Evidence map›Paper›PMID 9403706›Full record

ArticleThe American journal of pathology1997

Matrix vesicles in osteomalacic hypophosphatasia bone contain apatite-like mineral crystals.

H C Anderson, H H Hsu, D C Morris, K N Fedde, M P Whyte

Abstract readCase Reports
In one paragraph

Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.7field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 120 citations in OpenAlex.

  1. Trial
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  10. Ablation ofJBMR plus · 2021
    Article
  11. Review
  12. Hypophosphatasia in adolescents and adults: overview of diagnosis and treatment.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2020
    Review
  13. Review
  14. Review
  15. Dental Manifestations of Pediatric Bone Disorders.Current osteoporosis reports · 2017
    Review
  16. Review
  17. Article
  18. Skeletal Mineralization Deficits and Impaired Biogenesis and Function of Chondrocyte-Derived Matrix Vesicles in Phospho1(-/-) and Phospho1/Pi t1 Double-Knockout Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

H C AndersonDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City 66160, USA.
H H Hsu
D C Morris
K N Fedde
M P Whyte
University of Kansas Medical Center · US

Funding

MINERALIZATION STUDIES RELATED TO ORAL BIOLOGYR01DE005262 · NIDCR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ANDERSON, HARRISON CLARKE · 1985 to 2005
$1.8M
NIDCR NIH HHS DEO5262
6 · The paper itself

Abstract

Hypophosphatasia, a heritable disease characterized by deficient activity of the tissue nonspecific isoenzyme of alkaline phosphatase (TNSALP), results in rickets and osteomalacia. Although identification of TNSALP gene defects in hypophosphatasia establishes a role of ALP in skeletal mineralization, the precise function remains unclear. The initial site of mineralization (primary mineralization) normally occurs within the lumen of TNSALP-rich matrix vesicles (MVs) of growth cartilage, bone, and dentin. We investigated whether defective calcification in hypophosphatasia is due to a paucity and/or a functional failure of MVs secondary to TNSALP deficiency. Nondecalcified autopsy bone and growth plate cartilage from five patients with perinatal (lethal) hypophosphatasia were studied by nondecalcified light and electron microscopy to assess MV numbers, size, shape, and ultrastructure and whether hypophosphatasia MVs contain apatite-like mineral, as would be the case if these MVs retained their ability to concentrate calcium and phosphate internally despite a paucity of TNSALP in their investing membranes. We found that hypophosphatasia MVs are present in approximately normal numbers and distribution and that they are capable of initiating internal mineralization. There is retarded extravesicular crystal propagation. Thus, in hypophosphatasia the failure of bones to calcify appears to involve a block of the vectorial spread of mineral from initial nuclei within MVs, outwards, into the matrix. We conclude that hypophosphatasia MVs can concentrate calcium and phosphate internally despite a deficiency of TNSALP activity.

Indexed as

ApatitesBone and BonesBone MatrixCartilageCrystallizationFemaleGrowth PlateHumansHypophosphatasiaInfant, NewbornMaleOsteomalaciaPregnancyApatites

Identifiers

PMID9403706
PMCPMC1858375
OpenAlexW322800605

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.