Int J Stomatol ›› 2020, Vol. 47 ›› Issue (5): 616-620.doi: 10.7518/gjkq.2020052

• Reviews • Previous Articles    

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)


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

CLC Number: 

  • 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/
[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] Gong Tao,Li Yuqing,Zhou Xuedong.. Research progress on sugar transporter and regulatory mechanisms in Streptococcus mutans [J]. Int J Stomatol, 2022, 49(5): 506-510.
[2] Fan Yu,Cheng Lei. Smoking affects the oral microenvironment and its role in the progression of dental caries [J]. Int J Stomatol, 2021, 48(5): 609-613.
[3] Li Shijia,Chen Qiuyu,Zou Jing,Huang Ruijie. Effect of nicotine on the growth of oral bacteria in single or mixed species [J]. Int J Stomatol, 2021, 48(3): 305-311.
[4] Liu Shiyu, Tian Mi, Shi Liran, Pan Weilin, Wang Yiyao, Li Mingyun. Effect of nicotine and mecamylamine on growth of periodontal pathogens [J]. Inter J Stomatol, 2017, 44(4): 421-425.
[5] Chen Dongru, Wu Liping. Research progress on hypoxia inducible factor-1α and antisense hypoxia inducible factor-1α [J]. Inter J Stomatol, 2016, 43(5): 589-593.
[6] Hou Yubo1, Liu Xinchan2, Yu Haiyan1, Cui Leihua3, Yu Weixian4. Effect of gingipains on osteoclasts and osteoblasts [J]. Inter J Stomatol, 2016, 43(5): 609-613.
[7] Zheng Jinxuan, Wu Liping. Relationship between microRNA21 and stem cell [J]. Inter J Stomatol, 2014, 41(6): 716-719.
[8] Lu Xiaowen, Kou Liang, Du Li.. Pain development mediated by transient receptor potential vanillic and its regulatory mechanisms [J]. Inter J Stomatol, 2014, 41(1): 82-87.
[9] SHI Jun, LIU Xing-rong. Twist gene and dental pulp stem cells [J]. Inter J Stomatol, 2010, 37(3): 294-294~297.
Full text



[1] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[2] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[3] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[4] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[5] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[6] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .
[7] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .
[8] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .
[9] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .
[10] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .