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山东大学学报（医学版） ›› 2015, Vol. 53 ›› Issue (3): 32-35.doi: 10.6040/j.issn.1671-7554.0.2014.590

• 基础医学 • 上一篇    下一篇

甲状旁腺激素对大鼠牵张成骨过程中ONC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因表达的影响

杜腾飞1, 刘国明2, 郭小美3, Ching-Chang Ko3, 商红国2   

  1. 1. 潍坊医学院口腔系, 山东 潍坊 261053;
    2. 山东大学附属千佛山医院口腔科, 山东 济南 250014;
    3. 北卡罗莱纳大学口腔学院正畸科, 美国 北卡罗莱纳 27599-7454
  • 收稿日期:2014-09-08 修回日期:2015-01-22 出版日期:2015-03-10 发布日期:2015-03-10
  • 通讯作者: 商红国, E-mail:shanghongguo@163.com E-mail:shanghongguo@163.com
  • 基金资助:
    山东省自然科学基金(ZR2011HL022)

Effects of PTH on gene ONC, OPN, C-FOS, COL1, VEGF, RUNX2 and ALP during the distraction osteogenesis in rat mandible

DU Tengfei1, LIU Guoming2, GUO Xiaomei3, Ching-Chang Ko3, SHANG Hongguo2   

  1. 1. Department of Stomtology, Weifang Medical University, Weifang 261053, Shandong, China;
    2. Department of Stomtology, Qianfoshan Hospital Affiliated to Shandong University, Jinan 250014, Shandong, China;
    3. Department of Orthodontics, University of North Carolina, Chapel Hill, 27599-7454 North Carolina, USA
  • Received:2014-09-08 Revised:2015-01-22 Online:2015-03-10 Published:2015-03-10

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摘要： 目的 探讨甲状旁腺激素(PTH)对大鼠牵张成骨(DO)过程中ONC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因表达的影响。方法 30只雄性大鼠制备大鼠下颌骨DO模型。随机分5组, 每组6只。第1组(只有牵张无PTH), 术后8周取材, 应用HE染色及微CT检测, 以确定成骨情况。第2组(有牵张无PTH), 第3组(有牵张有PTH),第4组(无牵张有PTH), 第5组(对照组:无牵张无PTH)。2、3、4组及对照组术后1周取材, RT-PCR测定ONC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因的表达。结果 第1组, 新骨形成, 骨质充满牵张区, 骨质连续, 大鼠建模成功。RT-PCR检测结果显示, 2、3、4组与对照组比较, OPN、COL1、RUNX2、ALP基因表达有明显提高(P<0.05), 其中第3组最为明显。ONC、C-FOS、VEGF基因2、3、4组与对照组比较差异无统计学意义(P>0.05)。结论 PTH在DO过程中, 间歇性给以PTH的作用只有在牵张期发挥作用, 其对OPN、COL1、RUNX2、ALP 基因表达能够获得理想的协同作用。

关键词: 牵张成骨, 下颌骨, 大鼠, 甲状旁腺激素

Abstract: Objective To explore the effects of parathyroid hormone (PTH) on gene ONC, OPN, C-FOS, COL1, VEGF, RUNX2 and ALP during the distraction osteogenesis (DO) in rat mandible. Methods A total of 30 DO models were established with male rats, which were then randomly divided into 5 groups, with 6 animals in each group. Group 1(DO, no PTH) was harvested 8 weeks after surgery, and the tissues were tested using HE and micro-CT. Group 2 (DO, no PTH), Group 3(DO, PTH), Group 4 (no DO, PTH), Group 5 (control Group, no DO, no PTH) were harvested 1 week after surgery, and Real-time PCR was used to quantify the genes:ONC, OPN, C-FOS, COL1, VEGF, RUNX2 and ALP. Results In Group 1, histological test and micro-CT showed new bone formation in the gap. In Groups 2, 3 and 4, especially in Group 3, RT-PCR test showed that compared with the control group, OPN, COL1, RUNX2 and ALP genes were significantly increased (P<0.05), while ONC , C-FOS, and VEGF genes were not significantly different (P>0.05). Conclusion Intermittent administration of PTH increases bone formation only in the distraction period. PTH has synergetic effect on gene expressions of OPN, COL1, RUNX2 and ALP.

Key words: Mandible, Distraction osteogenesis, Rats, Parathyroid hormone

中图分类号: 

  • R782.2+3
[1] Winters R, Tatum SA. Craniofacial distraction osteogenesis[J]. Facial Plast Surg Clin North Am, 2014, 22(4):653-664.
[2] Papakostidis C, Bhandari M, Giannoudis M, et al. Distraction osteogenesis in the treatment of long bone defects of the lower limbs:effectiveness, complications and clinical results:a systematic review and meta-analysis[J]. Bone Joint J, 2013, 95-B(12):1673-1680.
[3] Pereira MA, Luiz de Freitas PH, da Rsosa TF, et al. Understanding distraction osteogenesis on the maxillofacial complex:a literature review[J]. J Oral Marcillafac Surg, 2007, 65(12):2518-2523.
[4] Ai-Aql ZS, Alagl AS, Graves DT, et al. Molecular mechanisms Controlling bone formation during fracture healing and distraction osteogeresis[J]. J Dent Res, 2008, 87(2):107-118.
[5] Yu JC, Fearon J, Havlik RJ, et al. Distraction osteogenesis of the craniofacial skeleton[J]. Plast Reconstr Surg, 2004, 114(1):1E-20E.
[6] Seebach C, Skripitz R, Andreassen TT, et al. Intermittent parathyroid hormone(1-34) enhances mechanical strength and density of new bone after distraction osteogenesis in rats[J]. J Orthop Res, 2004, 22(3):472-478.
[7] Hamann KL, lane NE. Parathyroid hormone update[J]. Rheum Dis Clin North Am, 2006, 32(4):703-719.
[8] John HC, Meyer MB, Benkusky NA, et al. The parathyroid hormone-regulated transcriptome in osteocytes:parallel actions with 1,25-Dihydroxyvitamin D3 to Oppose Gene Expression changes during differentiation and to promote mature cell function[J]. Bone, 2014 Nov 22. pii:S8756-3282(14)00418-9. doi:10.1016/j.bone.2014.11.010.
[9] 胡兆兴, 王维东, 范军届, 等. 内源性甲状旁腺激素促进小鼠骨折愈合[J]. 南京医科大学学报:自然科学版, 2014, 34(4):457-461. HU Zhaoxing, WANG Weidong, FAN Junjie, et al. Endogenous parathyroid hormone promotes fracture healing in mice[J]. Acta Univ Med Nanjing:Natural Science, 2014, 34(4):457-461.
[10] Ali MN, Kobayashi T, Tanaka M, et al. Effects of intermittent parathyroid hormone treatment on new bone formation during distraction osteogenesis in the rat mandible[J]. Oral Surg Oral Med Oral Pathol Oral Radiol, 2012, 114(1):e36-42.
[11] Barnes GL, Kakar S, Vora S, et al. Stimulation of fracture-healing with systemic intermittent parathyroid hormone treatment[J]. J Bone Joint Surg Am, 2008, 90 Suppl 1:120-127.
[12] Kaback LA, Soung do Y, Naik A, et al. Teriparatide(1-34 human PTH) regulation of osterix during fracture repair[J]. J Cell Biochem, 2008, 105(1):219-226.
[13] Bouletreau PJ, Warren SM, Longaker MT. The molecular biology of distraction osteogenesis[J]. J Craniomaxillofac Surg, 2002, 30(1):1-11.
[14] 何昇, 胡静, 宋健, 等. 间歇性低剂量全身应用甲状旁腺激素对兔下颌快速骨牵张的作用[J]. 口腔医学, 2014, 34(2):102-106. HE Sheng, HU Jing, SONG Jian, et al. The effects of PTH administration on rapid mandibular distraction osteogenesis in rabbits[J]. Stomatology, 2014, 34(2):102-106.
[15] Aleksyniene R, Thomsen JS, Eckardt H, et al. Parathyroid hormone PTH(1-34) increases the volume, mineral content, and mechanical properties of regenerated mineralizing tissue after distraction osteogenesis in rabbits[J]. Acta orthop, 2009, 80(6):716, 723.
[16] Koh AJ, Demiralp B, Neiva KG, et al. Cells of the osteoclast lineage as mediators of the anabolic actions of parathyroid hormone in bone[J].Endocrinology, 2005, 146(11):4584-4596.
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