Hypophosphatemia and Osteoblast Function in Human Bone Disease

Parfitt, A. M.; Villanueva, A. R.

doi:10.1007/978-1-4684-4259-5_27

Cited by 17 publications

(34 citation statements)

References 6 publications

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“…In aluminum-loaded animals, mineralized bone formation at the tissue level was substantially reduced from con- trol values in conjunction with reductions in the extent of double tetracycline labeling, and fewer osteoid seams were characterized by the presence of osteoblasts in Al. Thus, the number of sites of active bone formation was markedly altered by the administration of aluminum (7,8,(1)(2)(3)(4)(5)(6)(7)(8). The corrected rates of mineralized bone apposition were also low in Al, but the calculation of this variable of bone dynamics is based upon the fraction of osteoid surfaces that label with tetracycline (7,8).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the number of sites of active bone formation was markedly altered by the administration of aluminum (7,8,(1)(2)(3)(4)(5)(6)(7)(8). The corrected rates of mineralized bone apposition were also low in Al, but the calculation of this variable of bone dynamics is based upon the fraction of osteoid surfaces that label with tetracycline (7,8). Therefore, the corrected values for bone apposition only confirm the tissuebased measurements of bone formation in animals given aluminum.…”

Section: Discussionmentioning

confidence: 99%

“…5-rum sections of bone were stained using the modified Goldner technique and examined by light microscopy (14-16); 10-/im sections were mounted unstained in 10% glycerol and viewed by ejifluorescent illumination for the evaluation of tetracycline labels (14, 15). 5-,um sections were also stained by the aurine iricarboxylic acid method for histochemical determinations of the aluminum content of bone (9,14,15 of mineralized bone apposition, MARU is the uncorrected rate of mineralized bone apposition as determined from the width of separation of double tetracycline labels, and Fract1,b is the fraction of osteoid surfaces labeled with tetracycline (7,8). The total length of double tetracyclinelabeled bone surface plus one-half of the length of single tetracyclinelabeled surface was used for the calculation ofFract, (7,18).…”

Section: Methodsmentioning

confidence: 99%

“…The total length of double tetracyclinelabeled bone surface plus one-half of the length of single tetracyclinelabeled surface was used for the calculation ofFract, (7,18). The values for MARC represent the rate of apposition of mineralized bone averaged over the life span of an osteoid seam (7,8). The mineralization lag time was calculated by dividing the mean osteoid seam width by the corrected rate of mineralized bone apposition; the results are expressed in days.…”

Section: Methodsmentioning

confidence: 99%

“…Since bone formation may be suppressed in aluminum-related bone disease without concurrent histologic evidence of osteoid accumulation, it is possible that aluminum adversely affects the formation of bone and/or the synthesis ofcollagen in a manner independent of the putative role of aluminum to inhibit the process of mineralization. Bone blasts or as a consequence of reductions in the total number of active osteoblasts (7,8). Observations from clinical bone biopsy material indicate that the extent of active bone-forming surface is reduced in both the osteomalacic and aplastic lesions of aluminum-associated bone disease as judged by diminished or absent tetracycline uptake into bone (3,5,6,9).…”

Section: Introductionmentioning

confidence: 99%

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Tissue and cellular basis for impaired bone formation in aluminum-related osteomalacia in the pig.

Sedman¹,

Alfrey²,

Miller³

et al. 1987

J. Clin. Invest.

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Bone formation is impaired in aluminum-associated bone disease. Reductions in the number of osteoblasts or in the function of individual osteoblasts could account for this finding. Thus, quantitative bone histology and measurements of bone formation were done at three skeletal sites in piglets given aluminum (Al) parenterally, 1.5 mg/kg per d, for 8 wk (Al, n = 4) and in control animals (C, n = 4). Bone Al was 241±40 mg/kg per dry weight in Al and 1.6±0.9 in C, P < 0.001. All Al-treated animals developed osteomalacia with increases in osteoid seam width, osteoid volume, and mineralization lag time at each skeletal site, P < 0.05 vs. C for all values. Mineralized bone formation at the tissue level was lower in Al than in C, P < 0.05 for each skeletal site, due to reductions in active bone forming surface. Bone formation at the cellular level was similar in each group, however, and total osteoid production by osteoblasts did not differ in C and Al. Aluminum impairs the formation of mineralized bone in vivo by decreasing the number of active osteoblasts, and this change can be distinguished from the effect of aluminum to inhibit, either directly or indirectly, the calcification of osteoid. IntroductionReductions in the rate of formation of bone are a hallmark of

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Tissue and cellular basis for impaired bone formation in aluminum-related osteomalacia in the pig.

Sedman¹,

Alfrey²,

Miller³

et al. 1987

J. Clin. Invest.

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Errors in bone remodeling: Toward a unified theory of metabolic bone disease

1989

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Recent evidence suggests that skeletal adaptation is organized by a functional unit that includes cells of diverse origin working in coordination. Genetic and metabolic factors control and regulate the processes of modeling and remodeling, only rarely acting on the isolated individual functions of specific cell lines. Errors in the genetic or metabolic regulation of the functional unit affect the entire process of skeletal adaptation rather than specific elements of it. Viewed in this way, some metabolic bone diseases can be understood as relatively simple errors in factors that control the coordinated activities of the entire functional unit. This paper reviews the modeling and remodeling processes and demonstrates how abnormal morphological characteristics of bone tissue can be viewed as products of specific errors in the adaptive process.

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