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Macroscopically healthy articular cartilage with fibrillar-scale early tissue degeneration subject to impact loading results in greater extent of cell-death.
Journal of the Mechanical Behavior of Biomedical Materials ( IF 3.9 ) Pub Date : 2020-08-19 , DOI: 10.1016/j.jmbbm.2020.104043
J Workman 1 , S McGlashan 2 , A Thambyah 1
Affiliation  

From previous investigations it has been shown that there exists healthy-appearing articular cartilage that contains collagen fibril network destructuring. It is hypothesised that such sub-micron scale destructuring not only presents an increased vulnerability to tissue scale damage following impact loading, but an increase in cell death as well.

Cartilage-on-bone blocks from 12 patellae, six healthy (G0) and the other six with sub-micron fibrillar destructuring (G1), were obtained and subject to 2.3 J impact loading. Two sets of sub-samples were obtained for each block tested. One set was used to examine for the live/dead cell response using calcein-AM and propidium iodide staining, imaged with confocal microscopy. The tissue microstructural matrix was imaged from the other matched set, unstained and in its fully hydrated state, using differential interference contrast optical light microscopy. High speed imaging of the impact was used to calculate the velocity changes or coefficient of restitution (COR) and used as a proxy of energy that the tissue absorbed. A previously defined tissue matrix damage score was used to quantify the extent of fracturing and cracking in the matrix. The cell death (PCD) was counted and presented as a percentage against all cells live plus dead.

The energy absorbed was 36.5% higher in G1 than in G0 (p = 0.034). However, the damage score and PCD of samples in the G1 group was much larger than the G0 group, ~300% and 161% respectively. Microscopy showed that cell death is associated to both matrix compaction and further fibrillar destructuring from the ECM to the territorial matrix regions of the chondron.

Following impact loading, cartilage tissue that appears normal but contains sub-micron fibrillar matrix destructuring responds with significantly increased cell death.



中文翻译:

受到冲击负荷的具有纤维状规模的早期组织变性的宏观健康的关节软骨导致更大程度的细胞死亡。

从以前的研究表明,存在着健康的关节软骨,其中包含胶原纤维网络破坏。假设这种亚微米尺度的破坏不仅在冲击负荷后呈现出对组织尺度损伤的增加的脆弱性,而且还增加了细胞死亡。

获得了来自12个,骨,6个健康(G0)和其他6个具有亚微米原纤维破坏(G1)的-骨软骨块,并承受2.3 J冲击载荷。对于每个测试块,获得了两组子样本。使用共焦显微镜成像,使用钙黄绿素-AM和碘化丙啶染色,使用一组检查活/死细胞反应。使用微分干涉对比光学显微镜,从另一个匹配组对组织微结构基质成像,未染色且处于完全水合状态。撞击的高速成像用于计算速度变化或恢复系数(COR),并用作组织吸收能量的代理。先前定义的组织基质损伤评分用于量化基质中的破裂和破裂程度。

在G1中吸收的能量比在G0中高出36.5%(p = 0.034)。但是,G1组的样品的损伤评分和PCD远高于G0组,分别为〜300%和161%。显微镜检查表明,细胞死亡与基质压实以及从ECM到软骨素的领土基质区域的进一步原纤维破坏有关。

冲击负荷后,看似正常但含有亚微米原纤维基质破坏的软骨组织会明显增加细胞死亡。

更新日期:2020-08-19
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