国际口腔医学杂志

国际口腔医学杂志 ›› 2020, Vol. 47 ›› Issue (5): 616-620.doi: 10.7518/gjkq.2020052

• 综述 • 上一篇    

尼古丁对牙槽骨破骨细胞的作用及其机制的研究进展

杨佩佩(),杨羽晨,张强()   

  1. 南昌大学第一附属医院口腔颌面外科 南昌 330006
  • 收稿日期:2019-11-01 修回日期:2020-04-26 出版日期:2020-09-01 发布日期:2020-09-16
  • 通讯作者: 张强
  • 作者简介:杨佩佩,硕士,Email: 978566228@qq.com
  • 基金资助:
    国家自然科学基金(81560189);国家自然科学基金(81260169)

Advances in the mechanism and effect of nicotine on alveolar osteoclasts

Yang Peipei(),Yang Yuchen,Zhang Qiang()   

  1. Dept. of Oral and Maxillofacial Surgery, First Affiliated Hospital of Nanchang University, Nanchang 330006, China
  • Received:2019-11-01 Revised:2020-04-26 Online:2020-09-01 Published:2020-09-16
  • Contact: Qiang Zhang
  • Supported by:
    National Natural Science Foundation of China(81560189);National Natural Science Foundation of China(81260169)

RichHTML

33

PDF (PC)

248

摘要：

吸烟对牙周疾病具有促进作用,而尼古丁作为烟草中有毒化学物质之一,是导致牙周病包括牙龈出血、牙周袋形成、牙槽骨吸收、牙齿松动的重要诱因。牙槽骨的吸收是骨组织的动态平衡被破坏的后果,是指成骨细胞主导的骨形成和破骨细胞主导的骨吸收失去平衡。通过研究尼古丁对破骨细胞及其诱导因子的调控作用,可以阐明尼古丁对于骨代谢的特殊作用,从而进一步论证尼古丁对牙周病发展的诱导作用。本文就尼古丁对破骨细胞的作用及其机制的研究进展进行综述。

关键词: 尼古丁, 破骨细胞, 调控机制

Abstract:

Smoking can promote periodontal disease. As one of the toxic chemicals in tobacco, nicotine is an important cause of periodontal diseases, including gingival bleeding, periodontal pocket formation, alveolar bone absorption and tooth loosening. Alveolar bone resorption results from the disrupted dynamic balance of bone tissue, which refers to the imbalance of bone resorption regulated by osteoblasts and osteoclasts. The special effect of nicotine on bone metabolism was clarified by studying the regulatory effect of nicotine on osteoclasts and inducing factors. The inducing effect of nicotine on the development of periodontal disease was further analysed. This article reviewed the research progress on the effect of nicotine on osteoclasts.

Key words: nicotine, osteoclasts, regulatory mechanism

中图分类号: 

  • R781.4
[1] Wetscher GJ, Bagchi M, Bagchi D, et al. Free radical production in nicotine treated pancreatic tissue[J]. Free Radic Biol Med, 1995,18(5):877-882.
doi: 10.1016/0891-5849(94)00221-5 pmid: 7797095
[2] Kim JH, Patel S. Is it worth discriminating against patients who smoke? A systematic literature review on the effects of tobacco use in foot and ankle sur-gery[J]. J Foot Ankle Surg, 2017,56(3):594-599.
doi: 10.1053/j.jfas.2017.02.006 pmid: 28476393
[3] Kinane DF, Stathopoulou PG, Papapanou PN. Perio-dontal diseases[J]. Nat Rev Dis Primers, 2017,3:17038.
doi: 10.1038/nrdp.2017.38 pmid: 28805207
[4] Müller HP, Stadermann S, Heinecke A. Longitudinal association between plaque and gingival bleeding in smokers and non-smokers[J]. J Clin Periodontol, 2002,29(4):287-294.
doi: 10.1034/j.1600-051x.2002.290403.x pmid: 11966925
[5] Johnson TM. Smoking and periodontal disease[J]. US Army Med Dept J, 2017: 67-70.
[6] Chang YC, Huang FM, Tai KW, et al. Mechanisms of cytotoxicity of nicotine in human periodontal liga-ment fibroblast cultures in vitro[J]. J Periodont Res, 2002,37(4):279-285.
doi: 10.1034/j.1600-0765.2002.01612.x pmid: 12200972
[7] Kubota M, Yanagita M, Mori , et al. The effects of cigarette smoke condensate and nicotine on perio-dontal tissue in a periodontitis model mouse[J]. PLoS One, 2016,11(5):e0155594.
doi: 10.1371/journal.pone.0155594 pmid: 27203240
[8] Boyce BF, Xing LP. Functions of RANKL/RANK/OPG in bone modeling and remodeling[J]. Arch Bio-chem Biophys, 2008,473(2):139-146.
doi: 10.1016/j.abb.2008.03.018
[9] Christoph F, König F, Lebentrau S, et al. RANKL/RANK/OPG cytokine receptor system: mRNA ex-pression pattern in BPH, primary and metastatic pro-state cancer disease[J]. World J Urol, 2018,36(2):187-192.
doi: 10.1007/s00345-017-2145-y pmid: 29204705
[10] Li Y, Toraldo G, Li AM, et al. B cells and T cells are critical for the preservation of bone homeostasis and attainment of peak bone mass in vivo[J]. Blood, 2007,109(9):3839-3848.
doi: 10.1182/blood-2006-07-037994 pmid: 17202317
[11] Liu W, Zhang XL. Receptor activator of nuclear factor-κB ligand (RANKL)/RANK/osteoprotegerin system in bone and other tissues (review)[J]. Mol Med Rep, 2015,11(5):3212-3218.
doi: 10.3892/mmr.2015.3152 pmid: 25572286
[12] Sojod B, Chateau D, Mueller CG, et al. RANK/RANKL/OPG signalization implication in perio-dontitis: new evidence from a RANK transgenic mouse model[J]. Front Physiol, 2017,8:338.
doi: 10.3389/fphys.2017.00338 pmid: 28596739
[13] Lee HJ, Pi SH, Kim Y, et al. Effects of nicotine on antioxidant defense enzymes and RANKL expre-ssion in human periodontal ligament cells[J]. J Perio-dontol, 2009,80(8):1281-1288.
[14] De Vries TJ, Schoenmaker T, Aerts D, et al. M-CSF priming of osteoclast precursors can cause osteo-clastogenesis-insensitivity, which can be prevented and overcome on bone[J]. J Cell Physiol, 2015,230(1):210-225.
doi: 10.1002/jcp.24702 pmid: 24962140
[15] Zeng L, Xu YM, Xing GY. Effect of lipopolysac-charide on osteoclasts formation and bone resorption function and its mechanism[J]. Chin J Reparative Reconstr Surg, 2018,32(5):568-574.
[16] Amano S, Kawakami K, Iwahashi H, et al. Functional role of endogenous CD14 in lipopolysaccharide-stimulated bone resorption[J]. J Cell Physiol, 1997,173(3):301-309.
doi: 10.1002/(SICI)1097-4652(199712)173:3<301::AID-JCP1>3.0.CO;2-R pmid: 9369942
[17] Tanaka H, Tanabe N, Shoji M, et al. Nicotine and lipopolysaccharide stimulate the formation of osteo-clast-like cells by increasing macrophage colony-stimulating factor and prostaglandin E2 production by osteoblasts[J]. Life Sci, 2006,78(15):1733-1740.
doi: 10.1016/j.lfs.2005.08.017 pmid: 16266722
[18] 王晓庚, 刘文佳, 周洪, 等. 不同浓度破骨细胞分化因子和巨噬细胞集落刺激因子体外诱导大鼠破骨样细胞形成的研究[J]. 口腔医学, 2008,28(4):169-172.
Wang XG, Liu WJ, Zhou H , et al. Differentiation of osteoclast-like cells induced by using different con-centrations of M-CSF and RANKL[J]. Stomatology, 2008,28(4):169-172.
[19] Zhao QX. Osteoclast differentiation and gene regu-lation[J]. Front Biosci, 2007,12(1):2519.
doi: 10.2741/2252
[20] Pixley FJ, Stanley ER. CSF-1 regulation of the wan-dering macrophage: complexity in action[J]. Trends Cell Biol, 2004,14(11):628-638.
doi: 10.1016/j.tcb.2004.09.016 pmid: 15519852
[21] Yeo CE, Kang WY, Seong SJ, et al. Neuromedin B and its receptor silencing suppresses osteoclast gene-ration by modulating precursor proliferation via M- CSF/c-Fms/D-type cyclins[J]. Exp Cell Res, 2017,359(1):112-119.
doi: 10.1016/j.yexcr.2017.08.003 pmid: 28780306
[22] Chen C, Xie J, Rajappa R, et al. Interleukin-1β and tumor necrosis factor-α increase stiffness and impair contractile function of articular chondrocytes[J]. Acta Biochim Biophys Sin (Shanghai), 2015,47(2):121-129.
doi: 10.1093/abbs/gmu116
[23] Chen YH, Guo QS, Pan XH, et al. Smoking and impaired bone healing: will activation of cholinergic anti-inflammatory pathway be the bridge[J]. Int Orthop, 2011,35(9):1267-1270.
doi: 10.1007/s00264-011-1243-5
[24] 蒙超龙, 王祥, 段建民, 等. 肿瘤坏死因子-α对人牙周膜干细胞的增殖及成骨分化的影响[J]. 牙体牙髓牙周病学杂志, 2018,28(2):63-68.
Meng CL, Wang X, Duan JM , et al. The effects TNF-α on the proliferation and osteogenic differentiation of periodontal ligament stem cells[J]. Chin J Conserv Dent, 2018,28(2):63-68.
[25] Kobayashi K, Takahashi N, Jimi E, et al. Tumor necrosis factor alpha stimulates osteoclast differen-tiation by a mechanism independent of the ODF/RANKL-RANK interaction[J]. J Exp Med, 2000,191(2):275-286.
doi: 10.1084/jem.191.2.275 pmid: 10637272
[26] Azuma Y, Kaji K, Katogi R, et al. Tumor necrosis factor-α induces differentiation of and bone resorp-tion by osteoclasts[J]. J Biol Chem, 2000,275(7):4858-4864.
doi: 10.1074/jbc.275.7.4858 pmid: 10671521
[27] Mundy GR. Role of cytokines in bone resorption[J]. J Cell Biochem, 1993,53(4):296-300.
doi: 10.1002/jcb.240530405 pmid: 8300746
[28] Hapidin H, Othman F, Soelaiman IN, et al. Negative effects of nicotine on bone-resorbing cytokines and bone histomorphometric parameters in male rats[J]. J Bone Miner Metab, 2007,25(2):93-98.
doi: 10.1007/s00774-006-0733-9
[29] Costa-Rodrigues J, Rocha I, Fernandes MH. Complex osteoclastogenic inductive effects of nicotine over hydroxyapatite[J]. J Cell Physiol, 2018,233(2):1029-1040.
doi: 10.1002/jcp.25956 pmid: 28407244
[1] 余岳霖,孔卫东. 甲状旁腺激素受体1基因相关与原发性牙齿萌出障碍的研究进展[J]. 国际口腔医学杂志, 2023, 50(5): 573-580.
[2] 于乐蓉,李祥伟,艾虹. 牙髓干细胞干性维持的研究进展[J]. 国际口腔医学杂志, 2023, 50(4): 463-471.
[3] 龚涛,李雨庆,周学东. 变异链球菌糖转运及其调控机制的研究进展[J]. 国际口腔医学杂志, 2022, 49(5): 506-510.
[4] 赵曼竹,宋锦璘. 时钟基因在牙齿发育中表达分布与调控机制的研究进展[J]. 国际口腔医学杂志, 2022, 49(4): 380-385.
[5] 安宁,李姣,梅志丹. 骨保护素/核因子-κB受体活化因子/核因子κB-受体活化因子配体信号分子调控牙萌出的研究进展[J]. 国际口腔医学杂志, 2022, 49(1): 116-120.
[6] 范宇,程磊. 吸烟影响口腔微环境及其在龋病进展中的作用[J]. 国际口腔医学杂志, 2021, 48(5): 609-613.
[7] 李诗佳,陈秋宇,邹静,黄睿洁. 尼古丁对口腔细菌单独或混合培养时菌群数目调控的研究[J]. 国际口腔医学杂志, 2021, 48(3): 305-311.
[8] 吕辉,王华,孙雯. 辅助性T细胞17与牙周炎骨免疫[J]. 国际口腔医学杂志, 2020, 47(6): 661-668.
[9] 付世锦,曾刊,李鑫,杨静,汪成林,叶玲. 骨保护素/核因子κB受体活化因子配体影响肺癌细胞下颌骨与股骨转移差异的初步研究[J]. 国际口腔医学杂志, 2020, 47(5): 538-546.
[10] 孙坚炜,雷利红,谭静怡,陈莉丽. 微小RNA 155对骨免疫的调控及其在牙周炎中作用的研究进展[J]. 国际口腔医学杂志, 2020, 47(5): 607-615.
[11] 朱俊瑾,周佳琦,伍颖颖. 哺乳动物雷帕霉素靶蛋白复合物1介导的自噬对骨代谢的调控[J]. 国际口腔医学杂志, 2020, 47(1): 84-89.
[12] 卢可心,张迪亚,吴燕岷. 蛋白酶激活受体在牙周组织细胞中相关作用的研究进展[J]. 国际口腔医学杂志, 2019, 46(6): 657-662.
[13] 张誉泓,戚孟春,董伟,孙红. CaMKi>Ⅱδ基因沉默对破骨细胞分化功能及c-fosi>/c-juni>/CREBi>基因的影响[J]. 国际口腔医学杂志, 2019, 46(4): 420-425.
[14] 胡巍,王译凡,袁一方,李影,郭斌. 节律基因调控成骨和破骨活动机制的研究进展[J]. 国际口腔医学杂志, 2019, 46(3): 302-307.
[15] 高鑫,曾融生. 骨保护素在口腔领域的研究进展[J]. 国际口腔医学杂志, 2019, 46(3): 316-319.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
[1] 王昆润. 二甲亚砜和双氯芬酸并用治疗根尖周炎[J]. 国际口腔医学杂志, 1999, 26(06): .
[2] 汤庆奋,王学侠. 17β-雌二醇对人类阴道和口腔颊粘膜的渗透性[J]. 国际口腔医学杂志, 1999, 26(06): .
[3] 潘劲松. 颈总动脉指压和颈内动脉球囊阻断试验在大脑血液动力学中的不同影响[J]. 国际口腔医学杂志, 1999, 26(05): .
[4] 王昆润. 后牙冠根斜形牙折的治疗[J]. 国际口腔医学杂志, 1999, 26(05): .
[5] 杨锦波. 嵌合体防龋疫苗的研究进展[J]. 国际口腔医学杂志, 1999, 26(05): .
[6] 王昆润. 下颔骨成形术用网状钛板固定植骨块[J]. 国际口腔医学杂志, 1999, 26(04): .
[7] 汪月月,郭莉莉. 口腔机能与老化—痴呆危险因素流行病学研究[J]. 国际口腔医学杂志, 1999, 26(04): .
[8] 丁刚. 应用硬组织代用品种植体行丰颏术[J]. 国际口腔医学杂志, 1999, 26(04): .
[9] 田磊. 局部应用脂多糖后结合上皮反应性增生的变化[J]. 国际口腔医学杂志, 1999, 26(04): .
[10] 戴青. 口腔念珠菌病的新分类[J]. 国际口腔医学杂志, 1999, 26(04): .