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It’s been over 100 years since the discovery of parathyroid hormone (PTH), yet the in vivo mechanisms of action of PTH at the cellular and molecular levels are still not well understood. Despite a wealth of in vitro studies, none predicted the anabolic effect of PTH on the skeleton. The anabolic effect of PTH was initially observed using parathyroid gland extract (PTE) in young rats and rabbits (1, 2). At the time, the models were thought to reproduce, in part, the pathologic processes of hyperparathyroidism, in which an early destructive phase was followed by an ebullient reparative phase of bone formation (1). After the successful synthesis of hPTH 1-34 in the early 1970s (3), its anabolic phenomenon was revisited, and small clinical trials suggested that PTH could be used as an anabolic therapy for osteoporosis (4, 5). The data were viewed with scepticism, because the literature at the time was dominated by the notion that PTH was a hormone controlling calcium homeostasis, in part by stimulating bone resorption. In vitro, embryonic bone organ culture studies confirmed the original in vivo studies with PTE, by showing that PTH initially stimulated resorption and had a delayed, stimulatory effect on the rate of matrix synthesis (6). These data supported the concept of “coupling” between resorption and formation, with PTH as a key stimulator of bone turnover (6). However, in vivo data from rats and humans showed that PTH stimulated bone formation de novo, without a prior episode of resorption (7, 8).

Stemming bone loss by suppressing apoptosis