Bone Disease and Aluminum: Pathogenic Considerations

Abstract

Reductions in the formation of new bone matrix are a consistent finding in both clinical and experimental studies of aluminum-associated bone disease. This adverse effect of aluminum on collagen synthesis may be mediated through reductions in either the number or the cellular activity of osteoblasts. However, diminished matrix synthesis can be dissociated from histologic evidence of defective mineralization during aluminum loading. Thus, the toxicity of aluminum on bone is probably comprised of two components, one affecting collagen synthesis and the other affecting matrix mineralization. Adynamic bone may represent the histologic consequence of primary reductions in the formation of osteoid in the absence of defective matrix calcification. In contrast, concurrent disturbances in both matrix synthesis and calcification may account for the lesion of aluminum-associated osteomalacia. Although consistent with current clinical and experimental observations, confirmation of this hypothesis will require more careful longitudinal studies of bone growth and bone histology during aluminum loading.