Evidence map›Paper›PMID 32134561›Full record

ArticleJournal of cellular and molecular medicine2020

Reduction of SOST gene promotes bone formation through the Wnt/β-catenin signalling pathway and compensates particle-induced osteolysis.

Zai Hang Zhang, Xin Yu Jia, Jing Yi Fang, Hao Chai, Qun Huang, Chang She, Peng Jia, De Chun Geng, Wei Xu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Interaction between diabetes and osteoporosis: imbalance between inflammation and bone remodeling.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. CombiningFrontiers in cell and developmental biology · 2025
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. The role of wnt signaling in diabetes-induced osteoporosis.Diabetology & metabolic syndrome · 2023
    Review
  17. Article
  18. Article
  19. Crosstalk between bone and other organs.Medical review (2021) · 2022
    Review
  20. 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

9 authors at 1 institution in 1 country.

Zai Hang ZhangDepartment of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Xin Yu JiaDepartment of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Jing Yi FangThe Experiment Center, The Medical College of Soochow University, Suzhou, China.
Hao ChaiDepartment of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Qun HuangDepartment of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Chang SheDepartment of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Peng JiaDepartment of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China.
De Chun GengDepartment of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou, China.
Wei XuDepartment of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-6030-0668
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increase in bone resorption and/or the inhibition of bone regeneration caused by wear particles are the main causes of periprosthetic osteolysis. The SOST gene and Sclerostin, a protein synthesized by the SOST gene, are the characteristic marker of osteocytes and regulate bone formation and resorption. We aimed to verify whether the SOST gene was involved in osteolysis induced by titanium (Ti) particles and to investigate the effects of SOST reduction on osteolysis. The results showed osteolysis on the skull surface with an increase of sclerostin levels after treated with Ti particles. Similarly, sclerostin expression in MLO-Y4 osteocytes increased when treated with Ti particles in vitro. After reduction of SOST, local bone mineral density and bone volume increased, while number of lytic pores on the skull surface decreased and the erodibility of the skull surface was compensated. Histological analyses revealed that SOST reduction increased significantly alkaline phosphatase- (ALP) and osterix-positive expression on the skull surface which promoted bone formation. ALP activity and mineralization of MC3T3-E1 cells also increased in vitro when SOST was silenced, even if treated with Ti particles. In addition, Ti particles decreased β-catenin expression with an increase in sclerostin levels, in vivo and in vitro. Inversely, reduction of SOST expression increased β-catenin expression. In summary, our results suggested that reduction of SOST gene can activate the Wnt/β-catenin signalling pathway, promoting bone formation and compensated for bone loss induced by Ti particles. Thus, this study provided new perspectives in understanding the mechanisms of periprosthetic osteolysis.

Indexed as

3T3 CellsAdaptor Proteins, Signal TransducingAnimalsbeta CateninBone RegenerationCell DifferentiationMiceOsteoblastsOsteoclastsOsteocytesOsteogenesisOsteolysisSkullTitaniumWnt Signaling PathwayAdaptor Proteins, Signal Transducingbeta CateninCTNNB1 protein, mouseSost protein, mouseTitaniumosteoblastosteocyteosteolysisSOST/sclerostinwear debris

Identifiers

PMID32134561
PMCPMC7171346
OpenAlexW3010061902

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Registered trials

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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.