Definition of a Critical Size Osteochondral Knee Defect and its Negative Effect on the Surrounding Articular Cartilage in the Rat.
Definition of a Critical Size Osteochondral Knee Defect and its Negative Effect on the Surrounding Articular Cartilage in the Rat.
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DOI：
10.1016/j.joca.2017.05.006
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发表时间：
2017-09
影响因子：
7
通讯作者：
Luyten FP
中科院分区：
文献类型：
--
作者：
Katagiri H;Mendes LF;Luyten FP
关节创伤是诱发膝骨关节炎（OA）的因素。关于创伤后骨软骨缺损对整个关节的影响的知识有限。本研究旨在确定大鼠膝关节的临界大小骨软骨缺损，并探讨骨软骨缺损与周围关节表面退行性变之间的可能联系。在大鼠膝关节上建立了不同大小的圆柱形骨软骨缺损。通过宏观观察、组织学和免疫组织化学研究这些病变的自然过程。采用定量聚合酶链式反应（qPCR）技术检测体外培养的关节软骨细胞和il - 1β和成纤维细胞生长因子2 （FGF2）培养基中缺损周围关节软骨的基因表达。在0.9 mm直径的缺陷中，观察到自发关节表面愈合，但在16周时软骨下骨板也向上推进。直径大于1.4 mm的缺陷是临界尺寸，在任何时间点都不能成功愈合。重要的是，缺损周围的关节软骨表达FGF2和il - 1β，但不表达ACAN和Col2。在il - 1β和FGF2补充培养基中培养的软骨细胞失去了天然成纤维细胞生长因子受体- FGFr1/FGFr3的平衡，并表现出活力下降。大鼠骨软骨缺损的临界尺寸定义为直径1.4 mm。软骨下骨板快速前进。骨软骨缺损周围的关节软骨表现出分解代谢活性，表达il - 1β、FGF2和FGFr1/FGFr3平衡紊乱，可能启动早期骨关节炎疾病的过程。
Joint trauma is predisposing to the incidence of osteoarthritis (OA) of the knee. There is a limited knowledge on the impact of posttraumatic osteochondral defects on the whole joint. This study was designed to define a critical size osteochondral defect in the knee of rats and to investigate a possible association between osteochondral defects and degeneration of the surrounding joint surface. Cylindrical osteochondral defects of different sizes were created in the knee joint of rats. The natural course of these lesions was studied by macroscopic observation, histology, and immunohistochemistry. Gene expression of the articular cartilage surrounding the defects in vivo and of articular chondrocytes cultured in vitro in IL1β and fibroblast growth factor 2 (FGF2) supplemented media was evaluated by quantitative polymerase chain reaction (qPCR). In defects of 0.9 mm diameter, spontaneous joint surface healing was observed but also upward advancing of the subchondral bone plate at 16 weeks. Larger 1.4 mm diameter defects were critical size, not resulting in successful healing at any time point. Importantly, the articular cartilage surrounding the defects expressed FGF2 and IL1β, but not ACAN and Col2. Chondrocytes cultured in IL1β and FGF2 supplemented media lost the natural fibroblast growth factor receptors – FGFr1/FGFr3 balance and showed decreased viability. A critical size osteochondral defect was defined as 1.4 mm in diameter in rat. Subchondral bone plate advancement occured rapidly. The articular cartilage surrounding osteochondral defects showed catabolic activity with expression of IL1β, FGF2 and a disturbed FGFr1/FGFr3 balance, potentially initiating a process of early osteoarthritic disease.
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影响因子：
--
作者：
Aigner, T;Vornehm, SI;Bayliss, MT
通讯作者：
Bayliss, MT
DOI：
10.1302/0301-620x.94b4.27495
发表时间：
2012-04-01
影响因子：
--
作者：
Bentley, G.;Biant, L. C.;Carrington, R. W. J.
通讯作者：
Carrington, R. W. J.
影响因子：
4
作者：
Ellman, M. B.;Yan, D.;Ahmadinia, K.;Chen, D.;An, H. S.;Im, H. J.
通讯作者：
Im, H. J.
影响因子：
5.3
作者：
Kim, Sunny;Bosque, Jose;Marder, Richard
通讯作者：
Marder, Richard
影响因子：
6.4
作者：
Chu, Constance R.;Szczodry, Michal;Bruno, Stephen
通讯作者：
Bruno, Stephen