AIBD is characterized either by a low turnover osteomalacia or by an aplastic disease. Chemical analyses have shown these conditions to be present when bone aluminum levels are between 12 and 500 mgg-1. High levels of the metal in diseased bones have also been demonstrated using aluminum-specific histochemical bone stains.
Aluminum-induced osteodystrophic osteomalacia develops in the absence of hypophosphatemia. The condition does not respond to vitamin D therapy, but it may be prevented by hyperparathyroidism. The disease is progressive and produces a variety of symptoms, including severe bone pain, muscle pains, and multiple nontraumatic fractures. It is normal for AIBD patients to remain asymptomatic for many years before physical signs of the disease, including funnel chest deformity, sternal bowing, and loss of height, become evident.
At the histological level, AIBD is characterized by a low rate of bone formation. The disease is variable, but bone removed from most patients show an increased amount of unmineralized osteoid; an increase in bone volume; a very low rate of bone apposition; a patchy, irregular pattern of calcification; a reduction in the number of active osteoblasts and osteoclasts; and irregular, misshaped bone trabeculae.
Although the causation of AIBD is not firmly established, it seems likely that it is produced by impaired bone matrix mineralization and by decreased osteoclastic activity. The progress of AIBD may be halted, and even reversed, by repeated administration of the chelating agent desferrioximine.
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