Oegema T R, Carpenter R J, Hofmeister F, Thompson R C
Department of Orthopaedic Surgery, University of Minnesota, Minneapolis 55455, USA.
Microsc Res Tech. 1997 May 15;37(4):324-32. doi: 10.1002/(SICI)1097-0029(19970515)37:4<324::AID-JEMT7>3.0.CO;2-K.
The zone of calcified cartilage (ZCC) forms an important interface between cartilage and bone for transmitting force, attaching cartilage to bone, and limiting diffusion from bone to the deeper layers of cartilage. The height of the ZCC is a relatively constant percent of articular cartilage and the height is maintained by a balance between progression of the tidemark into the unmineralized cartilage and changing into bone by vascular invasion and bony remodeling. During its formation, the cells that form the ZCC have properties similar to the cells of the growth plate. In the adult, the ZCC becomes quiescent but not inactive. The ZCC may be reactivated in osteoarthritis and may progressively calcify the unmineralized cartilage. This might contribute to cartilage thinning which would increase the concentration of forces across the uncalcified cartilage leading to more damage. Although the subchondral bony plate remodels extensively in osteoarthritis, there is little evidence that a change in the biomechanics of the plate directly initiates the osteoarthritic process in cartilage. However, increased repair by endochondral ossification of vertical cracks in the ZCC that penetrate into the marrow space could contribute to progression via changes in the ZCC.
钙化软骨区（ZCC）在软骨与骨之间形成了一个重要界面，用于传递力量、将软骨附着于骨以及限制从骨到软骨深层的扩散。ZCC的高度占关节软骨的比例相对恒定，其高度通过潮线向未矿化软骨推进以及血管侵入和骨重塑转变为骨之间的平衡得以维持。在其形成过程中，形成ZCC的细胞具有与生长板细胞相似的特性。在成年人中，ZCC变得静止但并非无活性。ZCC可能在骨关节炎中被重新激活，并可能逐渐使未矿化软骨钙化。这可能导致软骨变薄，从而增加未钙化软骨上的力的集中，进而导致更多损伤。尽管在骨关节炎中软骨下骨板会广泛重塑，但几乎没有证据表明该板生物力学的改变直接引发软骨中的骨关节炎进程。然而，ZCC中穿透至骨髓腔的垂直裂缝通过软骨内成骨增加修复，可能会通过ZCC的变化导致病情进展。
