Effect of vertebral endplate composition on disc health

描述(申请人提供)：尽管大多数下腰痛的确切原因尚不清楚，但可以理解的是，腰椎间盘退行性损伤(IVD)在导致背痛的致病机制中起着核心作用。由于IVD是体内最大的无血管结构，椎间盘细胞的存活严重依赖于邻近椎体内毛细血管的营养供应。从毛细血管床到椎间盘细胞的营养供应的主要决定因素是椎体终板，它由透明软骨层和软骨下骨层组成，软骨下骨层支撑着广泛的骨髓接触通道(MCC)网络，毛细血管芽通过这些通道出现。据推测，椎体终板退行性过度矿化是限制IVD营养供应的中心因素，从而导致椎间盘退变。然而，这一过程是软骨下骨过度矿化和MCC闭塞的结果，还是由于软骨层本身的钙化，仍未得到解决。确定终板中最容易发生矿化过多的成分，对于理解营养物质供应丧失的机制至关重要。我们建议确定软骨下骨结构、软骨终板成分和组织之间的关系，以及身体腰椎IVD退变的开始和进展。

DESCRIPTION (provided by applicant): Although the exact origin of most cases of low back pain remains unknown, it is understood that degenerative damage to the intervertebral disc (IVD) plays a central role in the pathogenic mechanism leading to back pain. As the IVD is the largest avascular structure in the body, survival of disc cells is critically dependent on nutrient supply from capillaries within adjacent vertebra. A principal determinant of nutrient supply from capillary beds to disc cells is the vertebral endplate, which is composed of a hyaline cartilage layer and a subchondral bone layer that supports an extensive network of marrow contact channels (MCCs) through which capillary buds emerge. It is hypothesized that degenerative hypermineralization of the vertebral endplate is a central factor in restricting nutrient supply to the IVD, leading to disc degeneration. Nevertheless, whether this process is the result of subchondral bone hypermineralization and MCC occlusion, or instead due to calcification of the cartilage layer itself, remains unresolved. Identifying the component of the endplate that is most susceptible to hypermineralization is central to understanding the mechanism by which nutrient supply to the IVD is lost. We propose to determine the relationship between subchondral bone architecture, cartilaginous endplate composition and organization, and the initiation and progression of IVD degeneration in cadaveric human lumbar spines.