Osteitis fibrosa is a complication of hyperparathyroidism in which certain bones become abnormally weak and deformed.
Osteitis fibrosa cystica
The parathyroid glands are four glands in the neck that help control calcium use and removal by the body. They do this by producing parathyroid hormone, or PTH. PTH helps control calcium, phosphorus, and vitamin D levels within the blood and bone.
Too much parathyroid hormone (hyperparathyroidism) can lead to increased bone breakdown, which can cause bones to become weaker and more fragile. Many people with hyperthyroidism 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.
Rarely, parathyroid cancer may cause osteitis fibrosa.
Before 1950, about half of people diagnosed with hyperparathyroidism had osteitis fibrosa. Now it is uncommon, probably because patients with hyperparathyroidism are diagnosed earlier, before this complication has occurred.
People with severe hyperparathyroidism have a higher risk for developing 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 may cause nausea, constipation, fatigue, frequent urination, and weakness.
Exams and Tests
Blood tests show a high level of calcium, parathyroid hormone, and alkaline phosphatase (a bone chemical). Phosphorus may be low.
A bone x-ray may be done. People with hyperparathyroidism are more likely to have osteopenia (thin bones) or osteoporosis (very thin bones) than to have full-blown osteitis fibrosa.
Most of the bone problems from osteitis fibrosa can be reversed with surgery to remove the abnormal parathyroid gland(s). However, some people may choose to not have surgery, and instead be followed with blood tests and bone measurements.
If surgery is not possible, medications can sometimes be used to lower calcium levels.
Wysolmerski JJ. Insogna KL. The parathyroid glands, hypercalcemia, and hypocalcemia. In: Kronenberg HM, Schlomo M, Polansky KS, Larsen PR, eds. Williams Textbook of Endocrinology. 11th ed. St. Louis, MO: Elsevier Saunders; 2008:chap 266.
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.