Current Osteoporosis Reports

, Volume 10, Issue 1, pp 64–72

Sclerostin: Therapeutic Horizons Based Upon Its Actions

Future Therapeutics (P Miller, Section Editor)

DOI: 10.1007/s11914-011-0089-5

Cite this article as:
Costa, A.G. & Bilezikian, J.P. Curr Osteoporos Rep (2012) 10: 64. doi:10.1007/s11914-011-0089-5


Inactivating mutations of the SOST gene cause a reduction in sclerostin levels and are associated with high bone mass. The clinical phenotypes, sclerosteosis and van Buchem’s disease, were described in 1950s. Much later, it was learned that both diseases are due to loss-of-function mutations in the SOST gene. As a regulator of an important osteoanabolic pathway, Wnt, inactivation of SOST leads to a stimulation of the pathway it regulates. The high bone mass in patients with either sclerosteosis or van Buchem’s disease is associated with unusual skeletal strength; they do not fracture. Knowledge of this molecule and its actions led rather quickly to the development of anti-sclerostin antibodies that lead to marked increases in bone mass in both animals and human subjects. Blocking sclerostin action with anti-sclerostin antibodies is a promising new therapeutic approach to osteoanabolic therapy of osteoporosis.


Sclerostin Sclerostin antibodies Osteoporosis 

Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  1. 1.Department of Medicine, Division of Endocrinology, Metabolic Bone Diseases Unit, College of Physicians and SurgeonsColumbia UniversityNew YorkUSA
  2. 2.Department of Medicine, Division of EndocrinologySão Paulo Federal UniversitySão PauloBrazil

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