Abstract
Estrogen receptors critically regulate a number of steps in the pathways in osteoblasts and osteocytes activated by exposure to dynamic mechanical strain. It is these pathways that are responsible for converting the immediate effects of strain change into a coherent stimulus for (re)modelling. It is this stimulus that controls the (re)modelling responsible for matching bones’ architecture to their customary loading. Less effective processing of this strain-related stimulus will have the same downstream effects as the absence of strain. The (re)modelling consequences are the same as those of disuse; bone loss to a genetically determined minimum. Here we review studies showing involvement of the estrogen receptor in a number of bone cells’ early responses to mechanical stimulation. We hypothesise that the structurally inappropriate bone loss in post-menopausal women, and ageing men, that is associated with declining estrogen, is due in part to less effective processing of potentially osteogenic strain-related stimulation in osteoblasts and osteocytes due to reduced availability of estrogen receptors.
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