et al.Evaluation of different implant designs in a ligature-induced peri-implantitis model: a canine study[J]. Int J Oral Maxillofac Implants, 2015, 30(3): 534-534.
[8] Weinberg MA, Bral M.Laboratory animal models in periodontology[J]. J Clin Periodontol, 1999, 26(6): 335-340.
[9] Nguyen Vo TN, Hao J, Chou J, et al.Ligature induced peri-implantitis: tissue destruction and inflammatory progression in a murine model[J]. Clin Oral Implants Res, 2017, 28(2): 129-136.
[10] Huang B, Piao M, Zhang L, et al.Ligature-induced peri-implant infection in crestal and subcrestal implants: a clinical and radiographic study in dogs[J]. Peer J, 2015, 3: e1139.
[11] Pirih FQ, Hiyari S, Barroso AD, et al.Ligature-induced peri-implantitis in mice[J]. J Periodontal Res, 2014, 50(4): 519-524.
[12] Namgoong H, Kim MD, Ku Y, et al.Bone reconstruction after surgical treatment of experimental peri-implantitis defects at a sandblasted/acid-etched hydroxyapatite-coated implant: an experimental study in the dog[J]. J Clin Periodontol, 2015, 42(10): 960-966.
[13] Serino G, Turri A.Outcome of surgical treatment of peri-implantitis: results from a 2-year prospective clinical study in humans[J]. Clin Oral Implant Res, 2011, 22(11): 1214-1220.
[14] Passi D, Singh M, Dutta SR, et al.Newer proposed classification of peri-implant defects: A critical update[J]. J Oral Biol Craniofac Res, 2017, 7(1): 58-61.
[15] Froum SJ, Rosen PS.A proposed classification for peri-implantitis[J]. Int J Periodontics Restorative Dent, 2012, 32(5): 533-537.
[16] Atieh MA, Payne AG, Duncan WJ, et al.Immediate placement or immediate restoration/loading of single implants for molar tooth replacement: a systematic review and meta-analysis[J]. Int J Oral Maxillofac Implants, 2010, 25(2): 401-415.
[17] 郭磊, 洪峰, 王远勤. 即刻种植和早期种植对前牙美学区种植体周软组织影响的对比研究[J]. 口腔疾病防治, 2017,25(4): 702-711.
[18] van Kesteren CJ, Schoolfield J, West J, et al. A prospective. randomized clinical study of changes in soft tissue position following immediate and delayed implant placement[J]. Int J Oral Maxillofac Implants, 2010, 25(3): 562-570.
[19] Wong RL, Hiyari S, Yaghsezian A, et al.Comparing the healing. potential of late-stage periodontitis and peri-implantitis[J]. J Oral Implantol, 2017, 43(6): 437-445.
[20] Hamdy AA, Ebrahem MA.The effect of interleukin-1 allele 2 genotype (IL-1a^-889 and IL-1b⁺³⁹⁵⁴) on the individual's susceptibility to peri-implantitis: case-control study[J]. J Oral Implantol, 2011, 37(3): 325-334.
[21] Liao J, Li C, Wang Y, et al.Meta-analysis of the association between common interleukin-1 polymorphisms and dental implant failure[J]. Mol Biol Rep, 2014, 41(5): 2789-2798.
[22] Yaghobee S, Khorsand A, Rasouli Ghohroudi AA, et al.Assessment of interleukin-1beta and interleukin-6 in the crevicular fluid around healthy implants, implants with peri-implantitis, and healthy teeth: a cross-sectional study[J]. J Korean Assoc Oral Maxillofac Surg, 2014, 40(5): 220-224.
[23] Severino VO, Napimoga MH, de Lima Pereira SA. Expression of IL-6, IL-10, IL-17 and IL-8 in the peri-implantcrevicular fluid of patients with peri-implantitis[J]. Arch Oral Biol, 2011, 56(8): 823-828.
[24] Kadkhodazadeh M, Baghani Z, Ebadian AR, et al.IL-17 gene polymorphism is associated with chronic periodontitis and peri-implantitis in Iranian patients: a cross-sectional study[J]. Immunol Invest, 2013, 42(2): 156-163.
[25] Pirih FQ, Hiyari S, Leung HY, et al.A murine model of lipopolysaccharide-induced peri-implant mucositis and peri-implantitis[J]. J Oral Implantol, 2014, 41(5): e158-e164.