Research Article Open Access

Sclerostin: A Novel Key to Bone and Dental Treatment

Galli Carlo1, Lumetti Simone1, Manfredi Edoardo1, Macaluso Guido1 and Passeri Giovanni2
  • 1 Università di Parma Via Gramsci, Italy
  • 2 Università di Parma, Italy

Abstract

Problem statement: Tooth loss can induce dramatical remodeling of alveolar bone because of mechanical loading impairment and strategies to help maintain adequate bone levels for subsequent therapies are sorely needed. Recent discoveries have shown that osteocytes, matrix-embedded cells in bone, respond to mechanical stimulation by modulating the expression of the Sost gene, which encodes for the protein sclerostin. This protein can oppose the WNT canonical pathway, a signaling cascade which regulates osteoblastic differentiation and bone homeostasis and thus orchestrate bone turn-over according to the skeleton’s mechanical needs. Conclusion: Experimental attempts at Sclerostin inhibition have provided interesting data on a novel approach to decrease bone resorption and promote bone formation, with important implications for the orthopedic and dental field.

Current Research in Dentistry
Volume 3 No. 1, 2012, 18-26

DOI: https://doi.org/10.3844/crdsp.2012.18.26

Submitted On: 30 July 2012 Published On: 1 January 2013

How to Cite: Carlo, G., Simone, L., Edoardo, M., Guido, M. & Giovanni, P. (2012). Sclerostin: A Novel Key to Bone and Dental Treatment. Current Research in Dentistry, 3(1), 18-26. https://doi.org/10.3844/crdsp.2012.18.26

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Keywords

  • Sost protein
  • osteocyte
  • alveolar bone loss