肌成纤维细胞与颌骨放射性骨坏死

中国口腔颌面外科杂志 ›› 2014, Vol. 12 ›› Issue (4): 368-372.

肌成纤维细胞与颌骨放射性骨坏死

代天国, 何悦

上海交通大学医学院附属第九人民医院·
口腔医学院口腔颌面-头颈肿瘤科, 上海市口腔医学重点实验室,上海 200011

收稿日期:2013-08-13 出版日期:2014-07-10 发布日期:2014-08-20
通讯作者: 何悦,Tel:021-23271699-5395,E-mail:william5218 @126.com
作者简介:代天国（1987-）,男,在读硕士研究生,E-mail:paradisedai @163.com
基金资助:
国家自然科学基金（81271112,30973341）; 上海市教育委员会“曙光计划”（10SG19）

Myofibroblasts and osteoradionecrosis of jaw

DAI Tian-guo, HE Yue

Department of Oromaxillofacial Head and Neck Oncology, Ninth People’s Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine; Shanghai Key Laboratory of Stomatology. Shanghai 200011, China

Received:2013-08-13 Online:2014-07-10 Published:2014-08-20
Supported by:
Supported by National Natural Science Foundation of China (81271112, 30973341) and Dawn Plan of Shanghai Municipal Education Commission (10SG19)

摘要/Abstract

关键词: 颌骨放射性骨坏死, 肌成纤维细胞, 成纤维细胞, 放射诱导纤维萎缩

Abstract: Summary ORNJ is a most severely complication of radiation therapy for head and neck cancer. Up to now, the precise pathogenesis of ORNJ has not been fully clarified, the newest one is radiation-induced fibrosis. It is believed that the hard and soft tissue of radiation area formed lots of pathologic fibrosis tissue through a series of changes after irradiation; subsequently, the pathological fibrous tissue disintegration caused ORNJ. Myofibroblasts play an important role in the fibrosis of liver, lung, kidney and scleroderma, whether it also plays an equally important role in ORNJ has yet to be confirmed. This paper mainly demonstrated the simple pathogenesis of ORNJ, the characteristics of the myofibroblasts, relationship and distinction between myofibroblasts and fibroblasts, and myofibroblasts and ORNJ.

Key words: Osteoradionecrosis, Myofibroblasts, Fibroblasts, Radiation-induced fibro-atrophic process

中图分类号:

R739.8

代天国, 何悦. 肌成纤维细胞与颌骨放射性骨坏死[J]. 中国口腔颌面外科杂志, 2014, 12(4): 368-372.

DAI Tian-guo, HE Yue. Myofibroblasts and osteoradionecrosis of jaw[J]. China J Oral Maxillofac Surg, 2014, 12(4): 368-372.

参考文献

[1] Sciubba JJ, Goldenberg D. Oral complications of radiotherapy [J]. Lancet Oncol, 2006, 7 (2):175-183.
[2] Lyonsa A, Ghazalib N. Osteoradionecrosis of the jaws: current understanding of its pathophysiology and treatment [J]. Br J Oral Maxillofac Surg, 2008, 46(8): 653-660.
[3] Chrcanovic BR, Reher P, Sousa AA, et al. Osteoradionecrosis of the jaws-a current overview-part1: physiopathology and risk and predisposing factors [J]. J Oral Maxillofac Surg, 2010, 14(1): 3-16.
[4] Meyer I. Infectious diseases of the jaws[J]. J Oral Surg,1970,28(1): 17-26.
[5] Marx RE. Osteoradionecrosis: a new concept of its pathophyrsiology[J]. J Oral Maxillofac Surg,1983, 41(5): 283-288.
[6] Rudolph R, Tripuraneni P, Koziol JA, et al. Normal transcutaneous oxygen pressure in skin after radiation therapy for cancer [J]. Cancer, 1994, 74(11): 3063-3070.
[7] Annane D, Depondt J, Aubert P, et al. Hyperbaric oxygen therapy for radionecrosis of the jaw: a randomized, placebo-controlled double-blind trial from the ORN96 study group [J]. J Clin Onco, 2004, 22(24): 4893-4900.
[8] Delanian S, Lefaix JL. The radiation-induced fibroatropic process: therapeutic perspective via the antioxidant pathway [J]. Radiother Oncol, 2004, 73(2): 119-131.
[9] Vandekerckhove J, Weber K. At least six different actins are expressed in a higher mammal: an analysis base on the amino acid sequence of the amino-terminal tryptic peptide [J]. J Mol Biol, 1987, 126(4): 783-802.
[10] Wynn TA. Cellular and molecular mechanisms of fibrosis [J]. J Pathol, 2008, 214(2): 199-210.
[11] Watsky MA, Weber KT, Sun Y, et al. New insights into the mechanism of fibroblast to myofibroblast transformation and associated pathologies [J]. Int Rev Cell Mol Biol, 2010, 282: 165-192.
[12] Kis K, Liu X, Hagood JS. Myofibroblast differentiation and survival in fibrotic disease[J]. Expert Rev Mol Med,2011,13: e27.
[13] Lee CH, Shah B, Moioli EK, et al. CTGF directs fibroblast differentiation from human mesenchymal stem/stromal cell and defines connective tissue healing in a rodent injury moddl [J]. J Clin Invest, 2010, 120(9): 3340-3349.
[14] Hinz B, Phan SH, Thannickal VJ, et al. The myofibroblast: one function, multiple origins [J]. Am J Pathol, 2007, 170(6): 1807-1816.
[15] Horowitz JC, Rogers DS, Sharma V, et al. Combinatorial activation of FAK and AKT by transforming growth factor-β1 confers an anoikis resistant phenotype to myofibroblasts [J]. Cell Signal, 2007, 19(4): 761-771.
[16] Yin Z, Watsky MA. Chloride channel activity in human lung fibroblasts and myofibroblasts [J]. Am J Physiol Lung Cell Mol Physiol, 2005, 288(6): L1110-L1116.
[17] Cho HJ, Yoo J. Rho activation is required for transforming growth factor-β-induced epithelial-mesenchymal transition in lens epithelial cells [J]. Cell Biol Int, 2007, 31(10): 1225-1230.
[18] Moustakas A, Souchelnytskyi S, Heldin CH. Smad regulation in TGF-β signal transduction [J]. J Cell Sci, 2001, 114(Pt 24): 4359-4369.
[19] Nakao A, Afrakhte M, Morén A, et al. Identification of Smad7, a TGF-beta inducible antagonist of TGF-beta signaling [J]. Nature, 1997, 389(6651): 631-635.
[20] Sobral LM, Montan PF, Zecchin KG, et al. Smad7 blocks transforming growth factor-betal-induced gingival fibroblast-myofibroblast transition via inhibitory regulation of Smad2 and connective tissue growth factor [J]. J Periodontol, 2011, 82(4): 642-651.
[21] Marx RE, Tursun R. Suppurative osteomyelitis, bisphosphonate induced osteonecrosis, osteoradionecrosis: a blinded histopathologic comparison and its implications for the mechanism of each disease [J]. Int J Oral maxillofac Surg, 2012, 41(3): 283-289.
[22] Forbes SJ, Russo FP, Rey V, et al. A significant proportion of fibroblasts are of bone marrow origin in human liver fibrosis [J]. Gastroenterology, 2004, 126(4): 955-963.
[23] Zhuang Q, Zhang Z, Fu H, et al. Does radiation-induced fibrosis have an important role in pathophysiology of the osteoradionecrosis of jaw? [J]. Med Hypotheses, 2011, 77(1): 63-65.
[24] Tian L, He LS, Soni B, et al. Myofibroblasts and their resistance to apoptosis: a possible mechanism of osteoradionecrosis [J]. Clin Cosmet Investig Dent, 2012, 4: 21-27.
[25] Zeisberg M, Kalluri R. The role of epithelial-to-mesenchymal transition in renal fibrosis [J]. J Mol Med (Berl), 2004, 82(3): 175-181.
[26] Piera-Velazquez S, Li Z, Jimenez SA. Role of endothelial- mesenchymal transition (End-MET) in the pathogenesis of fibrotic disorders [J]. Am J Pathol, 2011, 179(3): 1074-1080.
[27] Schrimpf C, Duffield JS. Mechanisms of fibrosis: the role of the pericyte [J]. Curr Opin Nephrol Hypertens, 2011, 20(3): 297-305.
[28] 付洪海, 周咏, 张志愿, 等. TGF-β1过表达介导的放疗诱导成纤维细胞向肌成纤维细胞分化的体外研究 [J]. 中国口腔颌面外科杂志, 2012, 10(4): 266-270.
[29] Gervaz P, Morel P, Vozenin-Brotons MC. Molecular aspects of intestinal radiation-induced fibrosis[J]. Curr Mol Med,2009,9(3): 273-280.
[30] Wallach-Dayan SB, Golan-Gerstl R, Breuer R. Evasion of myofibroblasts from immune surveillance: a mechanism for tissue fibrosis [J]. Proc Natl Acad Sci USA, 2007, 104(51): 20460-20465.
[31] Rishi L, Gahlot S, Kathania M, et al. Pentoxifylline induces apoptosis in vitro in cutaneous T cell lymphoma (HuT-78) and enhances FasL mediated killing killing by upregulating Fas expression [J]. Biochem Pharmacol, 2009, 77(1): 30-45.
[32] Delanian S, Lefaix JL. Complete healing of severe osteoradionecrosis with treatment combining pentoxifylline, tocopherol and clodronate [J]. Br J Radiol, 2002, 75(839): 467-469.
[33] Xu J, Zheng Z, Fang D, et al. Early-stage pathogenic sequence of jaw osteoradionecrosis in vivo [J]. J Dent Res, 2012, 91(7): 702-708.
[34] Anan A, Baskin-Bey ES, Bronk SF, et al. Proteasome inhibition induces hepatic stellate cell apoptosis [J]. Hepatology, 2006, 43(2): 335-344.
[35] Garneau-Tsodikova S, Thannickal VJ. Protein kinase inhibitors in the treatment of pulmonary fibrosis [J]. Curr Med Chem, 2008, 15(25): 2632-2640.
[36] Wang Q, Wang Y, Hyde DM, et al. Reduction of bleomycin induced lung fibrosis by transforming growth factor β soluble receptor in hamsters [J]. Thorax, 1999, 54(9): 805-812.