国际口腔医学杂志 ›› 2016, Vol. 43 ›› Issue (3): 333-337.doi: 10.7518/gjkq.2016.03.018

• 综述 • 上一篇    下一篇

骨硬化蛋白对牙骨质形成的影响及其机制

陈甜,白丁   

  1. 口腔疾病研究国家重点实验室 华西口腔医院正畸科(四川大学) 成都 610041
  • 收稿日期:2015-07-10 修回日期:2016-01-15 出版日期:2016-05-01 发布日期:2016-05-01
  • 通讯作者: 白丁,教授,博士,Email:baiding@scu.edu.cn
  • 作者简介:陈甜,硕士,Email:chentian0629@qq.com
  • 基金资助:
    国家自然科学基金(11172190,81371171);高等学校博士学科专项科研基金(20130181110013)

Effect of sclerostin on cementogenesis and its mechanism

Chen Tian, Bai Ding   

  1. State Key Laboratory of Oral Diseases, Dept. of Orthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China) This study was supported by the National Natural Science Foundation of China(11172190, 81371171) and the Doctoral Program Foundation of Institution of Higher Education of China(20130181110013).
  • Received:2015-07-10 Revised:2016-01-15 Online:2016-05-01 Published:2016-05-01

摘要: 骨硬化蛋白是一种含有胱氨酸结的分泌型糖蛋白,可通过骨细胞突触传递至骨表面并作用于周围的成骨细胞,从而降低骨的发生发育速度。其机制在于骨硬化蛋白与无翅型小鼠乳房肿瘤病毒整合位点家族蛋白竞争性地结合辅助受体低密度脂蛋白受体相关蛋白5/6,促进β-连环蛋白磷酸化并降低β-连环蛋白水平,从而抑制成骨细胞的分化及活性。牙骨质为连接牙体和牙周组织间的桥梁,其功能在于维系牙体的稳固和牙周组织的健康。骨硬化蛋白参与并影响牙骨质的发生发育等各种生理性活动,因此进一步深入探讨骨硬化蛋白这一骨形成负性调控因子与牙骨质间的相互作用和机制,将有助于牙骨质相关再生领域的发展。

关键词: 牙骨质, 骨硬化蛋白, 无翅型小鼠乳房肿瘤病毒整合位点家族-β-连环蛋白-信号转导通路, 分子机制, 矿化组织, 牙骨质, 骨硬化蛋白, 无翅型小鼠乳房肿瘤病毒整合位点家族-β-连环蛋白-信号转导通路, 分子机制, 矿化组织

Abstract: Sclerostin, a secreted glycoprotein with a C-terminal cysteine knot-like domain protein, is produced by the osteocytes and has anti-anabolic effects on bone formation. Sclerostin is an antagonist of Wnt signaling pathway by binding to low density lipoprotein receptor-related protein-5/6 receptors and prompting the phosphorylation of β-catenin. Cementum is a specialized substance covering the root of a tooth and a dynamic entity within the periodontium sustaining the firmness of the tooth. Sclerostin has been identified during cementogenesis, in which the underlying mechanism is still obscure. On this basis, providing a comprehensive insight into the interactional and reciprocal molecular mechanism between sclerostin and cementum may facilitate cementogenesis-related tooth development and regeneration.

Key words: cementum, sclerostin, wingless-type mice mammary tumour virus integration site family-β-catenin-signal transduction pathway, molecular mechanism, mineralized tissues, cementum, sclerostin, wingless-type mice mammary tumour virus integration site family-β-catenin-signal transduction pathway, molecular mechanism, mineralized tissues

中图分类号: 

  • Q 51
[1] van Bezooijen RL, ten Dijke P, Papapoulos SE, et al. SOST/sclerostin, an osteocyte-derived negative regulator of bone formation[J]. Cytokine Growth Factor Rev, 2005, 16(3):319-327.
[2] Poole KE, van Bezooijen RL, Loveridge N, et al. Sclerostin is a delayed secreted product of osteocytes that inhibits bone formation[J]. FASEB J, 2005, 19(13):1842-1844.
[3] J?ger A, G?tz W, Lossd?rfer S, et al. Localization of SOST/sclerostin in cementocytes in vivo and in mineralizing periodontal ligament cells in vitro[J]. J Periodont Res, 2010, 45(2):246-254.
[4] Sawada T, Ishikawa T, Shintani S, et al. Ultrastructural immunolocalization of dentin matrix protein 1 on sharpey’s fibers in monkey tooth cementum[J]. Biotech Histochem, 2012, 87(5):360-365.
[5] Naka T, Yokose S. Spatiotemporal expression of sclerostin in odontoblasts during embryonic mouse tooth morphogenesis[J]. J Endod, 2011, 37(3):340-345.
[6] Lehnen SD, G?tz W, Baxmann M, et al. Immunohistochemical evidence for sclerostin during cementogenesis in mice[J]. Ann Anat, 2012, 194(5):415-421.
[7] Bao Xingfu, Liu Yuyan, Han Guanghong, et al. The effect on proliferation and differentiation of cementoblast by using sclerostin as inhibitor[J]. IJMS, 2013, 14(10):21140-21152.
[8] Kuchler U, Schwarze UY, Dobsak T, et al. Dental and periodontal phenotype in sclerostin knockout mice[J]. Int J Oral Sci, 2014, 6(2):70-76.
[9] Bosshardt DD. Are cementoblasts a subpopulation of osteoblasts or a unique phenotype[J]. J Dent Res, 2005, 84(5):390-406.
[10] Foster BL, Popowics TE, Fong HK, et al. Advances in defining regulators of cementum development and periodontal regeneration[J]. Curr Top Dev Biol, 2007, 78:47-126.
[11] van Bezooijen RL, Bronckers AL, Gortzak RA, et al. Sclerostin in mineralized matrices and van Buchem disease[J]. J Dent Res, 2009, 88(6):569-574.
[12] Bonewald LF. The amazing osteocyte[J]. J Bone Miner Res, 2011, 26(2):229-238.
[13] Fujii Y, Hoshino T, Kumon H. Molecular simulation analysis of the structure complex of C2 domains of DKK family members and β-propeller domains of LRP5/6: explaining why DKK3 does not bind to LRP5/6[J]. Acta Med Okayama, 2014, 68(2):63-78.
[14] Miao CG, Yang YY, He X, et al. Wnt signaling in liver fibrosis: progress, challenges and potential directions[J]. Biochimie, 2013, 95(12):2326-2335.
[15] McGee-Lawrence ME, Ryan ZC, Carpio LR, et al. Sclerostin deficient mice rapidly heal bone defects by activating β-catenin and increasing intramembranous ossification[J]. Biochem Biophys Res Commun, 2013, 441(4):886-890.
[16] Ellies DL, Economou A, Viviano B, et al. Wise regulates bone deposition through genetic interactions with Lrp5[J]. PloS one. 2014, 9(5):e96257.
[17] Zhang R, Yang G, Wu X, et al. Disruption of Wnt/β-catenin signaling in odontoblasts and cementoblasts arrests tooth root development in postnatal mouse teeth[J]. Int J Biol Sci, 2013, 9(3):228-236.
[18] Kim TH, Bae CH, Jang EH, et al. Col1a1-cre mediated activation of β-catenin leads to aberrant dentoalveolar complex formation[J]. Anat Cell Biol, 2012, 45(3):193-202.
[19] Kim TH, Lee JY, Baek JA, et al. Constitutive stabilization of ?-catenin in the dental mesenchyme leads to excessive dentin and cementum formation [J]. Biochem Biophys Res Commun, 2011, 412(4):549-555.
[20] 郑桂婷, 徐燕. WNT/β-连环蛋白信号转导通路在牙周组织再生中的作用[J]. 国际口腔医学杂志, 2013, 40(6):773-777.
Zheng GT, Xu Y. Effects of the wnt/β-catenin signal transduction pathway on periodontal tissue regeneration[J]. Int J Stomatol, 2013, 40(6):773-777.
[21] Du Y, Ling J, Wei X, et al. Wnt/β-catenin signaling participates in cementoblast/osteoblast differentiation of dental follicle cells[J]. Connect Tissue Res, 2012, 53(5):390-397.
[22] Silvério KG, Davidson KC, James RG, et al. Wnt/β-catenin pathway regulates bone morphogenetic protein (BMP2)-mediated differentiation of dental follicle cells[J]. J Periodont Res, 2012, 47(3):309-319.
[23] Nemoto E, Koshikawa Y, Kanaya S, et al. Wnt signaling inhibits cementoblast differentiation and promotes proliferation[J]. Bone, 2009, 44(5):805-812.
[24] Han P, Ivanovski S, Crawford R, et al. Activation of the canonical Wnt signaling pathway induces cementum regeneration[J]. J Bone Miner Res, 2015, 30(7):1160-1174.
[25] Sevetson B, Taylor S, Pan Y. Cbfa1/RUNX2 directs specific expression of the sclerosteosis gene (SOST)[J]. J Biol Chem, 2004, 279(14):13849-13858.
[26] Yang F, Tang W, So S, et al. Sclerostin is a direct target of osteoblast-specific transcription factor osterix[J]. Biochem Biophys Res Commun, 2010, 400(4):684-688.
[27] Fatherazi S, Matsa-Dunn D, Foster BL, et al. Phosphate regulates osteopontin gene transcription [J]. J Dent Res, 2009, 88(1):39-44.
[28] Rutherford RB, Foster BL, Bammler T, et al. Extracellular phosphate alters cementoblast gene expression[J]. J Dent Res, 2006, 85(6):505-509.
[29] Kogawa M, Wijenayaka AR, Ormsby RT, et al. Sclerostin regulates release of bone mineral by osteocytes by induction of carbonic anhydrase 2[J]. J Bone Miner Res, 2013, 28(12):2436-2448.
[30] Ryan ZC, Craig TA, Salisbury JL, et al. Enhanced prostacyclin formation and Wnt signaling in sclerostin deficient osteocytes and bone[J]. Biochem Biophys Res Commun, 2014, 448(1):83-88.
[31] Li F, Song N, Tombran-Tink J, et al. Pigment epithelium derived factor suppresses expression of Sost/Sclerostin by osteocytes: implication for its role in bone matrix mineralization[J]. J Cell Physiol, 2015, 230(6):1243-1249.
(本文采编 王晴)
[1] 郝福,孙睿. 头颈部鳞状细胞癌第二原发癌的研究进展[J]. 国际口腔医学杂志, 2019, 46(5): 585-592.
[2] 许彩薇,薛毅,吴仲寅. 骨硬化蛋白与牙周炎相关性的研究进展[J]. 国际口腔医学杂志, 2018, 45(6): 703-709.
[3] 谢成佳, 葛少华. 牙骨质撕裂的诊治进展[J]. 国际口腔医学杂志, 2017, 44(3): 315-319.
[4] 陈杰 郭维华 田卫东. 牙囊和上皮根鞘细胞成无细胞牙骨质的机制[J]. 国际口腔医学杂志, 2014, 41(3): 314-319.
[5] 欧伟1 孙卫斌2. 牙骨质蛋白1的生物学作用及应用前景[J]. 国际口腔医学杂志, 2014, 41(2): 209-212.
[6] 郑桂婷 徐燕. WNT/β-连环蛋白信号转导通路在牙周组织再生中的作用[J]. 国际口腔医学杂志, 2013, 40(6): 773-777.
[7] 刘勇 杨荣涛综述 李祖兵审校. 梅克尔软骨消亡的分子机制研究进展[J]. 国际口腔医学杂志, 2012, 39(3): 339-341.
[8] 林婷婷综述 陆尔奕审校. 骨硬化蛋白在骨组织改建中作用的分子机制[J]. 国际口腔医学杂志, 2012, 39(2): 269-272.
[9] 吴卫锋综述 郭淑娟 吴亚菲审校. 成牙骨质细胞的研究进展[J]. 国际口腔医学杂志, 2011, 38(1): 95-97.
[10] 杨力综述 蔡萍审校. 成牙骨质细胞培养方法的研究进展[J]. 国际口腔医学杂志, 2010, 37(01): 68-68~70.
[11] 王智, 靳淑梅综述 张君审校. 牙根吸收的原因与机制[J]. 国际口腔医学杂志, 2010, 37(01): 101-101~105.
[12] 席巧玲综述 陈智,张露审校. 牙周上皮剩余的研究进展[J]. 国际口腔医学杂志, 2009, 36(2): 205-205~207,210.
[13] 冯帆,汤炜,田卫东,. 牙周组织再生的调控机制[J]. 国际口腔医学杂志, 2008, 35(S1): -.
[14] 卢嘉静综述 葛振林审校. 正畸致牙根吸收的分子生物学研究进展[J]. 国际口腔医学杂志, 2008, 35(5): 599-599~601.
[15] 陆史俊综述 魏昕审校. 变异链球菌耐酸分子机制的研究进展[J]. 国际口腔医学杂志, 2008, 35(5): 534-534~536.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed   
[1] 张新春. 桩冠修复与无髓牙的保护[J]. 国际口腔医学杂志, 1999, 26(06): .
[2] 王昆润. 长期单侧鼻呼吸对头颅发育有不利影响[J]. 国际口腔医学杂志, 1999, 26(05): .
[3] 彭国光. 颈淋巴清扫术中颈交感神经干的解剖变异[J]. 国际口腔医学杂志, 1999, 26(05): .
[4] 杨凯. 淋巴化疗的药物运载系统及其应用现状[J]. 国际口腔医学杂志, 1999, 26(05): .
[5] 康非吾. 种植义齿下部结构生物力学研究进展[J]. 国际口腔医学杂志, 1999, 26(05): .
[6] 柴枫. 可摘局部义齿用Co-Cr合金的激光焊接[J]. 国际口腔医学杂志, 1999, 26(04): .
[7] 孟姝,吴亚菲,杨禾. 伴放线放线杆菌产生的细胞致死膨胀毒素及其与牙周病的关系[J]. 国际口腔医学杂志, 2005, 32(06): 458 -460 .
[8] 费晓露,丁一,徐屹. 牙周可疑致病菌对口腔黏膜上皮的粘附和侵入[J]. 国际口腔医学杂志, 2005, 32(06): 452 -454 .
[9] 庞莉苹,姚江武. 抛光和上釉对陶瓷表面粗糙度、挠曲强度及磨损性能的影响[J]. 国际口腔医学杂志, 2008, 35(S1): .
[10] 李子夏,包广洁. 龋病病因相关因素的激光扫描共聚焦显微镜研究[J]. 国际口腔医学杂志, 2008, 35(S1): .