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首页> 外文期刊>Journal of orthopaedic research >Effects of cartilage impact with and without fracture on chondrocyte viability and the release of inflammatory markers
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Effects of cartilage impact with and without fracture on chondrocyte viability and the release of inflammatory markers

机译：软骨影响与骨折对软骨细胞活力和炎症标志物释放的影响

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Post-traumatic arthritis (PTA) frequently develops after intra-articular fracture of weight bearing joints. Loss of cartilage viability and post-injury inflammation have both been implicated as possible contributing factors to PTA progression. To further investigate chondrocyte response to impact and fracture, we developed a blunt impact model applying 70%, 80%, or 90% surface-to-surface compressive strain with or without induction of an articular fracture in a cartilage explant model. Following mechanical loading, chondrocyte viability, and apoptosis were assessed. Culture media were evaluated for the release of double-stranded DNA (dsDNA) and immunostimulatory activity via nuclear factor kappa B (NF-κB) activity in Toll-like receptor (TLR) -expressing Ramos-Blue reporter cells. High compressive strains, with or without articular fracture, resulted in significantly reduced chondrocyte viability. Blunt impact at 70% strain induced a loss in viability over time through a combination of apoptosis and necrosis, whereas blunt impact above 80% strain caused predominantly necrosis. In the fracture model, a high level of primarily necrotic chondrocyte death occurred along the fracture edges. At sites away from the fracture, viability was not significantly different than controls. Interestingly, both dsDNA release and NF-κB activity in Ramos-Blue cells increased with blunt impact, but was only significantly increased in the media from fractured cores. This study indicates that the mechanism of trauma determines the type of chondrocyte death and the potential for post-injury inflammation.
机译：创伤后关节炎（PTA）经常在重量轴承关节内断裂后发生。软骨活力和后损伤后炎症都涉及PTA进展的可能导致因素。为了进一步研究软骨细胞对冲击和骨折的反应，我们开发了一种钝的冲击模型，施加70％，80％或90％的表面到表面压缩菌株，或不诱导软骨外植体模型中的关节骨折。在机械加载后，评估软骨细胞活力和细胞凋亡。评估培养培养基用于通过Toll样受体（TLR）中的核因子Kappa B（NF-κB）活性释放双链DNA（DSDNA）和免疫刺激活性的免疫因子 - 表达ramos-Blue报告细胞。高压缩菌株，有或没有关节骨折，导致软骨细胞活力显着降低。通过细胞凋亡和坏死的组合，70％菌株在70％菌株的钝性诱导活力随时间造成的损失，而钝性高于80％的菌株引起的钝性坏死。在裂缝模型中，沿着裂缝边缘发生高水平的正当性软骨细胞死亡。在远离骨折的地点，活力与对照没有显着不同。有趣的是，ramos-Blue细胞中的DSDNA释放和NF-κB活性随着钝性的影响而增加，但介质在裂缝核心中仅显着增加。本研究表明，创伤机制决定了软骨细胞死亡的类型和后损伤后炎症的潜力。

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