Osteitis fibrosa is a complication of hyperparathyroidism, a condition in which certain bones become abnormally weak and deformed.
The parathyroid glands are 4 tiny glands in the neck. These glands produce parathyroid hormone (PTH). PTH helps control calcium, phosphorus, and vitamin D levels in the blood and is important for healthy bones.
Too much parathyroid hormone (hyperparathyroidism) can lead to increased bone breakdown, which can cause bones to become weaker and more fragile. Many people with hyperparathyroidism develop osteoporosis. Not all bones respond to PTH in the same way. Some develop abnormal areas where the bone is very soft and has almost no calcium in it. This is osteitis fibrosa.
In rare cases, parathyroid cancer causes osteitis fibrosa.
Osteitis fibrosa may cause bone pain or tenderness. There may be fractures (breaks) in the arms, legs, or spine, or other bone problems.
Hyperparathyroidism itself may cause any of the following:
- Frequent urination
Exams and Tests
Blood tests show a high level of calcium, parathyroid hormone, and alkaline phosphatase (a bone chemical). Phosphorus level in the blood may be low.
Most of the bone problems from osteitis fibrosa can be reversed with surgery to remove the abnormal parathyroid gland(s). Some people may choose not to have surgery, and instead be followed with blood tests and bone measurements.
If surgery is not possible, medicines can sometimes be used to lower calcium level.
When to Contact a Medical Professional
Call your health care provider if you have bone pain, tenderness, or symptoms of hyperparathyroidism.
Routine blood tests done during a medical checkup or for another health problem usually detect a high calcium level before severe damage is done.
Osteitis fibrosa cystica; Hyperparathyroidism - osteitis fibrosa
Silverberg SJ, Bilezikian JP. Primary hyperparathyroidism. In: Jameson JL, De Groot LJ, de Kretser DM, et al, eds. Endocrinology: Adult and Pediatric. 7th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 63.
Thakker RV. The parathyroid glands, hypercalcemia and hypocalcemia. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine. 25th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 245.
Review Date 5/2/2016
Updated by: Brent Wisse, MD, Associate Professor of Medicine, Division of Metabolism, Endocrinology & Nutrition, University of Washington School of Medicine, Seattle, WA. Also reviewed by David Zieve, MD, MHA, Isla Ogilvie, PhD, and the A.D.A.M. Editorial team.