随着骨关节炎的进展，人类关节软骨和软骨下骨板的液压传导性增加。
Increased hydraulic conductance of human articular cartilage and subchondral bone plate with progression of osteoarthritis.
作者信息
Hwang Jennifer, Bae Won C, Shieu Wendy, Lewis Chad W, Bugbee William D, Sah Robert L
机构信息
University of California-San Diego, La Jolla, CA 92093-0412, USA.
出版信息
Arthritis Rheum. 2008 Dec;58(12):3831-42. doi: 10.1002/art.24069.
OBJECTIVE
Osteoarthritis (OA) is characterized by progressive degeneration of articular cartilage and remodeling of the subchondral bone plate, comprising calcified cartilage and underlying subchondral bone. Calcified cartilage remodeling due to upward invasion by vascular canals or to calcified cartilage erosion may contribute to biomechanical alteration of the osteochondral tissue and its subchondral bone plate component. The study hypothesis was that hydraulic conductance of osteochondral tissue and subchondral bone plate increases with structural changes indicative of increasing stages of OA.
METHODS
Osteochondral cores were harvested from the knees of cadaveric tissue donors and from discarded fragments from patients with OA undergoing knee surgery. The osteochondral cores from tissue donors were macroscopically normal, and the cores from patients with OA had partial-thickness or full-thickness erosion to bone. The cores were perfusion-tested to determine the hydraulic conductance, or ease of fluid flow, in their native state and after enzymatic removal of cartilage. Adjacent portions were analyzed by 3-dimensional histology for calcified cartilage, subchondral bone, and subchondral bone plate thickness and vascular canal density.
RESULTS
Hydraulic conductance of native osteochondral tissue and subchondral bone plate was higher (2,700-fold and 3-fold, respectively) in fully eroded samples than in normal samples. The calcified cartilage layer was thicker (1.5-fold) in partially eroded samples than in normal samples but thinner and incomplete in fully eroded samples. Subchondral bone plate vascularity was altered with increasing stages of OA.
CONCLUSION
During joint loading, increased hydraulic conductance of the osteochondral tissue and subchondral bone plate could have deleterious biomechanical consequences for cartilage. Increased fluid exudation from overlying and opposing cartilage, increased fluid depressurization, and increased cartilage tissue strains could lead to chondrocyte death and cartilage damage.
目的
骨关节炎（OA）的特征是关节软骨进行性退变以及软骨下骨板重塑，软骨下骨板由钙化软骨和其下方的软骨下骨组成。由于血管通道向上侵入或钙化软骨侵蚀导致的钙化软骨重塑，可能会导致骨软骨组织及其软骨下骨板成分的生物力学改变。本研究的假设是，骨软骨组织和软骨下骨板的水力传导率会随着提示OA进展阶段增加的结构变化而升高。
方法
从尸体组织供体的膝关节以及接受膝关节手术的OA患者废弃的碎片中获取骨软骨芯。来自组织供体的骨软骨芯在宏观上是正常的，而来自OA患者的骨软骨芯有部分厚度或全层骨侵蚀。对这些骨软骨芯进行灌注测试，以确定其在天然状态下以及酶解去除软骨后的水力传导率，即流体流动的难易程度。对相邻部分进行三维组织学分析，以测定钙化软骨、软骨下骨以及软骨下骨板的厚度和血管通道密度。
结果
完全侵蚀的样本中，天然骨软骨组织和软骨下骨板的水力传导率分别比正常样本高2700倍和3倍。部分侵蚀的样本中钙化软骨层比正常样本厚1.5倍，但在完全侵蚀的样本中更薄且不完整。软骨下骨板的血管化随着OA阶段的增加而改变。
结论
在关节负荷过程中，骨软骨组织和软骨下骨板水力传导率的增加可能会对软骨产生有害的生物力学影响。覆盖和相对软骨的液体渗出增加、液体减压增加以及软骨组织应变增加，可能会导致软骨细胞死亡和软骨损伤。
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