Lin Yu-Yu, Tanaka Nobuaki, Ohkuma Satoru, Iwabuchi Yasunori, Tanne Yuki, Kamiya Takashi, Kunimatsu Ryo, Huang Yu-Ching, Yoshioka Motoko, Mitsuyoshi Tomomi, Tanimoto Kotaro, Tanaka Eiji, Tanne Kazuo
Department of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical Sciences, Minami-ku, Hiroshima, Japan.
Eur J Oral Sci. 2010 Apr;118(2):151-8. doi: 10.1111/j.1600-0722.2010.00710.x.
Osteoarthritis (OA) sometimes occurs as a consequence of repeated microtrauma involved in parafunction, which may lead to microfracture in the subchondral bone. The aim of this in vitro study was to evaluate the effects of subchondral osteoblasts in loading with repeated excessive mechanical stress on the metabolism of overlying chondrocytes. A high-magnitude cyclic tensile stress of 15 kPa (30 cycles min(-1)) was applied to the cultured osteoblasts obtained from porcine mandibular condyles. The chondrocytes in alginate beads were then co-cultured with mechanically stressed or unstressed osteoblasts. Chondrocytes co-cultured with unstressed osteoblasts showed a phenotypic shift to hypertrophic chondrocytes, characterized by decreased expression of type II collagen, aggrecan, Sry-related HMG box (SOX-9), and cartilage oligomeric matrix protein (COMP) genes and increased expression of type X collagen and bone sialoprotein (BSP) genes, suggesting that the co-culture may change the chondrocyte differentiation to some extent. These changes were more distinct in chondrocytes co-cultured with excessively mechanically stressed osteoblasts. After co-culture with stressed osteoblasts, the expressions of matrix metalloproteinase (MMP)1, MMP3 and MMP13 genes were also enhanced and the synthesis of DNA, proteoglycan and collagen were significantly decreased in chondrocytes. These results demonstrate that alterations in cartilage metabolism can be induced by stressed osteoblasts, indicating a possible explanation for the onset and progression of OA.
骨关节炎(OA)有时是由于功能异常所涉及的反复微创伤导致的,这可能会引起软骨下骨的微骨折。这项体外研究的目的是评估反复施加过度机械应力对软骨下成骨细胞加载后,其上方软骨细胞代谢的影响。对从猪下颌髁突获取的培养成骨细胞施加15 kPa(30次循环/分钟)的高幅度循环拉伸应力。然后将藻酸盐珠中的软骨细胞与经机械应力处理或未经处理的成骨细胞共培养。与未经处理的成骨细胞共培养的软骨细胞表现出向肥大软骨细胞的表型转变,其特征是II型胶原蛋白、聚集蛋白聚糖、Sry相关高迁移率族盒(SOX-9)和软骨寡聚基质蛋白(COMP)基因的表达降低,而X型胶原蛋白和骨唾液酸蛋白(BSP)基因的表达增加,这表明共培养可能在一定程度上改变软骨细胞的分化。这些变化在与过度机械应力处理的成骨细胞共培养的软骨细胞中更为明显。与应激成骨细胞共培养后,软骨细胞中基质金属蛋白酶(MMP)1、MMP3和MMP13基因的表达也增强,并且DNA、蛋白聚糖和胶原蛋白的合成显著减少。这些结果表明,应激成骨细胞可诱导软骨代谢的改变,这为OA的发病和进展提供了一种可能的解释。