Evidence map›Paper›PMID 34196732›Full record

ReviewCellular and molecular life sciences : CMLS2021

Cortical bone development, maintenance and porosity: genetic alterations in humans and mice influencing chondrocytes, osteoclasts, osteoblasts and osteocytes.

Tsuyoshi Isojima, Natalie A Sims

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 70 citations in OpenAlex.

  1. Bone organic matrix quality indices associate with fragility fracture occurrence independently of bone mineral density values.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
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  4. miR-433 targets BMP and Indian hedgehog signaling to coordinate murine postnatal growth plate dynamics.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
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  12. Review
  13. Effects of stress on bone health in children.Frontiers in endocrinology · 2025
    Review
  14. Review
  15. Article
  16. Review
  17. Bone Loss in Diabetes Mellitus: Diaporosis.International journal of molecular sciences · 2024
    Review
  18. 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

2 authors at 2 institutions in 2 countries.

Tsuyoshi IsojimaSt. Vincent's Institute of Medical Research, 9 Princes St, Fitzroy, VIC, 3122, Australia.ORCID http://orcid.org/0000-0003-0011-0325
Natalie A SimsSt. Vincent's Institute of Medical Research, 9 Princes St, Fitzroy, VIC, 3122, Australia. nsims@svi.edu.au.ORCID http://orcid.org/0000-0003-1421-8468
St Vincent's Hospital Melbourne · AUSt Vincents Institute of Medical Research · AU

Funding

National Health and Medical Research Council 1154819
6 · The paper itself

Abstract

Cortical bone structure is a crucial determinant of bone strength, yet for many years studies of novel genes and cell signalling pathways regulating bone strength have focused on the control of trabecular bone mass. Here we focus on mechanisms responsible for cortical bone development, growth, and degeneration, and describe some recently described genetic-driven modifications in humans and mice that reveal how these processes may be controlled. We start with embryonic osteogenesis of preliminary bone structures preceding the cortex and describe how this structure consolidates then matures to a dense, vascularised cortex containing an increasing proportion of lamellar bone. These processes include modelling-induced, and load-dependent, asymmetric cortical expansion, which enables the cortex's transition from a highly porous woven structure to a consolidated and thickened highly mineralised lamellar bone structure, infiltrated by vascular channels. Sex-specific differences emerge during this process. With aging, the process of consolidation reverses: cortical pores enlarge, leading to greater cortical porosity, trabecularisation and loss of bone strength. Each process requires co-ordination between bone formation, bone mineralisation, vascularisation, and bone resorption, with a need for locational-, spatial- and cell-specific signalling pathways to mediate this co-ordination. We will discuss these processes, and a number of cell-signalling pathways identified in both murine and human genetic studies to regulate cortical bone mass, including signalling through gp130, STAT3, PTHR1, WNT16, NOTCH, NOTUM and sFRP4.

Indexed as

AnimalsBone DevelopmentChondrocytesCortical BoneHumansOsteoblastsOsteoclastsOsteocytesPorositySignal TransductionBone growthBone strengthCortical boneCortical porosityNotumsFRP4

Identifiers

PMID34196732
PMCPMC11073036
OpenAlexW3176734525

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.