Vasiliadis Elias S, Evangelopoulos Dimitrios Stergios, Kaspiris Angelos, Vlachos Christos, Pneumaticos Spyros G
3rd Department of Orthopaedics, School of Medicine, National and Kapodistrian University of Athens, KAT Hospital, 16541 Athens, Greece.
Laboratory of Molecular Pharmacology, Division for Orthopaedic Research, School of Health Sciences, University of Patras, 26504 Rion, Greece.
J Clin Med. 2021 Nov 14;10(22):5286. doi: 10.3390/jcm10225286.
Idiopathic scoliosis is a disorder of unknown etiology. Bone biopsies from idiopathic scoliosis patients revealed changes at cellular and molecular level. Osteocytic sclerostin is downregulated, and serum level of sclerostin is decreased. Osteocytes in idiopathic scoliosis appear to be less active with abnormal canaliculi network. Differentiation of osteoblasts to osteocytes is decelerated, while Wnt/β-catenin signaling pathway is overactivated and affects normal bone mineralization that leads to inferior mechanical properties of the bone, which becomes susceptible to asymmetrical forces and causes deformity of the spinal column. Targeting bone metabolism during growth by stimulating sclerostin secretion from osteocytes and restoring normal function of Wnt/β-catenin signaling pathway could, in theory, increase bone strength and prevent deterioration of the scoliotic deformity.
特发性脊柱侧凸是一种病因不明的疾病。对特发性脊柱侧凸患者进行的骨活检显示在细胞和分子水平上存在变化。骨细胞中的硬化蛋白表达下调，血清硬化蛋白水平降低。特发性脊柱侧凸患者的骨细胞活性似乎较低，其小管网络异常。成骨细胞向骨细胞的分化减缓，而Wnt/β-连环蛋白信号通路过度激活，影响正常的骨矿化，导致骨骼的力学性能较差，骨骼易受不对称力的影响，进而引起脊柱畸形。理论上，通过刺激骨细胞分泌硬化蛋白并恢复Wnt/β-连环蛋白信号通路的正常功能来靶向生长期间的骨代谢，可以增加骨强度并防止脊柱侧凸畸形恶化。
