Evidence map›Paper›PMID 34830568›Full record

ReviewJournal of clinical medicine2021

Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis.

Elias S Vasiliadis, Dimitrios Stergios Evangelopoulos, Angelos Kaspiris, Christos Vlachos, Spyros G Pneumaticos

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.4field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Observational
  2. Review
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Elias S Vasiliadis3rd Department of Orthopaedics, School of Medicine, National and Kapodistrian University of Athens, KAT Hospital, 16541 Athens, Greece.ORCID 0000-0003-2428-5250
Dimitrios Stergios Evangelopoulos3rd Department of Orthopaedics, School of Medicine, National and Kapodistrian University of Athens, KAT Hospital, 16541 Athens, Greece.
Angelos KaspirisLaboratory of Molecular Pharmacology, Division for Orthopaedic Research, School of Health Sciences, University of Patras, 26504 Rion, Greece.
Christos Vlachos3rd Department of Orthopaedics, School of Medicine, National and Kapodistrian University of Athens, KAT Hospital, 16541 Athens, Greece.
Spyros G Pneumaticos3rd Department of Orthopaedics, School of Medicine, National and Kapodistrian University of Athens, KAT Hospital, 16541 Athens, Greece.
National and Kapodistrian University of Athens · GRUniversity of Patras · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

idiopathic scoliosisosteocytessclerostinWnt signaling pathwayβ-catenin

Identifiers

PMID34830568
PMCPMC8618875
OpenAlexW3213991821

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.