Sclerostin Stimulates Osteocyte Support of Osteoclast Activity by a RANKL-Dependent Pathway
2011

Sclerostin's Role in Bone Resorption

publication Evidence: moderate

Author Information

Author(s): Wijenayaka Asiri R., Kogawa Masakazu, Lim Hui Peng, Bonewald Lynda F., Findlay David M., Atkins Gerald J.

Primary Institution: University of Adelaide

Hypothesis

Sclerostin may have a catabolic action through promotion of osteoclast formation and activity by osteocytes.

Conclusion

Sclerostin promotes osteoclastogenesis and increases osteoclast activity, suggesting it has a catabolic effect on bone.

Supporting Evidence

  • Sclerostin increased RANKL mRNA expression and decreased OPG mRNA expression.
  • Co-cultures with sclerostin showed increased osteoclastic resorption.
  • Sclerostin did not induce apoptosis in osteocyte-like cells.

Takeaway

Sclerostin is a protein that helps control bone health. It can make bone-eating cells more active, which can lead to bone loss.

Methodology

The study involved treating human primary pre-osteocyte cultures and mouse osteocyte-like cells with recombinant human sclerostin and measuring effects on gene expression and osteoclast activity.

Limitations

The study primarily used in vitro models, which may not fully replicate in vivo conditions.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0025900

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