软骨ADAMTS-7基因上调与股骨头坏死发生之间的相关性研究
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摘要
目的探讨软骨解聚蛋白样金属蛋白酶-7(ADAMTS-7)基因上调与股骨头坏死发生之间的相关性。方法前瞻性选2017年4月至2018年5月121例股骨颈骨折患者,将70例股骨头坏死患者作为观察组,余单纯性股骨颈骨折无骨关节炎的患者作为对照组。取患者软骨标本,采用苏木精伊红染色和番红O染色观察患者软骨退化情况,Mankin评分观察软骨的降解情况,对比两组ADAMTS-7、肿瘤坏死因子-α(TNF-α)平均光密度表达、ADAMTS-7mRNA相对水平。结果苏木精伊红染色显示对照组患者细胞结构正常,只有较少软骨细胞坏死,软骨膜轻度异常,观察组患者软骨膜明显异常,软骨细胞坏死明显增多;番红O染色显示:对照组番红O染色正常,潮线完整,观察组染色明显退化,观察组Ⅳ期患者重度退化,潮线不完整。观察组Mankin评分明显高于对照组,观察组Ⅳ期Mankin评分也高于Ⅱ～Ⅲ期;观察组ADAMTS-7平均光密度、TNF-α平均光密度、ADAMTS-7 mRNA高于对照组,观察组Ⅳ期ADAMTS-7平均光密度、TNF-α平均光密度、ADAMTS-7 mRNA高于Ⅱ～Ⅲ期。结论软骨ADAMTS-7基因上调与股骨头坏死发生之间存在相关性,且ADAMTS-7参与了软骨退化的整个过程,在股骨头坏死的早期ADAMTS-7基因上调,股骨头坏死患者Ⅳ期时呈现高表达。
Objective To explore the correlation between the upregulation of cartilage ADAMTS-7 gene and the occurrence of femoral head necrosis. Methods From April 2017 to May 2018,121 patients with femoral neck fractures,70 patients with femoral head necrosis were selected as observation group,and patients with simple femoral neck fracture without osteoarthritis as control group. The cartilage specimens were taken. The cartilage degradation was observed by hematoxylin and eosin staining and Safranin O staining. The degradation of cartilage was observed by Mankin score. The expression of ADAMTS-7,TNF-α average optical density and ADAMTS-7 mRNA were compared. Results Eosin staining showed that the cell structure of the control group was normal,with less chondrocyte necrosis and mild abnormal cartilage. In the observation group,the perichondrium was abnormal,and the chondrocyte necrosis was significantly increased. The Safranin O staining showed that the control group had normal red staining and complete tidal line. The staining of the observation group was significantly degraded,and the patients in stage Ⅳ of the observation group were severely degenerated and the tidal line was incomplete. The Mankin score of the observation group was significantly higher than that of the control group. The Mankin score of the observation group was also higher than that of the Ⅱ to Ⅲ stage. The average optical density,average optical density of TNF-α and ADAMTS-7 mRNA of the ADAMTS-7 in the observation group were higher than those in the control group. The average optical density,TNF-α average optical density and ADAMTS-7 mRNA of group Ⅳ ADAMTS-7 were higher than those of stage Ⅱ～Ⅲ. Conclusion There is correlation between upregulation of cartilage ADAMTS-7 gene and occurrence of femoral head necrosis,Moreover,ADAMTS-7 is involved in the whole process of cartilage degeneration,and the ADAMTS-7 gene is up-regulated in the early stage of femoral head necrosis,and the femoral head necrosis is highly expressed in the Ⅳ stage.
Objective To explore the correlation between the upregulation of cartilage ADAMTS-7 gene and the occurrence of femoral head necrosis. Methods From April 2017 to May 2018,121 patients with femoral neck fractures,70 patients with femoral head necrosis were selected as observation group,and patients with simple femoral neck fracture without osteoarthritis as control group. The cartilage specimens were taken. The cartilage degradation was observed by hematoxylin and eosin staining and Safranin O staining. The degradation of cartilage was observed by Mankin score. The expression of ADAMTS-7,TNF-α average optical density and ADAMTS-7 mRNA were compared. Results Eosin staining showed that the cell structure of the control group was normal,with less chondrocyte necrosis and mild abnormal cartilage. In the observation group,the perichondrium was abnormal,and the chondrocyte necrosis was significantly increased. The Safranin O staining showed that the control group had normal red staining and complete tidal line. The staining of the observation group was significantly degraded,and the patients in stage Ⅳ of the observation group were severely degenerated and the tidal line was incomplete. The Mankin score of the observation group was significantly higher than that of the control group. The Mankin score of the observation group was also higher than that of the Ⅱ to Ⅲ stage. The average optical density,average optical density of TNF-α and ADAMTS-7 mRNA of the ADAMTS-7 in the observation group were higher than those in the control group. The average optical density,TNF-α average optical density and ADAMTS-7 mRNA of group Ⅳ ADAMTS-7 were higher than those of stage Ⅱ～Ⅲ. Conclusion There is correlation between upregulation of cartilage ADAMTS-7 gene and occurrence of femoral head necrosis,Moreover,ADAMTS-7 is involved in the whole process of cartilage degeneration,and the ADAMTS-7 gene is up-regulated in the early stage of femoral head necrosis,and the femoral head necrosis is highly expressed in the Ⅳ stage.
引文
[1]赖永洁.金属蛋白酶ADAMTS-7在软脚骨发育以及骨关节炎发病机制中的作用研究[D].济南:山东大学,2011:1-181.
[2]赵红星,黄媛霞,徐海斌,等.股骨头坏死早期大鼠股骨头骨组织中基质金属蛋白酶及其相关抑制剂的表达[J].西安交通大学学报(医学版),2017,38(2):231-234.
[3]王建忠,武永刚,王坤正.激素性股骨头坏死患者骨组织MMP-2、MMP-9、TIMP-1、TIMP-2蛋白的表达[J].中华关节外科杂志(电子版),2012,6(1):91-96.
[4]王佳斌,艾江平.糖皮质激素性股骨头坏死骨组织OPG、RANKL、MMP-1、MMP-2、TIMP的表达变化及意义[J].山东医药,2011,51(42):91-92.
[5]白晓卉.ADAMTS-7和ADAMTS-12抑制软骨分化的功能研究[D].济南:山东大学,2009:1-219.
[6]祁雷,姚运峰,李子煜,吴晗,荆珏华.大鼠骨关节炎模型的建立及软骨组织中MMP-13和ADAMTS-5的表达[J].局解手术学杂志,2018,27(3):157-163.
[7]中国医师协会骨科医师分会显微修复工作委员会,中国修复重建外科专业委员会骨缺损及骨坏死学组,中华医学会骨科分会显微修复学组.成人股骨头坏死临床诊疗指南(2016)[J].中华骨科杂志,2016,36(15):945-954.
[8]中华医学会骨科学分会关节外科学组.股骨头坏死临床诊疗规范[J].中国矫形外科杂志,2016,24(1):49-54.
[9]孙伟,李子荣.股骨头坏死的分期与分型[J].中国骨与关节杂志,2017,6(6):465-468.
[10]Moody HR,Heard BJ,Frank CB,et al.Investigating the potential value of individual parameters of histological grading systems in a sheep model of cartilage damage:the Modified Mankin method[J].J Anat,2012,221(1):47-54.
[11]尹思,张长青.股骨头坏死与基因遗传多态性[J].国际骨科学杂志,2010,31(3):178-180,189.
[12]张璐,于芳,王利,等.新型金属蛋白酶ADAMTS-7促进体内和体外血管平滑肌细胞增殖[J].中国科学:生命科学,2015,45(4):381-388.
[13]姜棚菲,马张稳,张民泽,等.腰椎间盘退行性改变患者ADAMTS-7表达及其机制研究[J].实用医院临床杂志,2017,14(6):101-104.
[14]张璐,于芳,王利,等.新型金属蛋白酶ADAMTS-7促进体内和体外血管平滑肌细胞增殖[J].中国科学:生命科学,2015,45(4):381-388.
[15]赵程锦,周煜虎,王坤正.软骨ADAMTS-7基因上调与股骨头坏死发生之间的相关性研究[J].中国骨质疏松杂志,2017,23(6):727-733.
[16]Yu H,Zhu Y.Expression of ADAMTS-7 and ADAMTS-12 in the nucleus pulposus during degeneration of rat caudal intervetebral disc[J].J Vet Med Sci,2012,74(1):9-15.
[17]周惠琼,张奉春,Rob K will.肿瘤坏死因子-α和白细胞介素-1β对人骨关节炎软骨细胞蛋白聚糖代谢的影响[J].中华风湿病学杂志,2008,12(2):83-87.
[2]赵红星,黄媛霞,徐海斌,等.股骨头坏死早期大鼠股骨头骨组织中基质金属蛋白酶及其相关抑制剂的表达[J].西安交通大学学报(医学版),2017,38(2):231-234.
[3]王建忠,武永刚,王坤正.激素性股骨头坏死患者骨组织MMP-2、MMP-9、TIMP-1、TIMP-2蛋白的表达[J].中华关节外科杂志(电子版),2012,6(1):91-96.
[4]王佳斌,艾江平.糖皮质激素性股骨头坏死骨组织OPG、RANKL、MMP-1、MMP-2、TIMP的表达变化及意义[J].山东医药,2011,51(42):91-92.
[5]白晓卉.ADAMTS-7和ADAMTS-12抑制软骨分化的功能研究[D].济南:山东大学,2009:1-219.
[6]祁雷,姚运峰,李子煜,吴晗,荆珏华.大鼠骨关节炎模型的建立及软骨组织中MMP-13和ADAMTS-5的表达[J].局解手术学杂志,2018,27(3):157-163.
[7]中国医师协会骨科医师分会显微修复工作委员会,中国修复重建外科专业委员会骨缺损及骨坏死学组,中华医学会骨科分会显微修复学组.成人股骨头坏死临床诊疗指南(2016)[J].中华骨科杂志,2016,36(15):945-954.
[8]中华医学会骨科学分会关节外科学组.股骨头坏死临床诊疗规范[J].中国矫形外科杂志,2016,24(1):49-54.
[9]孙伟,李子荣.股骨头坏死的分期与分型[J].中国骨与关节杂志,2017,6(6):465-468.
[10]Moody HR,Heard BJ,Frank CB,et al.Investigating the potential value of individual parameters of histological grading systems in a sheep model of cartilage damage:the Modified Mankin method[J].J Anat,2012,221(1):47-54.
[11]尹思,张长青.股骨头坏死与基因遗传多态性[J].国际骨科学杂志,2010,31(3):178-180,189.
[12]张璐,于芳,王利,等.新型金属蛋白酶ADAMTS-7促进体内和体外血管平滑肌细胞增殖[J].中国科学:生命科学,2015,45(4):381-388.
[13]姜棚菲,马张稳,张民泽,等.腰椎间盘退行性改变患者ADAMTS-7表达及其机制研究[J].实用医院临床杂志,2017,14(6):101-104.
[14]张璐,于芳,王利,等.新型金属蛋白酶ADAMTS-7促进体内和体外血管平滑肌细胞增殖[J].中国科学:生命科学,2015,45(4):381-388.
[15]赵程锦,周煜虎,王坤正.软骨ADAMTS-7基因上调与股骨头坏死发生之间的相关性研究[J].中国骨质疏松杂志,2017,23(6):727-733.
[16]Yu H,Zhu Y.Expression of ADAMTS-7 and ADAMTS-12 in the nucleus pulposus during degeneration of rat caudal intervetebral disc[J].J Vet Med Sci,2012,74(1):9-15.
[17]周惠琼,张奉春,Rob K will.肿瘤坏死因子-α和白细胞介素-1β对人骨关节炎软骨细胞蛋白聚糖代谢的影响[J].中华风湿病学杂志,2008,12(2):83-87.