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首页> 外文期刊>Osteoarthritis and cartilage >Subchondral bone trauma causes cartilage matrix degeneration: an immunohistochemical analysis in a canine model.
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Subchondral bone trauma causes cartilage matrix degeneration: an immunohistochemical analysis in a canine model.

机译:软骨下骨损伤导致软骨基质变性:犬模型中的免疫组织化学分析。

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Joint instability was believed to be the main cause of osteoarthritis following non-fracture articular trauma. However, sudden high impact load through articular cartilage onto subchondral bone may also cause osteoarthritic changes. OBJECTIVE: We asked whether early osteoarthritic changes following transarticular impact may be depicted using immunofluorescence on unfixed cryosections to contribute to a more detailed understanding of degenerative processes of joint impaction. DESIGN: Transarticular impacts were applied to patellofemoral joints of 12 skeletally mature beagle dogs (age: 15-16 months) using a drop tower. Biopsies of impact areas were sampled after 6 months and processed for standard light microscopy on formalin-fixed sections and for immunofluorescence for collagen type I (col I), type II (col II) and aggrecan (AC) on unfixed cryosections. Gross morphology and immunofluorescence on cryosections were documented using a semi-quantitative scaling system, compared to healthy controls and to standard light microscopy. RESULTS: Four biopsies showed almost entirely fibrocartilaginous morphology, four appeared to be of preserved hyaline morphology with only minor signs of fibrocartilaginous remodelling and four showed preserved hyaline appearance. We found decrease in col II and AC expression in highly degenerative specimens as well as increase of col I expression. Increased col I expression in the pericellular matrix could even be depicted in specimens with intact hyaline morphology. DISCUSSION/CONCLUSION: Observations suggest that joint impaction causes early osteoarthritic changes after 6 months. Collagen network disruption seems to lead to AC loss, although other researchers found isolated AC loss without denaturation of col II using immunofluorescence in formalin-fixed specimens. This is the first study on effects of transarticular impact using immunofluorescence on unfixed cryosections.
机译:人们认为关节不稳是非骨折性关节损伤后骨关节炎的主要原因。但是,通过关节软骨突然施加到软骨下骨上的突然高冲击负荷也可能导致骨关节炎改变。目的:我们问是否可以通过对未固定的冰冻切片进行免疫荧光来描述经关节撞击后早期骨关节炎的变化,以有助于更详细地了解关节撞击的退化过程。设计:经跌倒塔对12具骨骼成熟的比格犬(年龄:15-16个月)的pa股关节施加经关节撞击。 6个月后对受影响区域进行活检,在福尔马林固定切片上进行标准光学显微镜检查,在未固定的冰冻切片上进行I型胶原(col I),II型(col II)和聚集蛋白聚糖(AC)的免疫荧光检测。与健康对照和标准光学显微镜相比,使用半定量缩放系统记录了冷冻切片上的总体形态和免疫荧光。结果:四次活检显示几乎完全呈纤维软骨样形态,其中四个表现为保留的透明玻璃酸盐形态,仅有轻微的纤维oc关节重塑迹象,另外四个显示为保留的透明玻璃酸盐外观。我们发现在高度退化的标本中col II和AC表达下降,以及col I表达增加。甚至在具有完整玻璃样形态的标本中,细胞周围基质中col I表达的增加也可以描述出来。讨论/结论:观察表明,关节撞击会导致6个月后早期骨关节炎的改变。胶原蛋白网络的破坏似乎会导致交流电的损失,尽管其他研究人员发现在福尔马林固定的标本中使用免疫荧光法可以分离出交流电而不会使col II变性。这是关于使用免疫荧光对未固定冰冻切片进行跨关节撞击影响的首次研究。

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