Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis
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 w...
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2021
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oai:doaj.org-article:bc55d6f9420944c9b327bd16794d78142021-11-25T18:01:24ZSclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis10.3390/jcm102252862077-0383https://doaj.org/article/bc55d6f9420944c9b327bd16794d78142021-11-01T00:00:00Zhttps://www.mdpi.com/2077-0383/10/22/5286https://doaj.org/toc/2077-0383Idiopathic 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.Elias S. VasiliadisDimitrios Stergios EvangelopoulosAngelos KaspirisChristos VlachosSpyros G. PneumaticosMDPI AGarticleidiopathic scoliosissclerostinosteocytesβ-cateninWnt signaling pathwayMedicineRENJournal of Clinical Medicine, Vol 10, Iss 5286, p 5286 (2021) |
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idiopathic scoliosis sclerostin osteocytes β-catenin Wnt signaling pathway Medicine R |
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idiopathic scoliosis sclerostin osteocytes β-catenin Wnt signaling pathway Medicine R Elias S. Vasiliadis Dimitrios Stergios Evangelopoulos Angelos Kaspiris Christos Vlachos Spyros G. Pneumaticos Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis |
description |
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. |
format |
article |
author |
Elias S. Vasiliadis Dimitrios Stergios Evangelopoulos Angelos Kaspiris Christos Vlachos Spyros G. Pneumaticos |
author_facet |
Elias S. Vasiliadis Dimitrios Stergios Evangelopoulos Angelos Kaspiris Christos Vlachos Spyros G. Pneumaticos |
author_sort |
Elias S. Vasiliadis |
title |
Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis |
title_short |
Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis |
title_full |
Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis |
title_fullStr |
Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis |
title_full_unstemmed |
Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis |
title_sort |
sclerostin and its involvement in the pathogenesis of idiopathic scoliosis |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/bc55d6f9420944c9b327bd16794d7814 |
work_keys_str_mv |
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