Vidal Bruno, Cascão Rita, Finnilä Mikko A J, Lopes Inês P, Saarakkala Simo, Zioupos Peter, Canhão Helena, Fonseca João E
Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.
Research Unit of Medical Imaging, Physics and Technology, Faculty of Medicine, University of Oulu, Oulu, Finland.
PLoS One. 2018 Jan 9;13(1):e0190920. doi: 10.1371/journal.pone.0190920. eCollection 2018.
Arthritis induces joint erosions and skeletal bone fragility.
The main goal of this work was to analyze the early arthritis induced events at bone architecture and mechanical properties at tissue level.
Eighty-eight Wistar rats were randomly housed in experimental groups, as follows: adjuvant induced arthritis (AIA) (N = 47) and a control healthy group (N = 41). Rats were monitored during 22 days for the inflammatory score, ankle perimeter and body weight and sacrificed at different time points (11 and 22 days post disease induction). Bone samples were collected for histology, micro computed tomography (micro-CT), 3-point bending and nanoindentation. Blood samples were also collected for bone turnover markers and systemic cytokine quantification.
At bone tissue level, measured by nanoindentation, there was a reduction of hardness in the arthritic group, associated with an increase of the ratio of bone concentric to parallel lamellae and of the area of the osteocyte lacuna. In addition, increased bone turnover and changes in the microstructure and mechanical properties were observed in arthritic animals, since the early phase of arthritis, when compared with healthy controls.
We have shown in an AIA rat model that arthritis induces very early changes at bone turnover, structural degradation and mechanical weakness. Bone tissue level is also affected since the early phase of arthritis, characterized by decreased tissue hardness associated with changes in bone lamella organization and osteocyte lacuna surface. These observations highlight the pertinence of immediate control of inflammation in the initial stages of arthritis.
关节炎会导致关节侵蚀和骨骼骨脆性增加。
本研究的主要目的是分析早期关节炎在组织水平上对骨结构和力学性能的影响。
88只Wistar大鼠被随机分为实验组，如下：佐剂诱导性关节炎（AIA）组（N = 47）和健康对照组（N = 41）。在22天内监测大鼠的炎症评分、踝关节周长和体重，并在不同时间点（疾病诱导后11天和22天）处死。收集骨样本进行组织学、显微计算机断层扫描（micro-CT）、三点弯曲和纳米压痕测试。还收集血样用于骨转换标志物和全身细胞因子的定量分析。
通过纳米压痕测量，在骨组织水平上，关节炎组的硬度降低，同时骨同心层与平行层的比例以及骨细胞陷窝面积增加。此外，与健康对照组相比，在关节炎动物中，从关节炎早期开始就观察到骨转换增加以及微观结构和力学性能的变化。
我们在AIA大鼠模型中表明，关节炎在骨转换、结构退化和力学弱点方面诱导了非常早期的变化。从关节炎早期开始，骨组织水平也受到影响，其特征是组织硬度降低，伴有骨板组织和骨细胞陷窝表面的变化。这些观察结果突出了在关节炎初始阶段立即控制炎症的相关性。
