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 (752 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 outer layer of bone. It is dense, rigid, strong, and forms concentric lamellar osteons.
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: Compact Bones; Compact Bone; Compact Bone Tissue; Substantia Compacta.
Where it fits in the MeSH classification
- Broader topics
- Bone and Bones
- Narrower topics
- Haversian System
Related concepts
- Osteons
Research landscape
PubMed indexes 2,888 records tagged with the MeSH heading “Cortical Bone” (counts retrieved 2026-10-31). 1,139 of them (39.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,159 records.
Reviews account for 119 records (4.1%) and meta-analyses for 16. Randomized controlled trials number 25 (0.9%) 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.
Show the data
| Period | Records |
|---|---|
| through 1999 | 412 |
| 2000-2009 | 178 |
| 2010-2019 | 1,159 |
| 2020 onward | 1,139 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 119 | 4.1% |
| Meta-analyses | 16 | 0.6% |
| Randomized controlled trials | 25 | 0.9% |
Method: PubMed query "Cortical 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 / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Osteocyte RANKL is required for cortical bone loss with age and is induced by senescence | 2020 | Research article Design not recorded in structured metadata | 103 | cc by PMID 32870816 · DOI · PMC7566701 |
| Assessing matrix quality by Raman spectroscopy helps predict fracture toughness of human cortical bone | 2019 | Research article Design not recorded in structured metadata | 60 | cc by PMID 31076574 · DOI · PMC6510799 |
| Periosteal CD68+ F4/80+ Macrophages Are Mechanosensitive for Cortical Bone Formation by Secretion and Activation of TGF-β1 | 2022 | Research article Design not recorded in structured metadata | 58 | cc by PMID 34854257 · DOI · PMC8787385 |
| Direct MRI of collagen | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42241079 · DOI · PMC13236022 |
Osteocyte RANKL is required for cortical bone loss with age and is induced by senescence [1]
Abstract reading summary — source excerpts
- Opening excerpt
- In aging mice, osteoclast number increases in cortical bone but declines in trabecular bone, suggesting that different mechanisms underlie age-associated bone loss in these 2 compartments.
- Closing excerpt
- Our results demonstrate the requirement of osteocyte-derived RANKL for age-associated cortical bone loss and suggest that increased Tnfsf11 expression with age results from accumulation of senescent cells in cortical bone.
- 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 (197 words)
In aging mice, osteoclast number increases in cortical bone but declines in trabecular bone, suggesting that different mechanisms underlie age-associated bone loss in these 2 compartments. Osteocytes produce the osteoclastogenic cytokine RANKL, encoded by Tnfsf11. Tnfsf11 mRNA increases in cortical bone of aged mice, suggesting a mechanism underlying the bone loss. To address this possibility, we aged mice lacking RANKL in osteocytes. Whereas control mice lost cortical bone between 8 and 24 months of age, mice lacking RANKL in osteocytes gained cortical bone during this period. Mice of both genotypes lost trabecular bone with age. Osteoclasts increased with age in cortical bone of control mice but not in RANKL conditional knockout mice. Induction of cellular senescence increased RANKL production in murine and human cell culture models, suggesting an explanation for elevated RANKL levels with age. Overexpression of the senescence-associated transcription factor Gata4 stimulated Tnfsf11 expression in cultured murine osteoblastic cells. Finally, elimination of senescent cells from aged mice using senolytic compounds reduced Tnfsf11 mRNA in cortical bone. Our results demonstrate the requirement of osteocyte-derived RANKL for age-associated cortical bone loss and suggest that increased Tnfsf11 expression with age results from accumulation of senescent cells in cortical bone.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32870816 · DOI · PMC7566701
Assessing matrix quality by Raman spectroscopy helps predict fracture toughness of human cortical bone [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Developing clinical tools that assess bone matrix quality could improve the assessment of a person's fracture risk.
- Closing excerpt
- While Raman-derived matrix properties appear useful to the assessment of fracture resistance of bone, the acquisition strategy to resolve the Amide I band needs to be identified.
- 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 (214 words)
Developing clinical tools that assess bone matrix quality could improve the assessment of a person's fracture risk. To determine whether Raman spectroscopy (RS) has such potential, we acquired Raman spectra from human cortical bone using microscope- and fiber optic probe-based Raman systems and tested whether correlations between RS and fracture toughness properties were statistically significant. Calculated directly from intensities at wavenumbers identified by second derivative analysis, Amide I sub-peak ratio I1670/I1640, not I1670/I1690, was negatively correlated with Kinit (N = 58; R2 = 32.4%) and J-integral (R2 = 47.4%) when assessed by Raman micro-spectroscopy. Area ratios (A1670/A1690) determined from sub-band fitting did not correlate with fracture toughness. There were fewer correlations between RS and fracture toughness when spectra were acquired by probe RS. Nonetheless, the I1670/I1640 sub-peak ratio again negatively correlated with Kinit (N = 56; R2 = 25.6%) and J-integral (R2 = 39.0%). In best-fit general linear models, I1670/I1640, age, and volumetric bone mineral density explained 50.2% (microscope) and 49.4% (probe) of the variance in Kinit. I1670/I1640 and v1PO4/Amide I (microscope) or just I1670/I1640 (probe) were negative predictors of J-integral (adjusted-R2 = 54.9% or 37.9%, respectively). While Raman-derived matrix properties appear useful to the assessment of fracture resistance of bone, the acquisition strategy to resolve the Amide I band needs to be identified.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31076574 · DOI · PMC6510799
Periosteal CD68+ F4/80+ Macrophages Are Mechanosensitive for Cortical Bone Formation by Secretion and Activation of TGF-β1 [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Mechanical force regulates bone density, modeling, and homeostasis.
- Closing excerpt
- The results suggest that periosteal myeloid-lineage cells respond to mechanical forces and consequently produce and activate TGF-β1 for periosteal bone formation.
- 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 (182 words)
Mechanical force regulates bone density, modeling, and homeostasis. Substantial periosteal bone formation is generated by external mechanical stimuli, yet its mechanism is poorly understood. Here, it is shown that myeloid-lineage cells differentiate into subgroups and regulate periosteal bone formation in response to mechanical loading. Mechanical loading on tibiae significantly increases the number of periosteal myeloid-lineage cells and the levels of active transforming growth factor β (TGF-β), resulting in cortical bone formation. Knockout of Tgfb1 in myeloid-lineage cells attenuates mechanical loading-induced periosteal bone formation in mice. Moreover, CD68+ F4/80+ macrophages, a subtype of myeloid-lineage cells, express and activate TGF-β1 for recruitment of osteoprogenitors. Particularly, mechanical loading induces the differentiation of periosteal CD68+ F4/80- myeloid-lineage cells to the CD68+ F4/80+ macrophages via signaling of piezo-type mechanosensitive ion channel component 1 (Piezo1) for TGF-β1 secretion. Importantly, CD68+ F4/80+ macrophages activate TGF-β1 by expression and secretion of thrombospondin-1 (Thbs1). Administration of Thbs1 inhibitor significantly impairs loading-induced TGF-β activation and recruitment of osteoprogenitors in the periosteum. The results suggest that periosteal myeloid-lineage cells respond to mechanical forces and consequently produce and activate TGF-β1 for periosteal bone formation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34854257 · DOI · PMC8787385
Direct MRI of collagen [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Collagen is the most abundant protein in the human body and has an important role in healthy tissue as well as in a range of prevalent diseases.
- Closing excerpt
- This capability suggests significant promise for biomedical science and clinical use.
- 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 (159 words)
Collagen is the most abundant protein in the human body and has an important role in healthy tissue as well as in a range of prevalent diseases. Medical research and diagnostics, hence, call for means of mapping collagen in vivo. Magnetic resonance imaging (MRI) is a natural candidate for this task, offering full 3D capability and versatile contrast non-invasively. However, collagen has so far been invisible to MRI due to extremely short lifetime of its resonances. Here, we report the direct imaging of collagen in vivo by magnetic resonance on the microsecond scale. The dynamics of resonance signals from collagen were first assessed in samples of bovine tendon and cortical bone. On this basis, imaging was performed at echo times down to 10 microseconds, yielding collagen-specific depiction by echo subtraction. The same approach was then extended for use in vivo, enabling direct collagen imaging of a human forearm. This capability suggests significant promise for biomedical science and clinical use.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42241079 · DOI · PMC13236022
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 The Role of Water Compartments in the Material Properties of Cortical Bone [5]
- Research article Quantitative 3D analysis of the canal network in cortical bone by micro-computed tomography [6]
- Research article Quantitative Computed Tomography-Current Status and New Developments [7]
- Research article Cortical Bone Porosity: What Is It, Why Is It Important, and How Can We Detect It? [8]
- Research article Woven bone overview: structural classification based on its integral role in developmental, repair and pathological bone formation throughout vertebrate groups [9]
- Research article Nuclear magnetic resonance studies of bone water [10]
References
- Kim HN, Xiong J, MacLeod RS, Iyer S, Fujiwara Y, Cawley KM, et al.. Osteocyte RANKL is required for cortical bone loss with age and is induced by senescence. . 2020. PMID 32870816 · DOI · PMC7566701
- Unal M, Uppuganti S, Timur S, Mahadevan-Jansen A, Akkus O, Nyman JS. Assessing matrix quality by Raman spectroscopy helps predict fracture toughness of human cortical bone. . 2019. PMID 31076574 · DOI · PMC6510799
- Deng R, Li C, Wang X, Chang L, Ni S, Zhang W, et al.. Periosteal CD68+ F4/80+ Macrophages Are Mechanosensitive for Cortical Bone Formation by Secretion and Activation of TGF-β1. . 2022. PMID 34854257 · DOI · PMC8787385
- Van Schoor JD, Weiger M, Baadsvik EL, Pruessmann KP. Direct MRI of collagen. . 2026. PMID 42241079 · DOI · PMC13236022
- Granke M, Does MD, Nyman JS. The Role of Water Compartments in the Material Properties of Cortical Bone. Calcif Tissue Int. 2015. PMID 25783011 · DOI · PMC4526331
- Cooper DM, Turinsky AL, Sensen CW, Hallgrímsson B. Quantitative 3D analysis of the canal network in cortical bone by micro-computed tomography. Anat Rec B New Anat. 2003. PMID 12964207 · DOI
- Engelke K. Quantitative Computed Tomography-Current Status and New Developments. J Clin Densitom. 2017. PMID 28712984 · DOI
- Cooper DM, Kawalilak CE, Harrison K, Johnston BD, Johnston JD. Cortical Bone Porosity: What Is It, Why Is It Important, and How Can We Detect It?. Curr Osteoporos Rep. 2016. PMID 27623679 · DOI
- Shapiro F, Wu JY. Woven bone overview: structural classification based on its integral role in developmental, repair and pathological bone formation throughout vertebrate groups. Eur Cell Mater. 2019. PMID 31571191 · DOI
- Wehrli FW, Fernández-Seara MA. Nuclear magnetic resonance studies of bone water. Ann Biomed Eng. 2005. PMID 15709708 · 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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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.