Osteocyte-derived RANKL is a critical mediator of the increased bone resorption caused by dietary calcium deficiency.

ABSTRACT: Parathyroid hormone (PTH) excess stimulates bone resorption. This effect is associated with increased expression of the osteoclastogenic cytokine receptor activator of nuclear factor κB ligand (RANKL) in bone. However, several different cell types, including bone marrow stromal cells, osteocytes, and T lymphocytes, express both RANKL and the PTH receptor and it is unclear whether RANKL expression by any of these cell types is required for PTH-induced bone loss. Here we have used mice lacking the RANKL gene in osteocytes to determine whether RANKL produced by this cell type is required for the bone loss caused by secondary hyperparathyroidism induced by dietary calcium deficiency in adult mice. Thirty days of dietary calcium deficiency caused bone loss in control mice, but this effect was b

SUBMITTER: Xiong J 

PROVIDER: S-EPMC4125539 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature