中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (24): 4402-4407.doi: 10.3969/j.issn.1673-8225.2012.24.007

• 骨组织构建 bone tissue construction • 上一篇    下一篇

骨保护素基因敲除小鼠腰椎间盘退变与腰椎骨质疏松

郝晓东，王善金，蒋雷生，蒋盛旦，郭 震，戴力扬   

  1. 上海交通大学医学院附属新华医院骨科，上海市 200092
  • 收稿日期:2012-02-08 修回日期:2012-03-23 出版日期:2012-06-10 发布日期:2013-11-05
  • 通讯作者: 戴力扬，主任医师，教授，博士生导师，上海交通大学医学院附属新华医院骨科，上海市 200092
  • 作者简介:郝晓东★，男，1984年生，内蒙古呼和浩特市人，汉族，上海交通大学医学院附属新华医院骨科在读硕士，主要从事脊柱外科基础与临床的研究。 hdd80@163.com
  • 基金资助:

    国家自然科学基金项目(U1032001)，课题名称：骨质疏松性椎体结构及功能异常的机制与脊柱退变的功能重建研究；国家自然科学基金项目(81171757)，课题名称：TGF-β/Smad7信号通路在椎间盘退变病理过程中作用与机制研究

Relationship between lumbar intervertebral disc degeneration and vertebral osteoporosis in osteoprotegerin gene knock-out mice

Hao Xiao-dong, Wang Shan-jin, Jiang Lei-sheng, Jiang Sheng-dan, Guo Zhen, Dai Li-yang   

  1. Department of Orthopedics, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
  • Received:2012-02-08 Revised:2012-03-23 Online:2012-06-10 Published:2013-11-05
  • Contact: Dai Li-yang, Chief physician, Professor, Doctoral supervisor, Department of Orthopedics, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
  • About author:Hao Xiao-dong★, Studying for master’s degree, Department of Orthopedics, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China hdd80@163.com

PDF

436

被引次数

19

摘要：

背景：骨保护素基因敲除小鼠已被证明会表现出明显的骨质疏松及骨关节炎表型。
目的：观察骨保护素基因敲除小鼠随年龄增长腰椎间盘退变和骨质疏松的动态变化关系。
方法：分别取出生后4，8，12周的骨保护素基因敲除纯合子小鼠及正常对照组小鼠的L3椎体和L4/5椎间盘，运用Micro-CT检测L3椎体松质骨微结构指标；用苏木精-伊红染色法观察L4/5椎间盘形态学，测量椎间盘及软骨终板高度。
结果与结论：骨保护素基因敲除纯合子小鼠组L3椎体骨小梁数量、骨小梁厚度、骨体积分数较正常组均明显下降(P < 0.05)，而骨小梁分离度、结构模型指数较正常小鼠增高(P < 0.05)。8周及12周的骨保护素基因敲除纯合子小鼠的L4/5椎间盘软骨终板出现退变征象，软骨终板排列不规则，并有骨髓腔组织进入软骨终板及外层纤维环。提示骨保护素基因在维持椎间盘正常的结构和功能方面起到重要作用，骨保护素基因缺失后可导致椎间盘退变和椎体骨质疏松。

关键词: 骨保护素, 椎间盘退变, 骨质疏松, 基因敲除, 核因子κB受体活化因子配基

Abstract:

BACKGROUND: Osteoprotegerin gene knock-out (OPG-/-) mice have been shown to demonstrate significant osteoporosis and osteoarthritis phenotype.
OBJECTIVE: To observe the relationship between lumbar intervertebral disc degeneration and vertebral osteoporosis in OPG-/- mice with aging.
METHODS: The third lumbar vertebrae (L3) and the L4/5 lumbar intervertebral discs (L4/5) from 4-, 8-, 12-week-old mice were harvested. Bone micro-architecture of the L3 was evaluated using Micro-CT; L4/5 was stained using hematoxylin and eosin for routine morphologic examination to measure the height of intervertebral disc and cartilage endplate.
RESULTS AND CONCLUSION: Compared with the control group, the third lumbar vertebras in OPG-/- mice appeared with significantly drop in bone mass: trabecular number, trabecular thickness and bone volume fraction significantly declined compared with normal mice of the same age, with a statistical difference between them (P < 0.05); while trabecular separation/spacing, structure model index increased compared with control group, and there ws a statistical difference between them (P < 0.05). Hematoxylin-eosin staining exhibited degeneration of the intervertebral disc and cartilage endplate in OPG-/- mice: irregular arrangement of cartilage endplate was observed, and bone marrow cavity tissue was observed in the endplate cartilage and annulus fibrosis. OPG gene plays a very important role in maintaining the structure and function of the normal intervertebral disc, the deletion of OPG gene causes intervertebral disc degeneration and vertebra osteoporosis.

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