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Review
. 2021 Nov 14;10(22):5286.
doi: 10.3390/jcm10225286.

Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis

Elias S Vasiliadis  1 , Dimitrios Stergios Evangelopoulos  1 , Angelos Kaspiris  2 , Christos Vlachos  1 , Spyros G Pneumaticos  1
Affiliations
Review

Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis

Elias S Vasiliadis et al. J Clin Med. .

Abstract

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.

Keywords: Wnt signaling pathway; idiopathic scoliosis; osteocytes; sclerostin; β-catenin.

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Conflict of interest statement

The authors declare no conflict of interest.

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