Chen Min-Huey, Wang Jue-Long, Wong Chi-Yin, Yao Chung-Chen, Chen Yi-Jane, Jiang Ching-Chuan
Department of Dentistry, National Taiwan University Hospital and School of Dentistry, College of Medicine, National Taiwan University, National Taiwan University Hospital, Taipei, Taiwan.
J Formos Med Assoc. 2005 Apr;104(4):264-72.
Softening of cartilage is the initial degenerative step of osteoarthritic cartilage by matrix degradation and corruption of interconnection of the collagen fibrillar network. The purpose of this study was to investigate the correlation of chondrocyte apoptosis, matrix degradation, and the corruption of collagen architecture in the development of severe swelling of osteoarthritic cartilage.
Twenty osteoarthritic and 7 normal femoral neck fractured cartilage samples were obtained from patients with knee osteoarthritis and normal patients with femoral neck fracture at the time of total hip joint replacement surgery. Apoptosis was verified by TUNEL (terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate nick end-labeling) staining and structural changes were observed under phase-contrast microscopy. Matrix degradation was evaluated by histochemical analysis of proteoglycans. Swelling tests were performed by immersing the cartilage slices in hypotonic solution. The results of ultrastructural study of collagen architecture of osteoarthritic cartilage performed by scanning electron microscopy before and after swelling were compared.
Matrix degradation was most prominent in the middle zone of osteoarthritic cartilage. The percentage of chondrocytes in osteoarthritic cartilage showing apoptosis ranged from 15 to 20% (average, 18%; standard deviation (SD) = 3.2%) and was correlated with the extent of structural changes and matrix degradation. The swelling strain of the osteoarthritic cartilage varied from 120 to 200% (average, 160%; SD = 40%) depending on the degree of matrix degradation and structural changes. The loss of interconnectivity of collagen fibrillar architecture was correlated with the increased swelling potential of osteoarthritic cartilage.
This study demonstrated that chondrocyte apoptosis was correlated with matrix degradation and the corruption of fibrillar architecture and that the extent of these manifestations correlated with the swelling potential of osteoarthritic cartilage. These findings also emphasize the importance of the fibrillar architecture in maintaining the mechanical properties of cartilage.
软骨软化是骨关节炎软骨退变的起始步骤，表现为基质降解和胶原纤维网络连接破坏。本研究旨在探讨骨关节炎软骨严重肿胀发展过程中软骨细胞凋亡、基质降解及胶原结构破坏之间的相关性。
在全髋关节置换手术时，从膝关节骨关节炎患者和股骨颈骨折正常患者中获取20份骨关节炎和7份正常股骨颈骨折软骨样本。通过TUNEL（末端脱氧核苷酸转移酶介导的dUTP缺口末端标记）染色验证细胞凋亡，并在相差显微镜下观察结构变化。通过蛋白聚糖的组织化学分析评估基质降解。将软骨切片浸入低渗溶液中进行肿胀试验。比较肿胀前后通过扫描电子显微镜对骨关节炎软骨胶原结构进行的超微结构研究结果。
基质降解在骨关节炎软骨的中间区域最为显著。骨关节炎软骨中显示凋亡的软骨细胞百分比为15%至20%（平均18%；标准差（SD）=3.2%），且与结构变化和基质降解程度相关。骨关节炎软骨的肿胀应变根据基质降解和结构变化程度在120%至200%之间变化（平均160%；SD = 40%）。胶原纤维结构连接性的丧失与骨关节炎软骨肿胀潜能增加相关。
本研究表明软骨细胞凋亡与基质降解及纤维结构破坏相关，且这些表现的程度与骨关节炎软骨的肿胀潜能相关。这些发现还强调了纤维结构在维持软骨力学性能方面的重要性。
