{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T11:50:03Z","timestamp":1768909803473,"version":"3.49.0"},"reference-count":82,"publisher":"MDPI AG","issue":"22","license":[{"start":{"date-parts":[[2021,11,14]],"date-time":"2021-11-14T00:00:00Z","timestamp":1636848000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JCM"],"abstract":"<jats:p>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\/\u03b2-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\/\u03b2-catenin signaling pathway could, in theory, increase bone strength and prevent deterioration of the scoliotic deformity.<\/jats:p>","DOI":"10.3390\/jcm10225286","type":"journal-article","created":{"date-parts":[[2021,11,14]],"date-time":"2021-11-14T20:48:36Z","timestamp":1636922916000},"page":"5286","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis"],"prefix":"10.3390","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2428-5250","authenticated-orcid":false,"given":"Elias S.","family":"Vasiliadis","sequence":"first","affiliation":[{"name":"3rd Department of Orthopaedics, School of Medicine, National and Kapodistrian University of Athens, KAT Hospital, 16541 Athens, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dimitrios Stergios","family":"Evangelopoulos","sequence":"additional","affiliation":[{"name":"3rd Department of Orthopaedics, School of Medicine, National and Kapodistrian University of Athens, KAT Hospital, 16541 Athens, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Angelos","family":"Kaspiris","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Pharmacology, Division for Orthopaedic Research, School of Health Sciences, University of Patras, 26504 Rion, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christos","family":"Vlachos","sequence":"additional","affiliation":[{"name":"3rd Department of Orthopaedics, School of Medicine, National and Kapodistrian University of Athens, KAT Hospital, 16541 Athens, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Spyros G.","family":"Pneumaticos","sequence":"additional","affiliation":[{"name":"3rd Department of Orthopaedics, School of Medicine, National and Kapodistrian University of Athens, KAT Hospital, 16541 Athens, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2021,11,14]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"38","DOI":"10.1097\/BLO.0b013e3180d09dcc","article-title":"Genetic association of complex traits: Using idiopathic scoliosis as an example","volume":"462","author":"Cheng","year":"2007","journal-title":"Clin. 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