Does deregulated PHOSPHO1 expression contribute to catabolic bone loss in hyperparathyroid hormone disorders?

A healthy skeleton during ageing is protective against osteoporosis (low bone mass) which causes pain, immobility and fractures.  Current therapies to combat osteoporosis include the use of parathyroid hormone (PTH) which when injected daily to patients can stimulate bone formation.  Intriguingly, in human disorders characterised by a continuous over-production of PTH, low bone mass is observed.  A better understanding of how PTH controls bone mass will help develop therapeutic strategies against bone pathologies induced by excessive PTH. Towards this goal our preliminary novel data has indicated that the amount of PHOSPHO1 – a bone specific protein essential for bone formation – is increased by intermittent PTH treatment; an observation consistent with the anabolic effects of intermittent PTH on bone.  The effects of continuous PTH exposure on PHOSPHO1 production is unknown and in this study we will correlate bone mass and PHOSPHO1 levels in mice treated with continuous PTH.