Histomorphometric evidence of deleterious effect of aluminum on osteoblasts

Vernejoul, M. C. De; Belenguer, Ricardo García; Halkidou, H.; Buisine, A.; Bielakoff, J.; Miravet, L

doi:10.1016/8756-3282(85)90401-6

Cited by 48 publications

(14 citation statements)

References 16 publications

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“…The fact that ABD may be seen without histological staining of aluminum (6 cases of 10) is quite unusual since up to now, this bone disease has only been reported with aluminum deposition at the osteoid-calcified bone inter face [14,27,28,[30][31][32], This suggests that factors other than aluminum may be involved in the pathogenesis of this lesion. This hypothesis is further supported by the fact that the plasma concentrations of aluminum are comparable in these patients and in the patients with OF and also because the cumulative doses of aluminum are lower in the ABD group.…”

Section: Relationship Between Aluminum Staining and Bone Status: Emermentioning

confidence: 99%

“…This could be due to a lower aluminum overload. It is known that this latter factor may lead not only to osteomalacia [6,7,12] but also to an osteoblastic depres sion [28,29] with [12,13] or without [14,27] osteopenia. The mechanisms involved in the exteriorization of these various forms of aluminic osteopathy are controversial: for Charhon et al [5,30] PTH may play a predominant role since plasma concentrations of PTH have been found higher in case of osteomalacia: for Andress et al [27] osteomalacia would be favored only by the higher rate of aluminum intoxication since the plasma alumi num concentrations after deferoxamine infusion were higher in case of osteomalacia whereas the plasma con centrations of PTH were comparable in osteomalacic and ABD groups.…”

Section: Prevalence O F the Various Histological Types O F Bone Diseasementioning

confidence: 99%

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Disappearance of Aluminic Bone Disease in a Long Term Asymptomatic Dialysis Population Restricting Al(OH)<sub>3</sub> Intake: Emergence of an Idiopathic Adynamic Bone Disease Not Related to Aluminum

Morinière

Cohen‐Solal

Belbrik

et al. 1989

Nephron

102

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In dialysis centers using reverse osmosis-treated water but not restricting Al(OH)₃ administration, a high prevalence of histological aluminum bone disease has been reported. To assess wether this is also the case in our center where Al(OH)₃ intake has always been restricted and even completely given up after 1980 thanks to high doses of CaCO₃, we reviewed 42 bone biopsies performed between 1975 and 1985 in patients dialyzed for a mean duration of 56 months. Seventeen of these patients had been dialyzed before 1978 with softened water moderately contamined by aluminum, 15 had always been dialyzed with reverse osmosis-treated water and 10 had been exclusively treated by hemofiltration. The prevalence of aluminum bone disease in the whole population was 9.5% (4 patients) and consisted only of adynamic bone disease, osteomalacia being totally absent. When the patients dialyzed with aluminum-contaminated water were excluded as well as 1 diabetic patient who had taken Al(OH)₃ for 1.5 years the prevalence of aluminum bone disease was null in this population. When the whole population is considered the prevalence of the other types of bone disease was 76% for osteitis fibrosa and 14.5% for a non-aluminic adynamic bone disease (6 cases). These latter cases differed from the osteitis fibrosa group only by a relative hypoparathyroidism not explained by higher plasma concentrations and higher oral cumulative doses of calcium, magnesium and aluminum or by lower plasma concentrations of phosphate and bicarbonate. None had previous parathyroidectomy, one had an unsuccessful transplantation and one was diabetic. Iron overload was excluded by negative Perls staining. Duration of dialysis was shorter for these patients than for those with osteitis fibrosa. Conclusions: (1) In the absence of parenteral aluminum contamination, exclusion of Al(OH)₃ allows to prevent completely aluminic bone disease. (2) A new uremic bone disease is described: the idiopathic adynamic bone disease associated with a relative hypoparathyroidism.

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Section: Relationship Between Aluminum Staining and Bone Status: Emermentioning

confidence: 99%

Section: Prevalence O F the Various Histological Types O F Bone Diseasementioning

confidence: 99%

Disappearance of Aluminic Bone Disease in a Long Term Asymptomatic Dialysis Population Restricting Al(OH)<sub>3</sub> Intake: Emergence of an Idiopathic Adynamic Bone Disease Not Related to Aluminum

Morinière

Cohen‐Solal

Belbrik

et al. 1989

Nephron

102

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“…Epidemiological observations do not support as obvi ously the role of aluminum toxicity for ABD as for generalized osteomalacia since this latter and not ABD was the type of aluminum bone disease which presented as an epidemy with a geographical clustering in associa tion with high aluminum content of the tap water and which disappeared after correct treatment of the water by reverse osmosis or deionization [28], ABD has been de scribed mainly in patients with relatively low aluminum burden because the main source of aluminum overload was the ingestion of aluminum-containing phosphate binders [7,[10][11][12][13][14][15].…”

Section: Evidence For the Responsibility Of Aluminum In Adynamic Bonementioning

confidence: 99%

“…i.e. with stainable aluminum covering less than 25% of the trabecular surface but with slightly increased plasma aluminum after deferoxamine or slightly in creased bone aluminum content measured biochemically [10][11][12][13][14][15],…”

Section: Introductionmentioning

confidence: 99%

Adynamic Bone Disease in Uremia: May It Be Idiopathic? Is It an Actual Disease?

Fournier¹,

Morinière²,

Solal

et al. 1991

Nephron

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“…It is characterized by low bone resorption and formation, and, in contrast to osteomalacia, the amount of osteoid tissue is normal or low. The condition was first described in the 1980s and was primarily ascribed to aluminum bone intoxication [1, 2, 3]. Even at the height of the aluminum epidemic, it was however clear that not all cases could be related to aluminum [4].…”

Section: Introductionmentioning

confidence: 99%

Causes and Consequences of Adynamic Bone Disease

Heaf¹

2001

Nephron

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Histomorphometric evidence of deleterious effect of aluminum on osteoblasts

Cited by 48 publications

References 16 publications

Disappearance of Aluminic Bone Disease in a Long Term Asymptomatic Dialysis Population Restricting Al(OH)<sub>3</sub> Intake: Emergence of an Idiopathic Adynamic Bone Disease Not Related to Aluminum

Disappearance of Aluminic Bone Disease in a Long Term Asymptomatic Dialysis Population Restricting Al(OH)<sub>3</sub> Intake: Emergence of an Idiopathic Adynamic Bone Disease Not Related to Aluminum

Adynamic Bone Disease in Uremia: May It Be Idiopathic? Is It an Actual Disease?

Causes and Consequences of Adynamic Bone Disease

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