The Hospital for Special Surgery, 535 East 70th Street, New York, USA.
Ther Adv Musculoskelet Dis. 2012 Aug;4(4):249-58. doi: 10.1177/1759720X12437353.
The articular cartilage and the subchondral bone form a biocomposite that is uniquely adapted to the transfer of loads across the diarthrodial joint. During the evolution of the osteoarthritic process biomechanical and biological processes result in alterations in the composition, structure and functional properties of these tissues. Given the intimate contact between the cartilage and bone, alterations of either tissue will modulate the properties and function of the other joint component. The changes in periarticular bone tend to occur very early in the development of OA. Although chondrocytes also have the capacity to modulate their functional state in response to loading, the capacity of these cells to repair and modify their surrounding extracellular matrix is relatively limited in comparison to the adjacent subchondral bone. This differential adaptive capacity likely underlies the more rapid appearance of detectable skeletal changes in OA in comparison to the articular cartilage. The OA changes in periarticular bone include increases in subchondral cortical bone thickness, gradual decreases in subchondral trabeular bone mass, formation of marginal joint osteophytes, development of bone cysts and advancement of the zone of calcified cartilage between the articular cartilage and subchondral bone. The expansion of the zone of calcified cartilage contributes to overall thinning of the articular cartilage. The mechanisms involved in this process include the release of soluble mediators from chondrocytes in the deep zones of the articular cartilage and/or the influences of microcracks that have initiated focal remodeling in the calcified cartilage and subchondral bone in an attempt to repair the microdamage. There is the need for further studies to define the pathophysiological mechanisms involved in the interaction between subchondral bone and articular cartilage and for applying this information to the development of therapeutic interventions to improve the outcomes in patients with OA.
关节软骨和软骨下骨形成了一种独特的生物复合材料,特别适合在关节间传递负荷。在骨关节炎的发展过程中,生物力学和生物学过程导致这些组织的成分、结构和功能特性发生改变。鉴于软骨和骨之间的紧密接触,任何一种组织的改变都会调节另一种关节成分的特性和功能。关节周围骨的变化往往在 OA 的早期发展中就已经发生。虽然软骨细胞也有能力根据负荷来调节其功能状态,但与相邻的软骨下骨相比,这些细胞修复和改变其周围细胞外基质的能力相对有限。这种差异适应性能力可能是 OA 中可检测到的骨骼变化比关节软骨更快出现的基础。关节周围骨的 OA 变化包括软骨下皮质骨厚度增加、软骨下骨小梁质量逐渐减少、边缘关节骨赘形成、骨囊肿形成以及关节软骨和软骨下骨之间的钙化软骨带进展。钙化软骨带的扩张导致关节软骨整体变薄。这个过程涉及的机制包括来自关节软骨深层区域的软骨细胞释放可溶性介质,以及微裂纹的影响,这些微裂纹试图修复微损伤,从而启动了钙化软骨和软骨下骨的局部重塑。需要进一步的研究来定义软骨下骨和关节软骨相互作用中涉及的病理生理机制,并将这些信息应用于治疗干预的发展,以改善 OA 患者的治疗效果。