期刊文献+

胫骨结构抬高术治疗髌股软骨病机理的研究 被引量:2

The Mechanism Study of Anterior Tibial Tubercle Advancementin the Treatment of Condromalacia Patellofemoral Joint
下载PDF
导出
摘要 为客观评价胫骨结节抬高术治疗髌股软骨病的机理,采用Fuij压敏片测压力和染色法测面积相结合,共测试8具新鲜离体膝关节标本,比较胫骨结节抬高术前后的髌股接触部位、面积和应力分布。发现胫骨结节抬高术后,髌骨的习惯性接触区位置向近端移行,这种现象有助于避开对软骨病灶区的挤压和应力集中,对缓解和消除髌股疼痛症状可能有利。因此,提出了“应力集中传导至软骨损伤区导致髌股疼痛”的设想。胫骨结节抬高术后,小屈膝角度(30°-60°)有一定的髌股减压作用,但随屈膝角度增加,髌股接触面积减小并出现压力分布不均或局部高压现象。胫骨结节抬高术后,“腱股接触”现象提早(60°)出现,对髌股关节生物力学行为可能造成影响。 In order to evaluate the mechanisms of Anterior Tibial Tubercle Advancement (ATTA) in the treatment of chondromalacia patellofemoral,we measured the contact site,contact area and stress distribution of thepatellofemoral joint before and after ATTA procedure in eight fresh human cadaver knee joints with the FujiPressure Sensitive Film and the dyeing method.The result showed that the habitual contact site transfered frominferior to superior site after ATTA , which could prevent cartilage lesion site from stress extrusion and concen-tration,and might reduce or relieve the patellofemoral pains. An assumption of 'the patellofemoral pains causedby stress concentration at chondromalacia site'was thus proposed for above findings.After ATTA,thepatallofemoral pressure was decreased only in 30°to 60° of knee flixion and became uneven or local high pres-sure in large degree of knee flexion.The contact area of patellofemoral joint was diminished with the increasingof knee flexion.The tendofemoral contact appeared in advance at 60°of knee flexion after ATTA,which couldaffect the biomechanical behavior of patellofemoral joint.
出处 《中国运动医学杂志》 CAS CSCD 北大核心 1998年第2期100-103,共4页 Chinese Journal of Sports Medicine
基金 国家自然科学基金青年基金
关键词 胫骨结节抬高术 髌股软骨病 治疗 anterior tibial tubercle advancement(ATTA),patellofemoral joint,biomechanics
  • 相关文献

同被引文献34

  • 1陈世益,白玉龙,许胜文,袁旬华.Q角对髌股关节接触面积和应力的影响[J].医用生物力学,1993,8(1):30-35. 被引量:2
  • 2毕五蝉 王亦璁.膝关节载荷系统紊乱所致关节软骨退变[J].中华骨科杂志,1991,11:240-242.
  • 3[4]Creamer P,Hochberg MC.Osteoarthritis[R].Lancet,1997,350:503-508.
  • 4[9]Vaishnaw AK,McNally JD,Elkon KB.Apoptosis in the rheumatic diseases[J].Arthritis Rheum,1997,40:1917-1927
  • 5[13]Hashimoto S,Setareh M,Ochs RL,et al.Fas/Fas ligand expression and induction of apoptosis in chondrocytes[J].Arthritis Rheum,1997,40:1794-1755.
  • 6[15]Roussel M.F.,Ashman R,A.,Sherr C.J.,et al.Inhibition of cell proliferation by the Mad I transcriptional repressor[J].Mol Cell Biol,1996;16:2796~2801.
  • 7[16]Packham G,Cleveland JL.c-myc and Apoptosis[J].BBA,1995,1242:11-28.
  • 8[20]Evan G.I.,Wyllie A.H.,Gilberg C.S.,et al.Induction of apoptosis in fibroblasts by c-myc protein[J].Cell,1992,69:119-128.
  • 9[21]Francisco JB,Robert LO,Herbert S,et al.Chondrocyte apoptosis induced by nitric oxide.Am J Pathol,1995,146:75-85.
  • 10[23]Blanco FJ,Guitian R,Vazquez-Martul E,et al.Osteoarthritis chondrocytes die by apoptosis:a possible pathway for osteoarthritis pathology[J].Arthritis Rheum,1998,41:284-289.

引证文献2

二级引证文献11

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部