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Avascular Necrosis (cont.)

Avascular Necrosis Causes

While the precise mechanism for the development of avascular necrosis is not known, it is suspected that interruption of the blood supply to the affected bone plays some role. This can occur when traumatic impact injures the blood vessels to the bone or when diseases produce areas of abnormal circulation.

There are many causes of avascular necrosis, but the vast majority of avascular necrosis is caused by either traumatic injury to the affected bone (such as fracture and dislocation), steroid medication usage (glucocorticoid medications such as prednisone and prednisolone, particularly when given in high doses), or excessive alcohol consumption.

Other risk factors for developing avascular necrosis include cigarette smoking, pregnancy, radiation and chemotherapy treatments, bone marrow and blood diseases (including sickle cell disease, leukemia, Gaucher's disease, thalassemia), and underwater diver's disease (from bone affects of Caisson disease, also known as dysbarism or "the bends"). Avascular necrosis occurs more frequently in patients with certain underlying diseases, including systemic lupus erythematosus, diabetes mellitus, vasculitis, and inflammatory bowel disease.

It is currently suspected by some researchers that intravenous bisphosphonate medications, including zoledronate (Zometa) and pamidronate (Aredia), which are used to reduce elevated calcium levels in patients with cancer and to treat osteoporosis, may increase the risk of avascular necrosis of the jaw bone. Ironically, bisphosphonates are actually used by some to treat the bone pain and decrease disability in patients with avascular necrosis (see treatment section below).

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