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Bone adaptation optimizes mass and structure, but the mechano-response is already reduced at maturation. Downregulation of sclerostin was believed to be a mandatory step in mechano-adaptation, but in young mice it was shown that load-induced formation can occur independent of sclerostin, a product of the  Sost  gene. We hypothesized that the bone formation and resorption response to loading is not affected by  Sost  deficiency, but is age-specific. Our findings indicate that the anabolic response to  in vivo  tibial loading was reduced at maturation in  Sost  Knockout (KO) and littermate control (LC) mice. Age affected all anabolic and catabolic parameters and altered  Sost  and Wnt target gene expression. While load-induced cortical resorption was similar between genotypes, loading-induced gains in mineralizing surface was enhanced in  Sost KO  compared to LC mice. Loading led to a downregulation in expression of the Wnt inhibitor  Dkk1 . Expression of  Dkk1  was greater in both control and loaded limbs of  Sost  KO compared to LC mice suggesting a compensatory role in the absence of  Sost . These data suggest physical activity could enhance bone mass concurrently with sclerostin-neutralizing antibodies, but treatment strategies should consider the influence of age on ultimate load-induced bone mass gains.

Sost deficiency led to a greater cortical bone formation response to mechanical loading and altered gene expression