信号转导和转录活化因子3在正畸力介导的骨改建中的表达

上海口腔医学 ›› 2016, Vol. 25 ›› Issue (6): 652-656.

信号转导和转录活化因子3在正畸力介导的骨改建中的表达

周巳入¹, 代庆刚², 张鹏¹, 河奈玲¹, 杨树亮³, 江凌勇¹

1.上海交通大学医学院附属第九人民医院·口腔医学院口腔颅颌面科,2.儿童口腔科, 上海市口腔医学重点实验室,上海 200011;;
3.浙江省永康市第一人民医院口腔科,浙江永康 321300

收稿日期:2016-09-18 出版日期:2016-12-25 发布日期:2016-12-29
通讯作者: 江凌勇,E-mail: jly117@sina.com
作者简介:周巳入（1992-）,女,硕士研究生,E-mail:13789278@qq.com
基金资助:
国家自然科学基金（81570950,81371121,30901698）; 上海市自然科学基金（13ZR1423700）; 上海交通大学医工交叉基金（YG2012MS40）; 上海交通大学SMC-晨星青年学者奖励计划优秀青年教师（B类计划）; 上海高校高峰高原学科建设项目

Expression of STAT3 in alveolar bone during orthodontic tooth movement in rats

ZHOU Si-ru¹, DAI Qing-gang², ZHANG Peng¹, HA Na-yong¹, YANG Shu-liang³, JIANG Ling-yong¹

1.Department of Oral and Craniomaxillofacial Science, 2.Department of Pediatric Dentistry, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine; Shanghai Key Laboratory of Stomatology. Shanghai 200011;
3.Department of Stomatology, First People's Hospital of Yongkang City. Yongkang 321300, Zhejiang Province, China

Received:2016-09-18 Online:2016-12-25 Published:2016-12-29

摘要/Abstract

摘要： 目的研究信号转导和转录活化因子3（signal transducer and activator of transcription 3,STAT3）在大鼠正畸牙移动过程中牙周组织内的表达规律。方法选用6周龄大鼠20只,构建大鼠左侧上颌第一磨牙正畸牙移动模型,分别于牙移动0、1、3、7 d各处死大鼠5只,取上颌第一磨牙及其周围牙周组织,行H-E染色和免疫组织化学染色,观察正畸牙移动过程中牙槽骨的改建及STAT3的表达变化。采用SPSS16.0软件包对数据进行统计学分析。结果大鼠左侧上颌第一磨牙在正畸力作用下不断近中移动。正畸力作用后,压力区破骨细胞显著增加（P<0.05）,张力区成骨细胞亦显著上升,牙槽骨改建增强。正畸力作用后,STAT3高表达于张力区成骨细胞内。统计学分析显示,正畸牙移动3、7 d的张力区,STAT3的表达均显著高于0 d（P<0.05）。结论正畸力可增强牙槽骨改建,张力区STAT3的表达改变可能与正畸牙移动的骨改建相关。

关键词: 正畸牙移动, 骨改建, 信号转导和转录活化因子3

Abstract: PURPOSE: To study the changes of expression of signal transducer and activator of transcription 3 (STAT3) during orthodontic tooth movement (OTM). METHODS: Twenty six-week-old SD rats were selected, the upper left first molars were moved by coil spring and lasted for 7 days. The maxillary tissues were obtained at 0, 1, 3, 7 d and subjected to histological study. Statistical analysis was performed using SPSS 16.0 software package. RESULTS: The main changes in alveolar bone during orthodontic tooth movement included significant increase in osteoblast number and bone formation in the tension area, and bone resorption in the pressure area. The positive cells of osteocalcin in the tension area increased during OTM. The expression of STAT3 increased in the tension area at 3 d and 7 d in comparison with that at 0 d. CONCLUSIONS: Orthodontic force can stimulate alveolar bone remolding. The expression of STAT3 in the tension area may have effects on alveolar bone remolding during orthodontic tooth movement.

Key words: Orthodontic tooth movement, Alveolar bone remolding, STAT3

中图分类号:

R783.5

周巳入, 代庆刚, 张鹏, 河奈玲, 杨树亮, 江凌勇. 信号转导和转录活化因子3在正畸力介导的骨改建中的表达[J]. 上海口腔医学, 2016, 25(6): 652-656.

ZHOU Si-ru, DAI Qing-gang, ZHANG Peng, HA Na-yong, YANG Shu-liang, JIANG Ling-yong. Expression of STAT3 in alveolar bone during orthodontic tooth movement in rats[J]. Shanghai Journal of Stomatology, 2016, 25(6): 652-656.

参考文献

[1] Nettelhoff L, Grimm S, Jacobs C, et al. Influence of mechanical compression on human periodontal ligament fibroblasts and osteoblasts [J]. Clin Oral Investig, 2016, 20(3): 621-629.
[2] Wang.C, Han J, Li Q, et al. Simulation of bone remodelling in orthodontic treatment[J]. Comput Methods Biomech Biomed Engin, 2014, 17(9): 1042-1050.
[3] Nakano T, Hotokezaka H, Hashimoto M, et al. Effects of different types of tooth movement and force magnitudes on the amount of tooth movement and root resorption in rats[J]. Angle Orthod, 2014, 84(6): 1079-1085.
[4] Meeran NA, Cellular response within the periodontal ligament on application of orthodontic forces[J]. J Indian Soc Periodontol, 2013, 17(1): 16-20.
[5] Goncalves CF, Desiderá AC, do Nascimento GC, et al. Experimental tooth movement and photobiomodulation on bone remodeling in rats [J]. Lasers Med Sci, 2016, 31(9): 1883-1890.
[6] Rodda SJ, McMahon AP. Distinct roles for Hedgehog and canonical Wnt signaling in specification, differentiation and maintenance of osteoblast progenitors [J]. Development, 2006, 133(16): 3231-3244.
[7] Resemann HK, Watson CJ, Lloyd-Lewis B. The Stat3 paradox: a killer and an oncogene [J]. Mol Cell Endocrinol, 2014, 382(1): 603-611.
[8] Cheon YH, Kim JY, Baek JM, et al. WHI-131 promotes osteoblast differentiation and prevents osteoclast formation and resorption in mice [J]. J Bone Miner Res, 2016, 31(2): 403-415.
[9] Mantila Roosa SM, Liu Y,Turner CH. Gene expression patterns in bone following mechanical loading [J]. J Bone Miner Res, 2011, 26(1): 100-112.
[10] 忻贤贞, 杨旭, 魏斌. SD大鼠咬合创伤模型的建立 [J]. 上海口腔医学, 2016, 25(3): 281-283.
[11] Persson M. A 100th anniversary: Sandstedt's experiments on tissue changes during tooth movement[J]. J Orthod, 2005, 32(1): 27-28.
[12] Krishnan V,Davidovitch Z. Cellular, molecular, and tissue-level reactions to orthodontic force[J]. Am J Orthod Dentofacial Orthop, 2006, 129(4): 469.e1-32.
[13] Meikle MC.The tissue, cellular, and molecular regulation of orthodontic tooth movement:100 years after Carl Sandstedt [J]. Euro J Orthod, 2006, 28(3): 221-240.
[14] Levy O, Ruvinov E, Reem T, et al. Highly efficient osteogenic differentiation of human mesenchymal stem cells by eradication of STAT3 signaling[J]. Int J Biochem Cell Biol, 2010, 42(11): 1823-1830.
[15] Minegishi Y, Saito M, Tsuchiya S, et al. Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome [J]. Nature, 2007, 448(7157): 1058-1062.
[16] Matsushita K, Itoh S, Ikeda S, et al. LIF/STAT3/SOCS3 signaling pathway in murine bone marrow stromal cells suppresses osteoblast differentiation[J]. J Cell Biochem, 2014, 115(7): 1262-1268.
[17] Holland SM, DeLeo FR, Elloumi HZ, et al. STAT3 mutations in the hyper-IgE syndrome[J]. N Engl J Med, 2007, 357(16): 1608-1619.
[18] Zhou H, Newnum AB, Martin JR, et al.Osteoblast/osteocyte-specific inactivation of Stat3 decreases load-driven bone formation and accumulates reactive oxygen species[J]. Bone, 2011, 49(3): 404-411.