Experimental aluminum-induced bone disease: studies in vivo.

The administration of aluminum to experimental animals can induce osteomalacia in previously normal bone. Aluminum exposure impairs the synthesis of new bone matrix which reduces bone formation. A specific action of aluminum to inhibit the mineralization of bone in vivo has not yet been demonstrated. The role of parathyroid hormone in the pathogenesis of the osteomalacia that develops after aluminum loading also remains uncertain. However, the occurrence of both osteomalacia and impaired bone formation in experimental animals following aluminum administration has been documented in the absence of reductions in the serum levels of PTH. The results of the animal studies completed to date are consistent with a direct adverse effect of aluminum to suppress new bone formation. This response of bone may be mediated through a toxic effect of aluminum on the osteoblast. Whether aluminum also disrupts the mineralization of bone by a mechanism separate from its effect on the osteoblast requires additional study.
AuthorsW G Goodman
JournalKidney international. Supplement (Kidney Int Suppl) Vol. 18 Pg. S32-6 (Feb 1986) ISSN: 0098-6577 [Print] UNITED STATES
PMID3517461 (Publication Type: Journal Article, Review)
Chemical References
  • Dihydroxycholecalciferols
  • Parathyroid Hormone
  • Aluminum
  • Aluminum (toxicity)
  • Animals
  • Calcification, Physiologic (drug effects)
  • Chick Embryo
  • Dihydroxycholecalciferols (metabolism)
  • Dogs
  • Kidney (metabolism)
  • Osteogenesis (drug effects)
  • Osteomalacia (chemically induced)
  • Parathyroid Hormone (secretion)
  • Rats

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