Bone and Joint Research Unit, Service of Rheumatology, IIS-Fundación Jiménez Díaz, Autonomous University of Madrid, Madrid, Spain.
Bone and Joint Research Unit, Service of Rheumatology, IIS-Fundación Jiménez Díaz, Autonomous University of Madrid, Madrid, Spain.
Osteoarthritis Cartilage. 2019 Aug;27(8):1229-1234. doi: 10.1016/j.joca.2019.04.013. Epub 2019 Apr 30.
We aimed to assess whether an increase in chondrocyte size might be a feature of the articular cartilage (AC) hypertrophic-like phenotype both in experimental and in human osteoarthritis (OA). The anatomical location of these enlarged cells in the cartilage layers was also evaluated.
Experimental OA was carried out in female rabbits alone or in combination with osteoporosis (OPOA). The rabbits were subjected to destabilization knee surgery to develop OA. Osteoporosis was induced with ovariectomy and methylprednisolone administration. Human OA samples obtained from knee replacement surgery were also studied. Cartilage lesions and chondrocyte size were assessed in AC sections. Immunostaining of type-X collagen and metalloproteinase-13 were used as markers of the AC hypertrophic transformation. Both the cell size and the gene expression of type-X collagen were further analyzed in primary murine chondrocyte cultures.
Compared to healthy AC, chondrocyte size was increased both in experimental and in human OA, in correlation with the severity of cartilage damage. No differences in chondrocyte size were found between deeper or more superficial regions of AC. In cell cultures, accretion of hypertrophic markers and cell enlargement were found to occur synchronized.
We observed an enhancement in the mean size of chondrocytes at the OA cartilage, which showed correlation with cartilage damage, both in human and in experimental OA. The enlarged chondrocytes were homogeneously distributed throughout the AC. Our results suggest that chondrocyte size could be a reliable measure of disease progression, of potential use in the histopathological assessment of OA cartilage.
我们旨在评估软骨细胞体积增大是否是实验性和人类骨关节炎（OA）关节软骨（AC）肥大样表型的特征。还评估了这些增大细胞在软骨层中的解剖位置。
单独或结合骨质疏松症（OPOA）对雌性兔进行实验性 OA。通过膝关节不稳定手术使兔子发生 OA。骨质疏松症通过卵巢切除术和甲基强的松龙给药诱导。还研究了来自膝关节置换手术的人类 OA 样本。在 AC 切片中评估软骨病变和软骨细胞大小。使用型-X 胶原和基质金属蛋白酶-13 的免疫染色作为 AC 肥大转化的标志物。进一步在原代鼠软骨细胞培养物中分析细胞大小和型-X 胶原的基因表达。
与健康 AC 相比，实验性和人类 OA 中的软骨细胞大小均增加，与软骨损伤的严重程度相关。在 AC 的深层或浅层区域之间未发现软骨细胞大小的差异。在细胞培养物中，发现肥大标志物的积累和细胞增大同步发生。
我们观察到 OA 软骨中软骨细胞平均大小增加，这与人类和实验性 OA 中的软骨损伤相关。增大的软骨细胞在 AC 中均匀分布。我们的结果表明，软骨细胞大小可能是疾病进展的可靠指标，在 OA 软骨的组织病理学评估中具有潜在用途。
