Centre for Comparative and Clinical Anatomy, University of Bristol, Bristol, United Kingdom.
Spine (Phila Pa 1976). 2012 Oct 15;37(22):1883-91. doi: 10.1097/BRS.0b013e318263ba59.
Mechanical and biochemical analyses of cadaveric and surgically removed discs.
To test the hypothesis that fissures in the annulus of degenerated human discs are mechanically and chemically conducive to the ingrowth of nerves and blood vessels.
Discogenic back pain is closely associated with fissures in the annulus fibrosus, and with the ingrowth of nerves and blood vessels.
Three complementary studies were performed. First, 15 cadaveric discs that contained a major annulus fissure were subjected to 1 kN compression, while a miniature pressure transducer was pulled through the disc to obtain distributions of matrix compressive stress perpendicular to the fissure axis. Second, Safranin O staining was used to evaluate focal loss of proteoglycans from within annulus fissures in 25 surgically removed disc samples. Third, in 21 cadaveric discs, proteoglycans (sulfated glycosaminoglycans [sGAGs]) and water concentration were measured biochemically in disrupted regions of annulus containing 1 or more fissures, and in adjacent intact regions.
Reductions in compressive stress within annulus fissures averaged 36% to 46%, and could have been greater at the fissure axis. Stress reductions were greater in degenerated discs, and were inversely related to nucleus pressure (R(2) = 47%; P = 0.005). Safranin O stain intensity indicated that proteoglycan concentration was typically reduced by 40% at a distance of 600 μm from the fissure axis, and the width of the proteoglycan-depleted zone increased with age (P < 0.006; R(2) = 0.29) and with general proteoglycan loss (P < 0.001; R(2) = 0.32). Disrupted regions of annulus contained 36% to 54% less proteoglycans than adjacent intact regions from the same discs, although water content was reduced only slightly.
Annulus fissures provide a low-pressure microenvironment that allows focal proteoglycan loss, leaving a matrix that is conducive to nerve and blood vessel ingrowth.
对尸体和手术切除的椎间盘进行机械和生化分析。
验证假设,即退化人类椎间盘的环纤维裂缝在机械和化学上有利于神经和血管的生长。
椎间盘源性腰痛与纤维环的裂缝密切相关,与神经和血管的生长有关。
进行了三项补充研究。首先,对含有大的环纤维裂缝的 15 个尸体椎间盘进行了 1 kN 的压缩,同时微型压力传感器通过椎间盘被拉出,以获得垂直于裂缝轴的基质压缩应力分布。其次,在 25 个手术切除的椎间盘样本中,使用番红 O 染色评估在环纤维裂缝内的蛋白聚糖的焦点损失。第三,在 21 个尸体椎间盘,在含有 1 个或更多裂缝的环的破坏区域和相邻的完整区域,通过生化方法测量蛋白聚糖(硫酸糖胺聚糖[sGAGs])和水浓度。
环纤维裂缝内的压缩应力平均降低了 36%至 46%,在裂缝轴上可能更大。在退化的椎间盘上,应力降低更大,与核压力呈负相关(R(2) = 47%;P = 0.005)。番红 O 染色强度表明,在距离裂缝轴 600 μm 的距离处,蛋白聚糖浓度通常降低 40%,而蛋白聚糖耗竭区的宽度随年龄增加(P < 0.006;R(2) = 0.29)和一般蛋白聚糖损失(P < 0.001;R(2) = 0.32)而增加。来自同一椎间盘的环的破坏区域的蛋白聚糖含量比相邻的完整区域低 36%至 54%,尽管水含量仅略有降低。
环纤维裂缝提供了一个低压微环境,允许局部蛋白聚糖丢失,留下有利于神经和血管生长的基质。