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 osteoclasts and osteocytes, both of which are responsible for the breakdown and maintaining of bone.
 Abnormalities affecting the parathyroid glands cause a surplus of PTH, which, in turn, increases the activity and frequency of osteoclasts 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.

Generally, the first bones to be affected are the fingers, facial bones, ribs, and pelvis.
Long bones, which are longer than they are wide, are also among the first affected.
As the disease progresses, any bone may be affected.
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 osteoclasts and osteocytes, both of which are responsible for the breakdown and maintaining of bone.  Abnormalities affecting the parathyroid glands cause a surplus of PTH, which, in turn, increases the activity and frequency of osteoclasts 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.
Generally, the first bones to be affected are the fingers, facial bones, ribs, and pelvis. Long bones, which are longer than they are wide, are also among the first affected. As the disease progresses, any bone may be affected.
Osteitis fibrosa cystica