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2014 ; 66
(ä): 146-54
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Osteocyte-derived RANKL is a critical mediator of the increased bone resorption
caused by dietary calcium deficiency
#MMPMID24933342
Xiong J
; Piemontese M
; Thostenson JD
; Weinstein RS
; Manolagas SC
; O'Brien CA
Bone
2014[Sep]; 66
(ä): 146-54
PMID24933342
show ga
Parathyroid hormone (PTH) excess stimulates bone resorption. This effect is
associated with increased expression of the osteoclastogenic cytokine receptor
activator of nuclear factor ?B 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 blunted in mice lacking RANKL in osteocytes. The increase in RANKL
expression in bone and the increase in osteoclast number caused by dietary
calcium deficiency were also blunted in mice lacking RANKL in osteocytes. These
results demonstrate that RANKL produced by osteocytes contributes to the
increased bone resorption and the bone loss caused by secondary
hyperparathyroidism, strengthening the evidence that osteocytes are an important
target cell for hormonal control of bone remodeling.