Department of Orthopedic Surgery and Graduate Program in Tissue Engineering and Regenerative Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Dev Dyn. 2010 Aug;239(8):2141-8. doi: 10.1002/dvdy.22350.
The goal of this mini-review is to address the long standing argument that the pathogenesis of disc disease is due to the loss and/or the replacement of the notochordal cells by other cell types. We contend that, although cells of different size and morphology exist, there is no strong evidence to support the view that the nucleus pulposus contains cells of distinct lineages. Based on lineage mapping studies and studies of other notochordal markers, we hypothesize that in all animals, including human, nucleus pulposus retains notochordal cells throughout life. Moreover, all cells including chondrocyte-like cells are derived from notochordal precursors, and variations in morphology and size are representative of different stages of maturation, and or, function. Thus, the most critical choice for a suitable animal model should relate more to the anatomical and mechanical characteristics of the motion segment than concerns of cell loss and replacement by non-notochordal cells.
本篇小综述旨在解决长期以来存在的争议,即椎间盘疾病的发病机制是由于脊索细胞的丢失和/或被其他细胞类型所取代。我们认为,尽管存在不同大小和形态的细胞,但没有强有力的证据支持核髓核含有不同谱系细胞的观点。基于谱系标记研究和其他脊索标记物的研究,我们假设在所有动物(包括人类)中,核髓核终生都保留脊索细胞。此外,所有细胞包括软骨细胞样细胞都源自脊索前体细胞,形态和大小的变化代表不同的成熟阶段,或者功能。因此,对于合适的动物模型,最关键的选择应该更多地与运动节段的解剖和力学特征有关,而不是与非脊索细胞的丢失和替代有关。