Effect of vertebral endplate composition on disc health

椎体终板成分对椎间盘健康的影响

• 批准号: 7055175
• 负责人: FRANK L ACOSTA
• 金额: $ 5.04万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-07-01 至 2007-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7055175
• 关键词: backache; calcification; capillary; cartilage; cell morphology; computed axial tomography; human tissue; hyaline substance; infrared spectrometry; interferometry; intervertebral disk; magnetic resonance imaging; nutrient bioavailability; pathologic process; postdoctoral investigator; postmortem; spine disorder

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.

描述（由申请人提供）：尽管大多数下背痛病例的确切起源仍然未知，但据了解，椎间盘（IVD）的退化性损害在导致背痛的致病机制中起着核心作用。由于IVD是体内最大的血管结构，因此椎间盘细胞的存活严重取决于相邻椎骨内毛细血管的营养供应。从毛细管床到圆盘细胞的营养供应的主要决定因素是椎骨终板，该底板由透明软骨层和软骨下骨层组成，该骨骼支持毛细血管芽出现的广泛的骨髓接触通道（MCC）网络。假设椎骨终板的退化性高矿化是限制对IVD养分供应的核心因素，导致椎间盘退化。然而，该过程是在软骨下骨高矿化和MCC遮挡的结果，还是由于软骨层本身的钙化而尚未解决。识别最容易受到高矿化的终板的组成部分，对于了解损失了IVD的营养供应的机制至关重要。我们建议确定软骨下骨结构，软骨末端板组成和组织之间的关系，以及尸体人类腰椎中IVD变性的起始和进展。