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Sclerostin: therapeutic horizons based upon its actions

Aline G Costa1, John P Bilezikian

  • 1Department of Medicine, Division of Endocrinology, Metabolic Bone Diseases Unit, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

Current Osteoporosis Reports
|January 12, 2012
PubMed

Insights

Inactivating mutations in the SOST gene lead to high bone mass and strength by reducing sclerostin. Anti-sclerostin antibodies show promise for treating osteoporosis by increasing bone mass.

Area of Science:

  • Genetics and Bone Biology
  • Molecular Endocrinology

Background:

  • The SOST gene encodes sclerostin, a key inhibitor of the Wnt signaling pathway.
  • Loss-of-function mutations in SOST cause sclerosteosis and van Buchem's disease, characterized by high bone mass and density.
  • Sclerostin's role in regulating bone metabolism is crucial for understanding skeletal diseases.

Purpose of the Study:

  • To review the role of SOST gene mutations and sclerostin in bone mass regulation.
  • To explore the therapeutic potential of targeting sclerostin for osteoanabolic therapies.

Main Methods:

  • Review of clinical phenotypes (sclerosteosis, van Buchem's disease) linked to SOST gene mutations.
  • Analysis of the Wnt pathway's regulation by sclerostin.
  • Examination of preclinical and clinical data on anti-sclerostin antibodies.

Main Results:

  • Inactivating SOST mutations lead to reduced sclerostin, Wnt pathway activation, and high bone mass.
  • Individuals with SOST mutations exhibit increased skeletal strength and resistance to fractures.
  • Anti-sclerostin antibodies effectively increase bone mass in animal models and human subjects.

Conclusions:

  • Sclerostin is a critical regulator of bone mass, and its inhibition is osteoanabolic.
  • Targeting sclerostin with antibodies represents a promising therapeutic strategy for osteoporosis and related bone conditions.

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