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Cancellous Bone

Anatomy and Physiology · NLM MeSH · updated 2026-10-31 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

A type of osseous tissue which makes up the inner part of bone.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (754 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

A type of osseous tissue which makes up the inner part of bone. It has a spongy, honeycomb-like structure with struts or trabecula and contains the bone marrow. It has higher rate of bone remodeling turnover than cortical bone.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Bone, Cancellous; Bones, Cancellous; Cancellous Bones; Spongy Bone; Bone, Spongy; Bones, Spongy; Spongy Bones; Trabecular Bone.

Where it fits in the MeSH classification

Broader topics
Bone and Bones

Related concepts

  • Bone Marrow
  • Bone Remodeling
  • Cortical Bone

Research landscape

PubMed indexes 2,628 records tagged with the MeSH heading “Cancellous Bone” (counts retrieved 2026-10-31). 1,469 of them (55.9%) were published from 2020 onward, and the busiest period so far is 2020 onward with 1,469 records.

Reviews account for 101 records (3.8%) and meta-analyses for 14. Randomized controlled trials number 47 (1.8%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.

PubMed records by publication periodthrough 1999: 0 records; 2000-2009: 0 records; 2010-2019: 1,230 records; 2020 onward: 1,469 records0through 199902000-20091,2302010-20191,4692020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19990
2000-20090
2010-20191,230
2020 onward1,469
Share of records by publication typeReviews: 3.8 percent; Meta-analyses: 0.5 percent; Randomized controlled trials: 1.8 percentReviews3.8% (101)Meta-analyses0.5% (14)Randomized controlled trials1.8% (47)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 2,628 PubMed records
TypeRecordsShare
Reviews1013.8%
Meta-analyses140.5%
Randomized controlled trials471.8%

Method: PubMed query "Cancellous Bone"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.

Reading the evidence in anatomy and physiology

Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
11β-HSD1 plays a critical role in trabecular bone loss associated with systemic glucocorticoid therapy
Fenton CG, Doig CL, Fareed S, Naylor A, Morrell AP, Addison O, et al.
2019Research article
Design not recorded in structured metadata
40cc by
PMID 31420008 · DOI · PMC6698000
Sub-trabecular strain evolution in human trabecular bone
Turunen MJ, Le Cann S, Tudisco E, Lovric G, Patera A, Hall SA, et al.
2020Research article
Design not recorded in structured metadata
36cc by
PMID 32796859 · DOI · PMC7429852
RSPO3 is important for trabecular bone and fracture risk in mice and humans
Nilsson KH, Henning P, El Shahawy M, Nethander M, Andersen TL, Ejersted C, et al.
2021Research article
Design not recorded in structured metadata
33cc by
PMID 34389713 · DOI · PMC8363747
Trabecular architecture of the medullary cavity: a comprehensive review of radiological patterns, pathological alterations
Chapala S, Kiyawat V, Gibson J, Chinniah P, Arora S, Shah A, et al.
2026Review article
Design not recorded in structured metadata
0cc by
PMID 42536418 · DOI · PMC13687762

11β-HSD1 plays a critical role in trabecular bone loss associated with systemic glucocorticoid therapy [1]

Research article Fenton CG, Doig CL, Fareed S, Naylor A, Morrell AP, Addison O, et al. · · 2019 · cited 40 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundDespite their efficacy in the treatment of chronic inflammation, the prolonged application of therapeutic glucocorticoids (GCs) is limited by significant systemic side effects including glucocorticoid-induced osteoporosis (GIOP).
Closing excerpt
This raises the intriguing possibility that therapeutic inhibitors of 11β-HSD1 may be effective in preventing GIOP in patients receiving therapeutic steroids.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (255 words)

BackgroundDespite their efficacy in the treatment of chronic inflammation, the prolonged application of therapeutic glucocorticoids (GCs) is limited by significant systemic side effects including glucocorticoid-induced osteoporosis (GIOP). 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) is a bi-directional enzyme that primarily activates GCs in vivo, regulating tissue-specific exposure to active GC. We aimed to determine the contribution of 11β-HSD1 to GIOP.MethodsWild type (WT) and 11β-HSD1 knockout (KO) mice were treated with corticosterone (100 μg/ml, 0.66% ethanol) or vehicle (0.66% ethanol) in drinking water over 4 weeks (six animals per group). Bone parameters were assessed by micro-CT, sub-micron absorption tomography and serum markers of bone metabolism. Osteoblast and osteoclast gene expression was assessed by quantitative RT-PCR.ResultsWild type mice receiving corticosterone developed marked trabecular bone loss with reduced bone volume to tissue volume (BV/TV), trabecular thickness (Tb.Th) and trabecular number (Tb.N). Histomorphometric analysis revealed a dramatic reduction in osteoblast numbers. This was matched by a significant reduction in the serum marker of osteoblast bone formation P1NP and gene expression of the osteoblast markers Alp and Bglap. In contrast, 11β-HSD1 KO mice receiving corticosterone demonstrated almost complete protection from trabecular bone loss, with partial protection from the decrease in osteoblast numbers and markers of bone formation relative to WT counterparts receiving corticosterone.ConclusionsThis study demonstrates that 11β-HSD1 plays a critical role in GIOP, mediating GC suppression of anabolic bone formation and reduced bone volume secondary to a decrease in osteoblast numbers. This raises the intriguing possibility that therapeutic inhibitors of 11β-HSD1 may be effective in preventing GIOP in patients receiving therapeutic steroids.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31420008 · DOI · PMC6698000

Sub-trabecular strain evolution in human trabecular bone [2]

Research article Turunen MJ, Le Cann S, Tudisco E, Lovric G, Patera A, Hall SA, et al. · · 2020 · cited 36 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
To comprehend the most detrimental characteristics behind bone fractures, it is key to understand the material and tissue level strain limits and their relation to failure sites.
Closing excerpt
In summary, this study investigated the local strains in whole trabecular structure at sub-trabecular resolution in human bone and confirmed the high strain magnitudes reported for single trabeculae under loading and, importantly extends its translation to the whole trabecular structure.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (237 words)

To comprehend the most detrimental characteristics behind bone fractures, it is key to understand the material and tissue level strain limits and their relation to failure sites. The aim of this study was to investigate the three-dimensional strain distribution and its evolution during loading at the sub-trabecular level in trabecular bone tissue. Human cadaver trabecular bone samples were compressed in situ until failure, while imaging with high-resolution synchrotron radiation X-ray tomography. Digital volume correlation was used to determine the strains inside the trabeculae. Regions without emerging damage were compared to those about to crack. Local strains in close vicinity of developing cracks were higher than previously reported for a whole trabecular structure and similar to those reported for single isolated trabeculae. Early literature on bone fracture strain thresholds at the tissue level seem to underestimate the maximum strain magnitudes in trabecular bone. Furthermore, we found lower strain levels and a reduced ability to capture detailed crack-paths with increased image voxel size. This highlights the dependence between the observed strain levels and the voxel size and that high-resolution is needed to investigate behavior of individual trabeculae. Furthermore, low trabecular thickness appears to be one predictor of developing cracks. In summary, this study investigated the local strains in whole trabecular structure at sub-trabecular resolution in human bone and confirmed the high strain magnitudes reported for single trabeculae under loading and, importantly extends its translation to the whole trabecular structure.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32796859 · DOI · PMC7429852

RSPO3 is important for trabecular bone and fracture risk in mice and humans [3]

Research article Nilsson KH, Henning P, El Shahawy M, Nethander M, Andersen TL, Ejersted C, et al. · · 2021 · cited 33 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
With increasing age of the population, countries across the globe are facing a substantial increase in osteoporotic fractures.
Closing excerpt
In conclusion, RSPO3 regulates vertebral trabecular bone mass and bone strength in mice and fracture risk in humans.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)

With increasing age of the population, countries across the globe are facing a substantial increase in osteoporotic fractures. Genetic association signals for fractures have been reported at the RSPO3 locus, but the causal gene and the underlying mechanism are unknown. Here we show that the fracture reducing allele at the RSPO3 locus associate with increased RSPO3 expression both at the mRNA and protein levels, increased trabecular bone mineral density and reduced risk mainly of distal forearm fractures in humans. We also demonstrate that RSPO3 is expressed in osteoprogenitor cells and osteoblasts and that osteoblast-derived RSPO3 is the principal source of RSPO3 in bone and an important regulator of vertebral trabecular bone mass and bone strength in adult mice. Mechanistic studies revealed that RSPO3 in a cell-autonomous manner increases osteoblast proliferation and differentiation. In conclusion, RSPO3 regulates vertebral trabecular bone mass and bone strength in mice and fracture risk in humans.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34389713 · DOI · PMC8363747

Trabecular architecture of the medullary cavity: a comprehensive review of radiological patterns, pathological alterations [4]

Review article Chapala S, Kiyawat V, Gibson J, Chinniah P, Arora S, Shah A, et al. · · 2026

Abstract reading summary — source excerpts
Opening excerpt
The trabecular bone of the medullary cavity is a complex 3D lattice essential for skeletal load distribution and metabolic homeostasis.
Closing excerpt
Understanding these morphological transitions is critical for the early detection of systemic metabolic diseases and the monitoring of localized mechanical failure.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (112 words)

The trabecular bone of the medullary cavity is a complex 3D lattice essential for skeletal load distribution and metabolic homeostasis. This article provides a narrative review of trabecular architecture, ranging from hierarchical nanoscopic fibrils to macroscopic stress trajectories. We analyze the radiological appearance of normal and pathological alterations, including thickening, breakage, faintness, rarefaction, and infiltration. Modalities such as high-resolution MRI, dual-energy CT, and the emerging photon-counting detector CT are evaluated for their diagnostic precision. Furthermore, we examine clinical indices like the Singh Index and the growing role of opportunistic CT screening. Understanding these morphological transitions is critical for the early detection of systemic metabolic diseases and the monitoring of localized mechanical failure.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42536418 · DOI · PMC13687762

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article A review of trabecular bone functional adaptation: what have we learned from trabecular analyses in extant hominoids and what can we apply to fossils? [5]
    Kivell TL · J Anat · 2016 · cited 135 times (Europe PMC)
  • Research article Use of Trabecular Bone Score (TBS) as a Complementary Approach to Dual-energy X-ray Absorptiometry (DXA) for Fracture Risk Assessment in Clinical Practice [6]
    Shevroja E, Lamy O, Kohlmeier L, Koromani F, Rivadeneira F, Hans D · J Clin Densitom · 2017 · cited 133 times (Europe PMC)
  • Research article Young's modulus of trabecular bone at the tissue level: A review [7]
    Wu D, Isaksson P, Ferguson SJ, Persson C · Acta Biomater · 2018 · cited 122 times (Europe PMC)
  • Research article Dual-energy X-ray Absorptiometry Monitoring with Trabecular Bone Score: 2019 ISCD Official Position [8]
    Krohn K, Schwartz EN, Chung YS, Lewiecki EM · J Clin Densitom · 2019 · cited 86 times (Europe PMC)
  • Research article The Trabecular Bone Score (TBS) Complements DXA and the FRAX as a Fracture Risk Assessment Tool in Routine Clinical Practice [9]
    Hans D, Šteňová E, Lamy O · Curr Osteoporos Rep · 2017 · cited 81 times (Europe PMC)
  • Research article Association between trabecular bone score and type 2 diabetes: a quantitative update of evidence [10]
    Ho-Pham LT, Nguyen TV · Osteoporos Int · 2019 · cited 78 times (Europe PMC)

References

  1. Fenton CG, Doig CL, Fareed S, Naylor A, Morrell AP, Addison O, et al.. 11β-HSD1 plays a critical role in trabecular bone loss associated with systemic glucocorticoid therapy. . 2019. PMID 31420008 · DOI · PMC6698000
  2. Turunen MJ, Le Cann S, Tudisco E, Lovric G, Patera A, Hall SA, et al.. Sub-trabecular strain evolution in human trabecular bone. . 2020. PMID 32796859 · DOI · PMC7429852
  3. Nilsson KH, Henning P, El Shahawy M, Nethander M, Andersen TL, Ejersted C, et al.. RSPO3 is important for trabecular bone and fracture risk in mice and humans. . 2021. PMID 34389713 · DOI · PMC8363747
  4. Chapala S, Kiyawat V, Gibson J, Chinniah P, Arora S, Shah A, et al.. Trabecular architecture of the medullary cavity: a comprehensive review of radiological patterns, pathological alterations. . 2026. PMID 42536418 · DOI · PMC13687762
  5. Kivell TL. A review of trabecular bone functional adaptation: what have we learned from trabecular analyses in extant hominoids and what can we apply to fossils?. J Anat. 2016. PMID 26879841 · DOI
  6. Shevroja E, Lamy O, Kohlmeier L, Koromani F, Rivadeneira F, Hans D. Use of Trabecular Bone Score (TBS) as a Complementary Approach to Dual-energy X-ray Absorptiometry (DXA) for Fracture Risk Assessment in Clinical Practice. J Clin Densitom. 2017. PMID 28734710 · DOI
  7. Wu D, Isaksson P, Ferguson SJ, Persson C. Young's modulus of trabecular bone at the tissue level: A review. Acta Biomater. 2018. PMID 30081232 · DOI
  8. Krohn K, Schwartz EN, Chung YS, Lewiecki EM. Dual-energy X-ray Absorptiometry Monitoring with Trabecular Bone Score: 2019 ISCD Official Position. J Clin Densitom. 2019. PMID 31383412 · DOI
  9. Hans D, Šteňová E, Lamy O. The Trabecular Bone Score (TBS) Complements DXA and the FRAX as a Fracture Risk Assessment Tool in Routine Clinical Practice. Curr Osteoporos Rep. 2017. PMID 28988401 · DOI
  10. Ho-Pham LT, Nguyen TV. Association between trabecular bone score and type 2 diabetes: a quantitative update of evidence. Osteoporos Int. 2019. PMID 31214749 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-31.

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All 542 articles in Anatomy and Physiology →

At a glance

2,628
PubMed records on this heading
56%
published since 2020
101
review articles
47
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

Related topics See all →

  • Cortical BoneAnatomy and Physiology
  • Bone MatrixAnatomy and Physiology
  • PeriosteumAnatomy and Physiology
  • Bone MarrowAnatomy and Physiology
  • CalcaneusAnatomy and Physiology

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