Chronic elevation of parathyroid hormone in mice reduces expression of sclerostin by osteocytes: a novel mechanism for hormonal control of osteoblastogenesis.

By T. Bellido, A. A. Ali, I. Gubrij, L. Plotkin, Q. Fu, Charles A. O’Brien, S. Manolagas, R. Jilka. Endocrinology, 2005

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Molecular and cellular mechanisms of the anabolic effect of intermittent PTH. (2007, background): “Administration of PTH to mice or rats caused a transient reduction in the level of sclerostin mRNA, the product of the Sost gene that is expressed exclusively in osteocytes [4,94].”
The Amazing Osteocyte (2010, background): “Mechanical loading also has been reported to reduce sclerostin expression,((50)) as does parathyroid hormone (PTH), which may account for some of the anabolic effect of PTH on bone formation.((51,52)) PTH also appears to reduce sclerostin levels in patients.”
From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. (2010, background): “Moreover, NAC suppresses Wnt-stimulated -catenin/TCF-mediated transcription, whereas it is well established that PTH stimulates Wnt signaling by suppressing the Wnt antagonist sclerostin (357, 358) and by activating LRP6 (96).”
Growth hormone, insulin-like growth factors, and the skeleton. (2008, background): “PTH decreases the expression of the Wnt antagonist, sclerostin, potentially leading to enhanced Wnt signaling, although Wnt signaling is not required to detect anabolic effects of PTH in murine models (171, 172).”