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The anabolic effect of PTH on bone is mediated by periostin


The impact of periostin (Postn) expression on bone metabolism was investigated by treating adult Postn knockout mice (Postn−/−) and wild-type mice with intermittent parathyroid hormone (PTH). PTH-induced bone markers were significantly lower in the periosteum of the Postn−/− mice, which also showed a lower response to PTH in terms of increases in bone mass, cortical bone volume and strength response.

Analysis of Wnt–β-catenin signaling demonstrated that the increased activity in this pathway, which is normally stimulated by PTH, did not occur in mice that lacked Postn. PTH stimulation of Postn expression normally inhibits Sost through the αVβ3 receptor and reduces expression of MEF2C. Postn therefore plays a crucial role in the anabolic response that occurs in the periosteum in response to PTH by suppressing Sost expression in osteocytes, stimulating osteoblasts and boosting Wnt signaling.

A potential therapeutic application is suggested by the observation that the PTH response in Postn−/− mice (an increase in bone mass) was partially restored by treatment with an anti-Sost antibody.

Editor's comment: It is interesting to examine whether the reduction in the anabolic effect of PTH after long-term daily injections is associated with a reduction in Postn expression. If that is the case, by increasing the expression of Postn, the anabolic effect of PTH may be enhanced and prolonged.

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