Mukoyama Shunsuke, Sasho Takahisa, Akatsu Yorikazu, Yamaguchi Satoshi, Muramatsu Yuta, Katsuragi Joe, Fukawa Taisuke, Endo Jun, Hoshi Hiroko, Yamamoto Yohei, Takahashi Kazuhisa
Graduate School of Medicine, Orthopedic Surgery, Chiba University, Chiba, Japan.
Cell Tissue Res. 2015 Feb;359(2):513-520. doi: 10.1007/s00441-014-2041-3. Epub 2014 Nov 19.
Partial thickness articular cartilage injuries (PTCIs) were not previously thought to heal spontaneously. Immature rats have the capacity for spontaneous repair of PTCIs, although it is a long-term process. Our aim has been to examine the spontaneous repair response mechanism in immature rats. Single linear PTCIs were created in 3-week-old and 12-week-old rats in the direction of joint motion. On day 1 and at 1, 2, and 4 weeks after PTCI, evaluations of histological changes and immunohistology at the injury site and in the surrounding cartilage were performed. Anti-CD105 and anti-CD166 antibodies (as stem cell markers to identify mesenchymal stem cells in reparative cartilage tissue) were used for immunohistological evaluations. To determine whether endogenous repair ability existed in articular cartilage, an ex vivo experiment was also carried out. Femoral condyles with PTCIs were incubated in Dulbecco's modified Eagle's medium containing 10% fetal bovine serum for 1 day and for 1 and 2 weeks. Histological changes were subsequently examined. Immature cartilage showed a higher repair response than did mature cartilage, and the response occurred immediately after PTCI. In immature rats, CD105- and CD166-positive cells were found in the superficial and transitional zones of the articular cartilage. Few CD166-positive cells were identified in mature articular cartilage. No significant in vivo differences in the spontaneous repair responses to PTCIs were observed between mature and immature groups. Thus, the repair response to PTCIs seems to be associated not only with CD105- and CD166-positive cells, but also with other perichondral factors.
部分厚度关节软骨损伤（PTCIs）以前被认为无法自发愈合。未成熟大鼠具有自发修复PTCIs的能力，尽管这是一个长期过程。我们的目的是研究未成熟大鼠的自发修复反应机制。在3周龄和12周龄大鼠的关节运动方向上制造单个线性PTCIs。在PTCIs后的第1天以及第1、2和4周，对损伤部位和周围软骨的组织学变化和免疫组织学进行评估。使用抗CD105和抗CD166抗体（作为干细胞标志物以识别修复性软骨组织中的间充质干细胞）进行免疫组织学评估。为了确定关节软骨中是否存在内源性修复能力，还进行了一项体外实验。将带有PTCIs的股骨髁在含有10%胎牛血清的杜尔贝科改良伊格尔培养基中孵育1天、1周和2周。随后检查组织学变化。未成熟软骨比成熟软骨表现出更高的修复反应，并且该反应在PTCIs后立即发生。在未成熟大鼠中，在关节软骨的表层和过渡区发现了CD105和CD166阳性细胞。在成熟关节软骨中很少发现CD166阳性细胞。在成熟组和未成熟组之间，未观察到对PTCIs的自发修复反应存在显著的体内差异。因此，对PTCIs的修复反应似乎不仅与CD105和CD166阳性细胞有关，还与其他软骨膜因子有关。
