Evidence map›Paper›PMID 38315213›Full record

ReviewEndocrine reviews2024

Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone.

Natalie Y Y Koh, Justyna J Miszkiewicz, Mary Louise Fac, Natalie K Y Wee, Natalie A Sims

Abstract readReview
In one paragraph

Review in Endocrine reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  6. Review
  7. Bone Organoids: A Novel Tool for Modeling and Managing Skeletal Disorders in Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
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  14. Article
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  17. Article
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  20. Observational
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.

Natalie Y Y KohBone Cell Biology & Disease Unit, St. Vincent's Institute of Medical Research, Fitzroy, VIC 3065, Australia.ORCID 0009-0007-6339-2207
Justyna J MiszkiewiczSchool of Social Science, The University of Queensland, Brisbane, QLD 4072, Australia.ORCID 0000-0002-9769-2706
Mary Louise FacBone Cell Biology & Disease Unit, St. Vincent's Institute of Medical Research, Fitzroy, VIC 3065, Australia.ORCID 0000-0001-5660-2770
Natalie K Y WeeBone Cell Biology & Disease Unit, St. Vincent's Institute of Medical Research, Fitzroy, VIC 3065, Australia.ORCID 0000-0002-7314-2646
Natalie A SimsBone Cell Biology & Disease Unit, St. Vincent's Institute of Medical Research, Fitzroy, VIC 3065, Australia.ORCID 0000-0003-1421-8468

Funding

an EH Flack Fellowship from the MarionAustralian Research CouncilNHMRCphilanthropic support to StUniversity of Melbourne
6 · The paper itself

Abstract

Preclinical models (typically ovariectomized rats and genetically altered mice) have underpinned much of what we know about skeletal biology. They have been pivotal for developing therapies for osteoporosis and monogenic skeletal conditions, including osteogenesis imperfecta, achondroplasia, hypophosphatasia, and craniodysplasias. Further therapeutic advances, particularly to improve cortical strength, require improved understanding and more rigorous use and reporting. We describe here how trabecular and cortical bone structure develop, are maintained, and degenerate with aging in mice, rats, and humans, and how cortical bone structure is changed in some preclinical models of endocrine conditions (eg, postmenopausal osteoporosis, chronic kidney disease, hyperparathyroidism, diabetes). We provide examples of preclinical models used to identify and test current therapies for osteoporosis, and discuss common concerns raised when comparing rodent preclinical models to the human skeleton. We focus especially on cortical bone, because it differs between small and larger mammals in its organizational structure. We discuss mechanisms common to mouse and human controlling cortical bone strength and structure, including recent examples revealing genetic contributors to cortical porosity and osteocyte network configurations during growth, maturity, and aging. We conclude with guidelines for clear reporting on mouse models with a goal for better consistency in the use and interpretation of these models.

Indexed as

Cortical BoneDisease Models, AnimalAnimalsBone DiseasesHumansMiceRatsRodentiaageingbone developmentcortical bonecortical porositymouse modelsosteocytesosteoporosispreclinical research

Identifiers

PMID38315213
PMCPMC11244217

What OpenQuestion holds

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LicenceCC BY
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.