Increased hydraulic conductance of human articular cartilage and subchondral bone plate with progression of osteoarthritis.
Increased hydraulic conductance of human articular cartilage and subchondral bone plate with progression of osteoarthritis.
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DOI:
10.1002/art.24069
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发表时间:
2008-12
影响因子:
--
通讯作者:
Sah, Robert L.
中科院分区:
文献类型:
--
作者:
Hwang, Jennifer;Bae, Won C.;Shieu, Wendy;Lewis, Chad W.;Bugbee, William D.;Sah, Robert L.
Osteoarthritis (OA) is characterized by progressive degeneration of articular cartilage and remodeling of the subchondral bone plate (ScBP), comprised of calcified cartilage (CC) and underlying subchondral bone (ScB). CC remodeling due to upward invasion by vascular canals or to CC erosion may contribute to biomechanical alteration of the osteochondral (OC) tissue and its ScBP component. The study hypothesis was that hydraulic conductance of OC tissue and ScBP increases with structural changes indicative of increasing stages of OA. OC cores were harvested from knees of cadaveric tissue donors and from discarded fragments of OA knee surgery patients. Tissue donor cores were macroscopically normal, and OA cores had partial- or full-thickness erosion to bone. 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-D histology for CC, ScB, and ScBP thickness and vascular canal density. The hydraulic conductances of native OC tissue and ScBP were higher (2700- and 3-fold) in fully eroded samples than normal samples. The CC layer was thicker (1.5-fold) in partially eroded samples than normal samples, but thinner and incomplete in fully eroded samples. ScBP vascularity was altered with increasing stages of OA. During joint loading, increased hydraulic conductance of the OC tissue and ScBP 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.
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