[Parathyroid hormone : its anabolic action on bone]

PTH actions on bone are exerted through multiple pathways from G-proteins coupled to a receptor PTH1R that is expressed on osteoblastic lineage cells. Physiological action of PTH may be through increased expression of RANKL, resulting in increased bone resorption and Ca( + + ) release from bone matrix by osteoclasts. Bone anabolic action of PTH by intermittent treatment is explained by ( I ) proliferation of osteogenic precursor cells, ( II ) differentiation of osteoblasts, ( III ) inhibition of apoptosis in osteoblastic cells, and ( IV ) inhibition of canonical Wnt inhibitor secretion from osteocytes. Two of these mechanisms ( II and III ) could be secondary to increased osteoclastogenesis after induction of RANKL in osteoblastic cells. Mechanisms involved in ( I ) might be controversial depending on cellular status including differentiation stages and cell density, and thus need to be clarified by further studies.