Orthopaedic Research Center, Department of Clinical Sciences, College of Veterinary Medicine, Colorado State University, 300 West Drake Rd,, Fort Collins, Colorado CO 80523, USA.
BMC Musculoskelet Disord. 2013 Feb 1;14:54. doi: 10.1186/1471-2474-14-54.
It is well documented that osteoarthritis (OA) can develop following traumatic joint injury and is the leading cause of lameness and subsequent wastage of equine athletes. Although much research of injury induced OA has focused on cartilage, OA is a disease that affects the whole joint organ.
In this study, we investigated the impact of synovial cells on the progression of an OA phenotype in injured articular cartilage. Injured and control cartilage were cultured in the presence of synoviocytes extracted from normal equine synovium. Synoviocytes and cartilage were evaluated for catabolic and anabolic gene expression. The cartilage was also evaluated histologically for loss of extracellular matrix molecules, chondrocyte cell death and chondrocyte cluster formation.
The results indicate synoviocytes exert both positive and negative effects on injured cartilage, but ultimately protect injured cartilage from progressing toward an OA phenotype. Synoviocytes cultured in the presence of injured cartilage had significantly reduced expression of aggrecanase 1 and 2 (ADAMTS4 and 5), but also had increased expression of matrix metalloproteinase (MMP) -1 and reduced expression of tissue inhibitor of metalloproteinases 1 (TIMP-1). Injured cartilage cultured with synoviocytes had increased expression of both collagen type 2 and aggrecanase 2. Histologic examination of cartilage indicated that there was a protective effect of synoviocytes on injured cartilage by reducing the incidence of both focal cell loss and chondrocyte cluster formation, two major hallmarks of OA.
These results support the importance of evaluating more than one synovial joint tissue when investigating injury induced OA.
有大量文献记载，骨关节炎（OA）可继发于创伤性关节损伤，是导致马运动家畜跛行和随后淘汰的主要原因。虽然许多关于损伤诱导性 OA 的研究都集中在软骨上，但 OA 是一种影响整个关节器官的疾病。
在这项研究中，我们研究了滑膜细胞对受伤关节软骨中 OA 表型进展的影响。在存在从正常马滑膜中提取的滑膜细胞的情况下，对受伤和对照软骨进行培养。对滑膜细胞和软骨进行分解代谢和合成代谢基因表达的评估。还对软骨进行组织学评估，以评估细胞外基质分子的丧失、软骨细胞死亡和软骨细胞簇形成。
结果表明滑膜细胞对受伤软骨既有积极影响，也有消极影响，但最终可防止受伤软骨向 OA 表型进展。在存在受伤软骨的情况下培养的滑膜细胞中，聚集蛋白水解酶 1 和 2（ADAMTS4 和 5）的表达明显降低，但基质金属蛋白酶（MMP）-1的表达增加，组织金属蛋白酶抑制剂 1（TIMP-1）的表达降低。与滑膜细胞共培养的受伤软骨中，Ⅱ型胶原和聚集蛋白水解酶 2 的表达均增加。软骨的组织学检查表明，滑膜细胞对受伤软骨具有保护作用，可减少局灶性细胞丢失和软骨细胞簇形成的发生率，这是 OA 的两个主要特征。
这些结果支持在研究损伤诱导性 OA 时，评估一个以上滑膜关节组织的重要性。
