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Cellular actions of parathyroid hormone on bone

E. Ambrogini,R. Jilka

Published 2020 in Unknown venue

ABSTRACT

Abstract Parathyroid hormone (PTH) stimulates bone remodeling by modulating the synthesis of critical proosteoclastogenic factors, mainly RANKL, and the level of proosteoblastogenic signals that couple bone formation to bone resorption. Coupling involves growth factors released from the bone matrix during resorption and/or from osteoclasts as well as other PTH-regulated proosteoblastogenic events such as Wnt signaling. In contrast, daily injections of PTH cause bone accretion by improving coupling, resulting in overfill of resorption cavities. This effect is due to inhibition of apoptosis of osteoblasts and their progenitors and to stimulation of differentiation. In addition, intermittent PTH reactivates the quiescent lining cell descendants of osteoblasts. Overfill of resorption cavities and lining cell activation does not occur under physiologic conditions or in hyperparathyroidism. Thus, the anabolic effect of PTH results from the intensification of ongoing mechanisms as well as induction of novel mechanisms that require pulsatile exposure to high levels of PTH.

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