Aluminum localization in bone from hemodialyzed patients: Relationship to matrix mineralization

Abstract

It has been suggested that in uremic bone, aluminum interferes with normal mineralization. Aluminum content and aluminum localization were studied in iliac crest biopsies of two groups of patients on regular hemodialysis; one group had histologic osteomalacia, and little or no bone resorption (group 1); the other, osteitis fibrosa and no mineralization defect (group 2). Group 1 patients had significantly higher plasma aluminum concentrations than those of group 2. No difference was found in bone aluminum content, which was above normal in both groups. In the bone samples of the osteomalacic subjects, aluminum was mainly localized at the limit between osteoid and calcified tissue, the site where the bone mineral is normally first deposited. Osteomalacia could not be related to hypocalcemia or to phosphate depletion. Active vitamin D derivatives (25-hydroxycholecalciferol and 1alpha-hydroxycholecalciferol) failed to prevent or to improve the bone disease. In the bone samples of group 2 subjects, aluminum could not be localized by the methods used, except in the two cases with greatly elevated bone aluminum, where it was mainly localized on cement lines. In group 2 subjects, immunoreactive parathyroid hormone plasma concentration, osteoclast surface, and marrow fibrosis were significantly higher than they were in group 1 subjects. It is concluded that in bone from uremic patients on regular dialysis, aluminum can induce a particular form of osteomalacia, resistant to the vitamin D active derivatives. The bone disease is only observed in the absence of severe secondary hyperparathyroidism. This suggests that parathyroid hormone may be involved in the development of the aluminum-induced mineralization defect.

Bactericidal strontium-releasing injectable bone cements based on bioactive glasses

“…chains by Al 3þ ); however, as aluminium is a known neurotoxin [20] and also negatively affects bone mineralization [21][22][23], dental GPCs are not ideal for orthopaedic applications. Efforts have been made to replace aluminium with iron [24] or zinc [25]; however, these also have drawbacks and particularly too high a zinc release has been shown to result in cytotoxic reactions [26].…”

Nutritional Aspects of Aluminium Toxicity

“…Patients with end-stage renal disease were undergoing haemodialysis with Al-contaminated water (Platts et al 1977;Parkinson et al 1979) or receiving oral Alcontaining phosphate-binding gels, or both (Bournerais et al 1983;Andreoli et al 1984 In both types of patients Al was located in the bone-osteoid surface either by histochemical staining with aurin tricarboxylic acid (Buchanan et al 1981 ;Ott et al 1982Ott et al , 1983 or by electron-microprobe analysis (Cournot-Witmer et al 1981). The stain was quantified by measuring the amount of surface taking up the stain.…”

Mechanism Underlying the Aluminum-Induced Stimulation of Bone Nodule Formation by Rat Calvarial Osteoblasts

“…[1][2][3][4][5][6][7][8][9] It has been shown in the present study that the short term treatment of calvarial osteoblasts with Al 3+ at 10 -7 M increases the BN formation. Serum levels of Al 3+ in normal subjects are in the order of 10 -7 M, while those in patients with end-stage renal disease undergoing hemodialysis therapy often exceed 5 × 10 -6 M. 23,24) It is therefore possible that the physiological level of Al 3+ serves as a positive regulator of bone formation although in vivo experiments in which the circulating level of Al 3+ is maintained at a low concentration range will be required to prove this assumption.…”

“…[1][2][3][4] However, the mechanism by which Al 3+ produces the osteodystrophy is controversial. Decreased numbers of osteoblasts and accumulation of Al 3+ at the mineralization front have been observed in human biopsy samples [5][6][7] and in bone tissues from experimental animal models, 8) suggesting that Al 3+ may physicochemically inhibit the formation and growth of hy-…”