 The effects of OFC on bone are largely dependent on the duration of the disease and the level of parathyroid hormone (PTH) produced. PTH is responsible for maintaining a homeostatic calcium concentration in the blood. It activates the parathyroid-hormone related protein receptor located on osteoblasts and osteocytes, both of which are responsible for the building and calcification of bone. Abnormalities affecting the parathyroid glands cause a surplus of PTH, which, in turn, increases the activity and frequency of osteoblasts and osteocytes. Increased PTH levels trigger the release of stored calcium through the dissolution of old bone, as well as the conservation of serum calcium through a cessation in the production of new bone.
