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The relationship between apoptosis of endplate chondrocytes and aging and degeneration of the intervertebral disc.

机译:终板软骨细胞凋亡与椎间盘衰老和变性之间的关系。

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STUDY DESIGN: Apoptosis in cervical intervertebral disc cells and cartilaginous endplate cells was examined by the nick end labeling (TUNEL) technique during the process of natural aging and in a mouse experimental spondylosis model. OBJECTIVES: To determine the role of apoptosis in aging and degeneration of intervertebral discs by monitoring chronologic changes in the quantity and localization of apoptotic cells. SUMMARY OF BACKGROUND DATA: Apoptosis occurs within human intervertebral discs, but little is known about the pathologic significance of this process. On the other hand, the cartilaginous endplate is known to decrease in thickness and to disappear with aging and degeneration. The cause of this age-related change remains unclear. METHODS: A mouse spondylosis model was prepared via surgical resection of the posterior spinal element in 12 mice to examine the experimentally induced spondylosis process. Eighteen naturally aged mice were also used to examine the influence of aging. Paraffin-embedded midsagittal sections of the cervical spine were obtained 2, 3, 6, and 12 months after surgery in the spondylosis model and in the age-matched naturally aged mice, as well as in 4-week-old and 18-month-old naturally aged mice. Sections were stained with hematoxylin and eosin, safranin-O, and the TUNEL procedure. The number of apoptotic cells and vital cells were counted in the cartilaginous endplate of the intervertebral disc excluding the growth cartilage, and the degree of disappearance of the cartilaginous endplate was evaluated. RESULTS: Apoptosis, particularly noticeable in the cartilaginous endplate, increased with age and resulted in a marked decrease in cell density. Subsequently, the structure of the cartilaginous endplate began to disappear. Apoptosis was more evident and the structure of the cartilaginous endplate began to disappear more rapidly in the surgically treated group than in the naturally aged group. CONCLUSIONS: TUNEL-positive cells in the cartilaginous endplate increased with age, with destruction of the cartilaginous endplate after apoptosis (TUNEL-positive cell death). The application of the spondylosis model increased the incidence of apoptosis preceding the development of spondylosis. This suggests that apoptosis plays a role in the age-related changes seen in the cartilaginous endplate of the intervertebral disc and in the experimentally induced spondylosis process.
机译:研究设计:在自然衰老过程中和小鼠实验性脊椎病模型中,通过缺口末端标记(TUNEL)技术检查了颈椎间盘细胞和软骨终板细胞的凋亡。目的:通过监测凋亡细胞的数量和位置的时间顺序变化,确定凋亡在椎间盘老化和变性中的作用。背景数据概述:细胞凋亡发生在人的椎间盘内,但对该过程的病理学意义了解甚少。另一方面,已知软骨终板的厚度减小并且随着老化和变性而消失。这种与年龄有关的变化的原因尚不清楚。方法:通过外科切除12只小鼠的后脊髓元件,制备了小鼠脊柱病模型,以检查实验性诱发的脊柱病过程。还使用了十八只自然衰老的小鼠来检查衰老的影响。在脊柱病模型,年龄匹配的自然衰老小鼠以及4周龄和18个月大的小鼠中,在手术后2、3、6和12个月获得石蜡包埋的颈椎中矢状断面。自然老化的老老鼠。用苏木精和曙红,番红O-O和TUNEL方法对切片进行染色。计数除生长软骨外的椎间盘的软骨终板中的凋亡细胞和活细胞的数目,并评估软骨终板的消失程度。结果:细胞凋亡,尤其是在软骨终板中,随着年龄的增长而增加,并导致细胞密度显着下降。随后,软骨终板的结构开始消失。与自然衰老组相比,在手术治疗组中凋亡更明显,并且软骨终板的结构开始更快消失。结论:软骨终板中的TUNEL阳性细胞随年龄增长而增加,凋亡后软骨终板破坏(TUNEL阳性细胞死亡)。脊椎病模型的应用增加了脊柱病发展之前细胞凋亡的发生率。这表明凋亡在椎间盘的软骨终板和实验诱导的脊椎病过程中看到的与年龄有关的变化中起作用。

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