Hoemann Caroline D, Lafantaisie-Favreau Charles-Hubert, Lascau-Coman Viorica, Chen Gaoping, Guzmán-Morales Jessica
Department of Chemical Engineering, Ecole Polytechnique, Montreal, Quebec, Canada.
J Knee Surg. 2012 May;25(2):85-97. doi: 10.1055/s-0032-1319782.
In the knee joint, the purpose of the cartilage-bone interface is to maintain structural integrity of the osteochondral unit during walking, kneeling, pivoting, and jumping--during which tensile, compressive, and shear forces are transmitted from the viscoelastic articular cartilage layer to the much stiffer mineralized end of the long bone. Mature articular cartilage is integrated with subchondral bone through a approximately 20 to approximately 250 microm thick layer of calcified cartilage. Inside the calcified cartilage layer, perpendicular chondrocyte-derived collagen type II fibers become structurally cemented to collagen type I osteoid deposited by osteoblasts. The mature mineralization front is delineated by a thin approximately 5 microm undulating tidemark structure that forms at the base of articular cartilage. Growth plate cartilage is anchored to epiphyseal bone, sometimes via a thin layer of calcified cartilage and tidemark, while the hypertrophic edge does not form a tidemark and undergoes continual vascular invasion and endochondral ossification (EO) until skeletal maturity upon which the growth plates are fully resorbed and replaced by bone. In this review, the formation of the cartilage-bone interface during skeletal development and cartilage repair, and its structure and composition are presented. Animal models and human anatomical studies show that the tidemark is a dynamic structure that forms within a purely collagen type II-positive and collagen type I-negative hyaline cartilage matrix. Cartilage repair strategies that elicit fibrocartilage, a mixture of collagen type I and type II, are predicted to show little tidemark/calcified cartilage regeneration and to develop a less stable repair tissue-bone interface. The tidemark can be regenerated through a bone marrow-driven growth process of EO near the articular surface.
在膝关节中,软骨-骨界面的作用是在行走、跪、旋转和跳跃过程中维持骨软骨单元的结构完整性,在此期间,拉伸、压缩和剪切力从粘弹性关节软骨层传递到长骨的硬得多的矿化末端。成熟的关节软骨通过一层约20至约250微米厚的钙化软骨与软骨下骨整合。在钙化软骨层内部,垂直的软骨细胞衍生的II型胶原纤维在结构上与成骨细胞沉积的I型胶原类骨质结合。成熟的矿化前沿由在关节软骨底部形成的一层约5微米厚的薄起伏潮标结构界定。生长板软骨有时通过一层薄的钙化软骨和潮标锚定在骨骺骨上,而肥大边缘不形成潮标,会经历持续的血管侵入和软骨内成骨(EO),直到骨骼成熟,此时生长板被完全吸收并被骨替代。在本综述中,介绍了骨骼发育和软骨修复过程中软骨-骨界面的形成及其结构和组成。动物模型和人体解剖学研究表明,潮标是一种动态结构,在纯II型胶原阳性和I型胶原阴性的透明软骨基质内形成。预计引发纤维软骨(I型和II型胶原的混合物)的软骨修复策略显示出很少的潮标/钙化软骨再生,并形成稳定性较差的修复组织-骨界面。潮标可以通过关节表面附近的骨髓驱动的EO生长过程再生。