中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (20): 3636-3640.doi: 10.3969/j.issn.1673-8225.2011.20.007

• 软骨组织构建 cartilage tissue construction • 上一篇    下一篇

基质金属蛋白酶和胶原在创伤关节软骨组织中的表达

杨  军，娄德全，周振东，张钦明   

  1. 中国医科大学附属盛京医院脊柱创伤骨科，辽宁省沈阳市 110004
  • 收稿日期:2010-11-24 修回日期:2011-01-29 出版日期:2011-05-14 发布日期:2011-05-14
  • 通讯作者: 杨军，中国医科大学附属盛京医院脊柱创伤骨科，辽宁省沈阳市 110004 yangj1@sj-hospital.org
  • 作者简介:杨军☆，男，1962年生，山东省招远县人，汉族，1985年中国医科大学毕业，博士，副教授，主要从是创伤骨科方面的研究。
  • 基金资助:

    辽宁省教育厅课题基金资助项目(L2010652)。

Expressions of matrix metalloproteinase and collagen in articular cartilages after trauma

Yang Jun, Lou De-quan, Zhou Zhen-dong, Zhang Qin-ming   

  1. Department of Orthopaedics, Shengjing Hospital of China Medical University, Shenyang  110004, Liaoning Province, China
  • Received:2010-11-24 Revised:2011-01-29 Online:2011-05-14 Published:2011-05-14
  • Contact: Yang Jun , Department of Orthopaedics, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning Province, China yangj1@sj-hospital. org
  • About author:Yang Jun☆, Doctor, Associate professor, Department of Orthopaedics, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning Province, China yangj1@sj-hospital. org
  • Supported by:

    the Foundation of Education Department of Liaoning Province, No. L2010652*

PDF

370

被引次数

21

摘要：

背景：研究发现，基质金属蛋白酶和胶原参与关节软骨组织机体生理重建及病理破坏。
目的：观察膝关节骨软骨缺损及表面软骨缺损动物模型关节软骨组织中胶原及基质金属蛋白酶的表达变化。
方法：雌性SD大鼠48只随机分为3组：骨软骨缺损组在双膝关节制作骨软骨缺损模型，表面缺损组在双膝关节制作表面软骨缺损，对照组双膝关节制作关节囊切开。分别于术后4、8、12周取股骨髁标本，行苏木精-伊红染色，免疫组化检测Ⅰ型胶原、Ⅱ型胶原、基质金属蛋白酶3的表达。
结果与结论：骨软骨缺损组术后4周缺损中有少量新生组织生成，8及12周可见到纤维组织填充，修复组织细胞外基质Ⅰ型胶原免疫组化染色阳性，Ⅱ型胶原免疫组化染色阴性，关节软骨组织中基质金属蛋白酶3表达增高。表面缺损组表面软骨缺损4及8周未见修复迹象，12周可见微量纤维组织填充，细胞外基质Ⅰ型胶原免疫组化染色阳性，Ⅱ型胶原免疫组化染色阴性，术后表面缺损组关节软骨组织基质金属蛋白酶3表达增高。对照组关节软骨组织Ⅰ型胶原免疫组化染色阴性，Ⅱ型胶原免疫组化染色阳性，基质金属蛋白酶3低表达，无形态学异常改变。说明机械性损伤可以导致关节软骨细胞外基质成分发生改变，丧失其原有的生物学特性而退变，基质金属蛋白酶3在损伤后的软骨组织中表达增高，使细胞外基质的降解增加，是导致关节软骨退变的重要因素。

关键词: 基质金属蛋白酶, 胶原, 关节软骨退变, 关节软骨缺损, 骨关节炎

Abstract:

BACKGROUND: Previously studies demonstrated that matrix metalloproteinase (MMP) and collagen participate in physiological restitution and pathological damage of articular cartilages.
OBJECTIVE: To explore the expressions of MMP and collagen in cartilage tissues in knee articular cartilages defects and surface defects models.
METHODS: Forty-eight SD female rats were used in this experiment. These rats were randomly divided into three groups. Group A (full-thickness defect group): a full-thickness cylindrical osteochondral defect was created in both condyles of femur. Group B (surface cartilage defect group): several partial-thickness articular cartilage defects in both condyles of femur. Group C (control group) was the opposite as shum-perative control. The rats were sacrificed at 4, 8, and 12 weeks. The expressions of collagen Ⅰ, collagen Ⅱ, and MMP-3 in each group were evaluated by hematoxylin-eosin staining and immunohistochemical analyses.
RESULTS AND CONCLUSION: In group A, a small amount of new organization generated at 4 weeks after operation; the defects were filled with fibrous tissues at 8 and 12 weeks after operation; Type Ⅰ collagen was positive expressed, type Ⅱ collagen negative expressed and MMP-3 expression increased. In group B, no signs of repair were found at 4 and 8 weeks after operation; the defects were filled with small volume of fibrous tissues, in which type Ⅰ collagen was positive while type Ⅱ collagen was negative; MMP-3 expression were increased. In group C, the articular cartilages were normal, type Ⅰ collagen was negative, type Ⅱ collagen was positive, and MMP-3 expression was low expressed; no morphological abnormal change could be seen. Mechanical injury can make articular cartilage extracellular matrix composition changed and loss of their original biological characteristics. MMP-3 expression in injured cartilage tissues is increased that leads to high matrix degradation. Thus, MMP-3 is an important factor for articular cartilage degeneration.

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