Sclerostin: A Novel Key to Bone and Dental Treatment

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.