Morphology of the human vertebral endplate.

Morphology of the human vertebral endplate.
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DOI:
10.1002/jor.21513
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发表时间:
2012-02
影响因子:
2.8
通讯作者:
Lotz, Jeffrey C.
Lotz, Jeffrey C.
中科院分区:
医学3区
文献类型:
--
作者:
Rodriguez, Azucena G.;Rodriguez-Soto, Ana E.;Burghardt, Andrew J.;Berven, Sigurd;Majumdar, Sharmila;Lotz, Jeffrey C.

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据推测,椎间盘细胞营养不良是退行性变的一个促成因素,并因椎体终板硬化而加剧。然而,终板形态和退变之间的定量关系是不可用的。我们研究了终板骨微结构与椎间盘退变指标的关系,如形态学分级、蛋白多糖含量和细胞密度。椎间核心样本[n=96,14例受试者,L1-L5节段,年龄35-85岁(64±16岁),1级(n=4)、2级(n=32)、3级(n=44)、4级(n=10)、5级(n=6)],包括软骨下骨、软骨终板和邻近的髓核。使用μCT分析椎体终板的形态,并收集邻近的核组织进行生化和细胞分析。分析椎体终板形态与邻近椎间盘退变的关系。与流行的观点相反,随着椎间盘退变的进展,椎体终板孔隙度增加50 - 130%,骨小梁厚度减少20 - 50%(p<0.05)。我们还观察到随着终板变得更加多孔,核细胞密度增加(R2=0.33,p<0.05),蛋白多糖含量降低(R2=0.47,p<0.05)。我们的数据表明终板硬化不是椎间盘退变的基本因素。相反,在我们的样本中观察到相反的情况,随着年龄和退变,终板变得越来越多孔。由于缺血性椎间盘细胞行为通常与退行性变化相关,因此这可能与其他因素有关,例如脊椎毛细血管的质量,而不是介入组织的渗透性降低。
It is presumed that poor intervertebral disc cell nutrition is a contributing factor in degeneration, and is exacerbated by vertebral endplate sclerosis. Yet, quantitative relationships between endplate morphology and degeneration are unavailable. We investigated how endplate bone microstructure relates to indices of disc degeneration, such as morphologic grade, proteoglycan content, and cell density. Intervertebral core samples [n=96, 14 subjects, L1–L5 level, ages 35–85 (64±16 yrs.), degeneration grade 1(n=4), grade 2(n=32), grade 3(n=44), grade 4(n=10), grade 5(n=6)] that included subchondral bone, cartilage endplate and adjacent nucleus were harvested from human cadaveric lumbar spines. The morphology of the vertebral endplate was analyzed using μCT and the adjacent nucleus tissue was collected for biochemical and cellular analyses. Relationships between vertebral endplate morphology and adjacent disc degeneration were analyzed. Contrary to the prevailing notion, vertebral endplate porosity increased between 50 and 130% and trabecular thickness decreased by between 20 and 50% with advancing disc degeneration (p<0.05). We also observed that nucleus cell density increased (R2=0.33, p<0.05) and proteoglycan content decreased (R2=0.47, p<0.05) as the endplate became more porous. Our data suggest that endplate sclerosis is not a fundamental factor contributing to disc degeneration. Rather, the opposite was observed in our samples, as the endplate became progressively more porous with age and degeneration. Since ischemic disc cell behavior is commonly associated with degenerative change, this may be related to other factors such as the quality of vertebral capillaries, as opposed to decreased permeability of intervening tissues.
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