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Targeted Deletion of the Sclerostin Gene in Mice Results in Increased Bone Formation and Bone Strength

Journal of Bone and Mineral Research · 2008 · Vol. 23(6) · pp. 860–869

Xiaodong Li(Amgen (United States))Michael S. Ominsky(Amgen (United States))Qing‐Tian Niu(Amgen (United States))Ning Sun(Amgen (United States))Betsy Daugherty(Amgen (United States))Diane D’Agostin(Amgen (United States))Carole Kurahara(Amgen (United States))Yongming Gao(Amgen (United States))Jin Cao(Amgen (United States))Jianhua Gong(Amgen (United States))Frank Asuncion(Amgen (United States))Mauricio Barrero(Amgen (United States))Kelly Warmington(Amgen (United States))Denise Dwyer(Amgen (United States))Marina Stolina(Amgen (United States))Sean Morony(Amgen (United States))Ildiko Sarosi(Amgen (United States))Paul J. Kostenuik(Amgen (United States))David L. Lacey(Amgen (United States))W. Scott Simonet(Amgen (United States))Hua Zhu Ke(Amgen (United States))Chris Pászty✉(Amgen (United States))

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Abstract

SOST KO mice have a high bone mass phenotype characterized by marked increases in BMD, bone volume, bone formation, and bone strength. These results show that sclerostin is a key negative regulator of a powerful, evolutionarily conserved bone formation pathway that acts on both trabecular and cortical bone.

Bone health and osteoporosis research Bone Metabolism and Diseases Dermatological and Skeletal DisordersSclerostinFemurOsteoclastOsteoblastBone mineralOsteocyteInternal medicineEndocrinologyOsteoporosisDensitometry

MeSH terms

AnimalsBone and BonesCalciumFemaleGenetic MarkersGlycoproteinsMaleOsteogenesisPhenotypePhosphatesStress, MechanicalTomography, X-Ray ComputedBiomarkersBone DensityGene Deletion