Benneker Lorin M, Heini Paul F, Alini Mauro, Anderson Suzanne E, Ito Keita
AO Research Institute, Davos, Switzerland.
Spine (Phila Pa 1976). 2005 Jan 15;30(2):167-73. doi: 10.1097/01.brs.0000150833.93248.09.
Intervertebral disc degeneration was evaluated by morphologic appearance, magnetic resonance imaging, and by biochemical matrix composition. Caliber and distribution of openings of the adjacent vertebral osseous endplates were measured.
Correlation between occlusion of vertebral endplate openings and intervertebral disc degeneration was quantified.
Calcifications of vertebral endplates with disease and age have suggested insufficient nutrition as a mechanism for intervertebral disc degeneration. It has been proposed that occlusion of endplate openings, which contain vascular sources for the disc, may limit the transport of nutrients, leading to disc degeneration.
Fresh magnetic resonance images from 39 human lumbar discs were scored. Sectioned discs with endplates were morphologically graded. Samples of nuclear and anular regions were evaluated for proteoglycan and collagen contents. Backlight microscopic images of 4 endplate regions were obtained, and caliber and distribution of endplate openings for each disc were measured. Analysis of variance regression models were used to assess correlation between endplate openings and disc degeneration.
The decrease in opening density significantly correlated to morphologic degeneration grade, best for openings with 20 to 50 im equivalent diameter and in the nuclear region. Although the density of 20 to 50 im openings also significantly indirectly correlated to age, it was not as strong as the correlation to degeneration grade. Opening density was also significantly correlated to proteoglycan content in all regions. However, all other biochemical parameters as well as the T2 intensity score showed only weak or no correlation to opening density.
A high indirect correlation between the density of openings in the osseous endplate (particularly of the size of the capillary buds) and the morphologic degeneration grade of the disc support the hypothesis that occlusion of these openings may deprive the cells of nutrients, leading to insufficient maintenance of the extracellular matrix and disc degeneration.
通过形态学表现、磁共振成像以及生化基质成分评估椎间盘退变情况。测量相邻椎体骨终板开口的口径和分布。
量化椎体终板开口闭塞与椎间盘退变之间的相关性。
随着疾病和年龄增长，椎体终板钙化提示营养不足是椎间盘退变的一种机制。有人提出，包含椎间盘血管来源的终板开口闭塞可能会限制营养物质的运输，导致椎间盘退变。
对39例人类腰椎间盘的新鲜磁共振图像进行评分。对带有终板的椎间盘切片进行形态学分级。评估髓核和纤维环区域样本的蛋白聚糖和胶原蛋白含量。获取4个终板区域的背光显微镜图像，测量每个椎间盘终板开口的口径和分布。使用方差分析回归模型评估终板开口与椎间盘退变之间的相关性。
开口密度的降低与形态学退变分级显著相关，对于等效直径为20至50μm且位于髓核区域的开口相关性最佳。虽然20至50μm开口的密度也与年龄显著间接相关，但其与退变分级的相关性不如与退变分级的相关性强。开口密度在所有区域也与蛋白聚糖含量显著相关。然而，所有其他生化参数以及T2强度评分与开口密度仅显示出微弱或无相关性。
骨终板开口密度（尤其是毛细血管芽的大小）与椎间盘形态学退变分级之间的高度间接相关性支持了这样一种假设，即这些开口的闭塞可能使细胞缺乏营养，导致细胞外基质维持不足和椎间盘退变。
