Abstract：
Spinal stenosis (SS) is a multifactorial polyetiological condition characterized by the narrowing of the spinal canal. This condition is a common source of pain among people over 50 years old. We perform a systematic review of molecular and genetic mechanisms that cause SS. The five main mechanisms of SS were found to be ossification of the posterior longitudinal ligament (OPLL), hypertrophy and ossification of the ligamentum flavum (HLF/OLF), facet joint (FJ) osteoarthritis, herniation of the intervertebral disc (IVD), and achondroplasia. FJ osteoarthritis, OPLL, and HLF/OLFLF/OLF have all been associated with an over-abundance of transforming growth factor beta and genes related to this phenomenon. OPLL has also been associated with increased bone morphogenetic protein 2. FJ osteoarthritis is additionally associated with Wnt/β-catenin signaling and genes. IVD herniation is associated with collagen type I alpha 1 and 2 gene mutations and subsequent protein dysregulation. Finally, achondroplasia is associated with fibroblast growth factor receptor 3 gene mutations and fibroblast growth factor signaling. Although most publications lack data on a direct relationship between the mutation and SS formation, it is clear that genetics has a direct impact on the formation of any pathology, including SS. Further studies are necessary to understand the genetic and molecular changes associated with SS.
摘要：
椎管狭窄（SS）是一种多因素多病因疾病，其特征是椎管狭窄。这种情况是50岁以上人群的常见疼痛来源。我们对引起SS的分子和遗传机制进行了系统的回顾。发现SS的五个主要机制是后纵韧带骨化（OPLL），黄韧带（HLF/OLF）的肥大和骨化，小关节（FJ）骨关节炎，椎间盘突出症（IVD），和软骨发育不全。FJ骨关节炎,OPLL,和HLF/OLFLF/OLF都与转化生长因子β和与此现象相关的基因过量有关。OPLL也与骨形态发生蛋白2的增加有关。FJ骨关节炎还与Wnt/β-连环蛋白信号传导和基因相关。IVD疝与I型胶原α1和2基因突变以及随后的蛋白质失调有关。最后,软骨发育不全与成纤维细胞生长因子受体3基因突变和成纤维细胞生长因子信号传导有关。尽管大多数出版物缺乏有关突变与SS形成之间直接关系的数据，很明显，遗传学对任何病理的形成都有直接影响，包括SS。需要进一步的研究来了解与SS相关的遗传和分子变化。
