Subfailure damage in ligament: a structural and cellular evaluation

Subfailure damage in ligament: a structural and cellular evaluation
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DOI:
10.1152/jappl.2002.92.1.362
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发表时间:
2002-01-01
影响因子:
3.3
通讯作者:
Vanderby, R
Vanderby, R
中科院分区:
医学2区
文献类型:
--
作者:
Provenzano, PP;Heisey, D;Vanderby, R

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从宏观结构角度(指整个韧带作为一个结构)和微观细胞角度评估韧带亚失效损伤。以新鲜收获的大鼠内侧副韧带(mcl)为模型进行离体实验。韧带预加载0.1 N,以建立长度(和应变)测量的一致参考点。韧带结构损伤的特征是亚失效拉伸后组织长度的不可恢复差异。还评估了单次亚破坏拉伸后组织的力学性能(通过预加载状态下测量的应力与应变曲线)(n = 6对,每个拉伸韧带施加不同的拉伸幅度)。含有坏死细胞的区域被用来表征单次拉伸后的细胞损伤。值得注意的是,受损细胞的数量没有被量化,细胞面积和荧光面积之间的差异是未知的。结构和细胞损伤被表示为亚失效MCL菌株的功能并进行了比较。统计分析表明,结构损伤发生在5.14%应变时(参考预加载长度)。高于损伤阈值的亚破坏应变通过延长趾区(即增加松弛度)以及降低切向模量和极限应力来改变MCL应力-应变曲线的形状。韧带应变明显低于结构损伤阈值时,细胞损伤发生。这种细胞损伤可能是轻度扭伤韧带自然愈合过程的一部分。
Subfailure damage in ligaments was evaluated macroscopically from a structural perspective (referring to the entire ligament as a structure) and microscopically from a cellular perspective. Freshly harvested rat medial collateral ligaments (MCLs) were used as a model in ex vivo experiments. Ligaments were preloaded with 0.1 N to establish a consistent point of reference for length (and strain) measurements. Ligament structural damage was characterized by nonrecoverable difference in tissue length after a subfailure stretch. The tissue's mechanical properties (via stress vs. strain curves measured from a preloaded state) after a single subfailure stretch were also evaluated (n = 6 pairs with a different stretch magnitude applied to each stretched ligament). Regions containing necrotic cells were used to characterize cellular damage after a single stretch. It should be noted that the number of damaged cells was not quantified and the difference between cellular area and area of fluorescence is not known. Structural and cellular damage were represented and compared as functions of subfailure MCL strains. Statistical analysis indicated that the onset of structural damage occurs at 5.14% strain (referenced from a preloaded length). Subfailure strains above the damage threshold changed the shape of the MCL stress-strain curve by elongating the toe region (i.e., increasing laxity) as well as decreasing the tangential modulus and ultimate stress. Cellular damage was induced at ligament strains significantly below the structural damage threshold. This cellular damage is likely to be part of the natural healing process in mildly sprained ligaments.