Attenuated bone aluminum deposition in nonuremic beagles with reduced bone remodeling

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Abstract

Excess bone aluminum accumulates in uremic subjects after parathyroidectomy. To evaluate whether decreased bone remodeling caused by parathyroidectomy augments bone aluminum deposition, we administered aluminum chloride (0.75 mg/kg iv 3 times/wk) or vehicle to thyroparathyroidectomized (TPTX) and sham-operated (Sham) nonuremic beagles for 8 wk. TPTX alone effectively lowered plasma parathyroid hormone concentrations (8.2 ± 2.8 vs. 27 ± 2.2 pg/ml) and consequently suppressed bone remodeling, as evidenced by the diminished resorptive surface (0.8 ± 0.3 vs. 4.0 ± 0.5%), osteoid surface (0.5 ± 0.2 vs. 13.3 ± 2.3%), and bone formation rate (1.8 ± 0.6 vs. 15.5 ± 2.2%/yr) compared with untreated Shams. Aluminum treatment resulted in no further suppression of bone remodeling in TPTX dogs and did not cause osteomalacia. Aluminum-treated TPTX dogs, however, accumulated much less total bone (28.1 ± 4.5 μg/g) and surface aluminum (3.8 ± 1.4%) than similarly treated Shams (61.4 ± 5.6 μg/g; 12.2 ± 2.7%, respectively) despite displaying higher plasma aluminum concentrations (1,209 ± 330 vs. 181 ± 18 μg/l). These observations illustrate that diminished bone turnover retards rather than augments bone aluminum accumulation. Thus bone aluminum deposition after parathyroidectomy in uremic subjects is not likely to be the result of passive aluminum accumulation on inactive bone surface. Further studies are needed to determine whether factors, such as prior bone aluminum accumulation and/or the degree of preexistent hyperosteoidosis, modulate aluminum accumulation after parathyroidectomy.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume258
Issue number4 21-4
StatePublished - 1990
Externally publishedYes

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Bone Remodeling
Aluminum
Bone
Bone and Bones
Parathyroidectomy
Dogs
Osteomalacia
Plasmas
Parathyroid Hormone
Osteogenesis

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Endocrinology
  • Physiology

Cite this

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title = "Attenuated bone aluminum deposition in nonuremic beagles with reduced bone remodeling",
abstract = "Excess bone aluminum accumulates in uremic subjects after parathyroidectomy. To evaluate whether decreased bone remodeling caused by parathyroidectomy augments bone aluminum deposition, we administered aluminum chloride (0.75 mg/kg iv 3 times/wk) or vehicle to thyroparathyroidectomized (TPTX) and sham-operated (Sham) nonuremic beagles for 8 wk. TPTX alone effectively lowered plasma parathyroid hormone concentrations (8.2 ± 2.8 vs. 27 ± 2.2 pg/ml) and consequently suppressed bone remodeling, as evidenced by the diminished resorptive surface (0.8 ± 0.3 vs. 4.0 ± 0.5{\%}), osteoid surface (0.5 ± 0.2 vs. 13.3 ± 2.3{\%}), and bone formation rate (1.8 ± 0.6 vs. 15.5 ± 2.2{\%}/yr) compared with untreated Shams. Aluminum treatment resulted in no further suppression of bone remodeling in TPTX dogs and did not cause osteomalacia. Aluminum-treated TPTX dogs, however, accumulated much less total bone (28.1 ± 4.5 μg/g) and surface aluminum (3.8 ± 1.4{\%}) than similarly treated Shams (61.4 ± 5.6 μg/g; 12.2 ± 2.7{\%}, respectively) despite displaying higher plasma aluminum concentrations (1,209 ± 330 vs. 181 ± 18 μg/l). These observations illustrate that diminished bone turnover retards rather than augments bone aluminum accumulation. Thus bone aluminum deposition after parathyroidectomy in uremic subjects is not likely to be the result of passive aluminum accumulation on inactive bone surface. Further studies are needed to determine whether factors, such as prior bone aluminum accumulation and/or the degree of preexistent hyperosteoidosis, modulate aluminum accumulation after parathyroidectomy.",
author = "Leigh Quarles",
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T1 - Attenuated bone aluminum deposition in nonuremic beagles with reduced bone remodeling

AU - Quarles, Leigh

PY - 1990

Y1 - 1990

N2 - Excess bone aluminum accumulates in uremic subjects after parathyroidectomy. To evaluate whether decreased bone remodeling caused by parathyroidectomy augments bone aluminum deposition, we administered aluminum chloride (0.75 mg/kg iv 3 times/wk) or vehicle to thyroparathyroidectomized (TPTX) and sham-operated (Sham) nonuremic beagles for 8 wk. TPTX alone effectively lowered plasma parathyroid hormone concentrations (8.2 ± 2.8 vs. 27 ± 2.2 pg/ml) and consequently suppressed bone remodeling, as evidenced by the diminished resorptive surface (0.8 ± 0.3 vs. 4.0 ± 0.5%), osteoid surface (0.5 ± 0.2 vs. 13.3 ± 2.3%), and bone formation rate (1.8 ± 0.6 vs. 15.5 ± 2.2%/yr) compared with untreated Shams. Aluminum treatment resulted in no further suppression of bone remodeling in TPTX dogs and did not cause osteomalacia. Aluminum-treated TPTX dogs, however, accumulated much less total bone (28.1 ± 4.5 μg/g) and surface aluminum (3.8 ± 1.4%) than similarly treated Shams (61.4 ± 5.6 μg/g; 12.2 ± 2.7%, respectively) despite displaying higher plasma aluminum concentrations (1,209 ± 330 vs. 181 ± 18 μg/l). These observations illustrate that diminished bone turnover retards rather than augments bone aluminum accumulation. Thus bone aluminum deposition after parathyroidectomy in uremic subjects is not likely to be the result of passive aluminum accumulation on inactive bone surface. Further studies are needed to determine whether factors, such as prior bone aluminum accumulation and/or the degree of preexistent hyperosteoidosis, modulate aluminum accumulation after parathyroidectomy.

AB - Excess bone aluminum accumulates in uremic subjects after parathyroidectomy. To evaluate whether decreased bone remodeling caused by parathyroidectomy augments bone aluminum deposition, we administered aluminum chloride (0.75 mg/kg iv 3 times/wk) or vehicle to thyroparathyroidectomized (TPTX) and sham-operated (Sham) nonuremic beagles for 8 wk. TPTX alone effectively lowered plasma parathyroid hormone concentrations (8.2 ± 2.8 vs. 27 ± 2.2 pg/ml) and consequently suppressed bone remodeling, as evidenced by the diminished resorptive surface (0.8 ± 0.3 vs. 4.0 ± 0.5%), osteoid surface (0.5 ± 0.2 vs. 13.3 ± 2.3%), and bone formation rate (1.8 ± 0.6 vs. 15.5 ± 2.2%/yr) compared with untreated Shams. Aluminum treatment resulted in no further suppression of bone remodeling in TPTX dogs and did not cause osteomalacia. Aluminum-treated TPTX dogs, however, accumulated much less total bone (28.1 ± 4.5 μg/g) and surface aluminum (3.8 ± 1.4%) than similarly treated Shams (61.4 ± 5.6 μg/g; 12.2 ± 2.7%, respectively) despite displaying higher plasma aluminum concentrations (1,209 ± 330 vs. 181 ± 18 μg/l). These observations illustrate that diminished bone turnover retards rather than augments bone aluminum accumulation. Thus bone aluminum deposition after parathyroidectomy in uremic subjects is not likely to be the result of passive aluminum accumulation on inactive bone surface. Further studies are needed to determine whether factors, such as prior bone aluminum accumulation and/or the degree of preexistent hyperosteoidosis, modulate aluminum accumulation after parathyroidectomy.

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