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 (619 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
The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.
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: Marrow, Bone; Red Marrow; Marrow, Red; Yellow Marrow; Marrow, Yellow; Marrow.
Where it fits in the MeSH classification
- Broader topics
- Immune System
Research landscape
PubMed indexes 74,816 records tagged with the MeSH heading “Bone Marrow” (counts retrieved 2026-10-31). 7,840 of them (10.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 46,045 records.
Reviews account for 5,658 records (7.6%) and meta-analyses for 109. Randomized controlled trials number 575 (0.8%) 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.
Show the data
| Period | Records |
|---|---|
| through 1999 | 46,045 |
| 2000-2009 | 8,788 |
| 2010-2019 | 12,143 |
| 2020 onward | 7,840 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,658 | 7.6% |
| Meta-analyses | 109 | 0.1% |
| Randomized controlled trials | 575 | 0.8% |
Method: PubMed query "Bone Marrow"[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 |
|---|---|---|---|---|
| Bone marrow breakout lesions act as key sites for tumor-immune cell diversification in multiple myeloma | 2025 | Research article Design not recorded in structured metadata | 23 | cc by PMID 39919199 · DOI · PMC7619224 |
| Inflammatory stromal and T cells mediate human bone marrow niche remodeling in clonal hematopoiesis and myelodysplasia | 2025 | Research article Design not recorded in structured metadata | 21 | cc by PMID 41253811 · DOI · PMC12627676 |
| Single-cell spatial transcriptomics reveals immunotherapy-driven bone marrow niche remodeling in AML | 2025 | Research article Design not recorded in structured metadata | 21 | cc by PMID 40632867 · DOI · PMC12239967 |
| comBO: A combined human bone and lympho-myeloid bone marrow organoid for preclinical modeling of hematopoietic disorders | 2026 | Research article Design not recorded in structured metadata | 12 | cc by PMID 41734765 · DOI · PMC7618947 |
Bone marrow breakout lesions act as key sites for tumor-immune cell diversification in multiple myeloma [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The bone marrow microenvironment plays a crucial role in the development of multiple myeloma.
- Closing excerpt
- These analyses identify breakout lesions as a hotspot for tumor-immune cell interactions and diversification, representing a key event in myeloma pathogenesis.
- 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 (149 words)
The bone marrow microenvironment plays a crucial role in the development of multiple myeloma. As the disease progresses, malignant myeloma cells can evolve to survive outside the bone marrow. However, the processes underlying bone marrow independence and their consequences for immune control remain poorly understood. Here, we conducted single-cell and spatial multiomics analyses of bone marrow-confined intramedullary disease and paired breakout lesions that disrupt the cortical bone. These analyses revealed a distinct cellular microenvironment and architectural features of breakout lesions, characterized by extensive areas of malignant plasma cells interspersed with lesion-specific solitary natural killer and macrophage populations, as well as focal accumulations of immune cell agglomerates. Within these agglomerates, spatially confined T cell clones expanded alongside various immune cells, coinciding with the local genomic evolution of tumor cells. These analyses identify breakout lesions as a hotspot for tumor-immune cell interactions and diversification, representing a key event in myeloma pathogenesis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39919199 · DOI · PMC7619224
Inflammatory stromal and T cells mediate human bone marrow niche remodeling in clonal hematopoiesis and myelodysplasia [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Somatic mutations in hematopoietic stem/progenitor cells (HSPCs) can lead to clonal hematopoiesis of indeterminate potential (CHIP) and progression to myelodysplastic syndromes (MDS).
- Closing excerpt
- These findings position iMSCs as central mediators of early BM niche dysfunction and potential therapeutic targets for intercepting pre-malignant hematopoiesis.
- 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 (175 words)
Somatic mutations in hematopoietic stem/progenitor cells (HSPCs) can lead to clonal hematopoiesis of indeterminate potential (CHIP) and progression to myelodysplastic syndromes (MDS). Using single-cell and anatomical profiling of a large cohort of human bone marrow (BM), we show that the HSPC BM niche in CHIP and MDS is undergoing inflammatory remodeling. This includes loss of CXCL12⁺ adipogenic stromal cells and the emergence of a distinct population of inflammatory mesenchymal stromal cells (iMSCs), which arise in CHIP and become more prevalent in MDS. Functional studies in primary BM HSPC-MSC co-cultures reveals that healthy aged and CHIP HSPCs activate stromal support, while MDS HSPCs fail to do so. In contrast, MDS blasts further suppress HSPC support and trigger inflammation, indicating disease-stage-specific stromal disruption. In parallel, we show that iMSCs retain partial support and angiogenic potential in MDS, coinciding with expanded BM vasculature. Additionally, we identify IFN-responsive T cells that preferentially interact with iMSCs, potentially reinforcing local inflammation. These findings position iMSCs as central mediators of early BM niche dysfunction and potential therapeutic targets for intercepting pre-malignant hematopoiesis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41253811 · DOI · PMC12627676
Single-cell spatial transcriptomics reveals immunotherapy-driven bone marrow niche remodeling in AML [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Given the graft-versus-leukemia effect observed with allogeneic hematopoietic stem cell transplantation in refractory or relapsed acute myeloid leukemia (AML), immunotherapies have been explored in nontransplant settings.
- Closing excerpt
- These findings provide insights into immune interactions in AML and may inform therapeutic strategies.
- 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 (142 words)
Given the graft-versus-leukemia effect observed with allogeneic hematopoietic stem cell transplantation in refractory or relapsed acute myeloid leukemia (AML), immunotherapies have been explored in nontransplant settings. We applied a multiomic approach to examine bone marrow interactions in patients with AML treated with pembrolizumab and decitabine. Using extensively trained nuclear and membrane segmentation models, we achieved precise transcript assignment and deep learning-based image analysis. To address read-depth limitations, we integrated single-cell RNA sequencing with single-cell spatial transcriptomics from the same sample. Quantifying cell-cell distances at the edge level enabled more accurate tumor microenvironment analysis, revealing global and local immune cell enrichment near leukemia cells postpembrolizumab treatment, potentially linked to clinical response. Furthermore, ligand-receptor analysis indicated potential alterations in specific signaling pathways between leukemia and immune cells following immunotherapy treatment. These findings provide insights into immune interactions in AML and may inform therapeutic strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40632867 · DOI · PMC12239967
comBO: A combined human bone and lympho-myeloid bone marrow organoid for preclinical modeling of hematopoietic disorders [4]
Abstract reading summary — source excerpts
- Opening excerpt
- The bone marrow is the primary site of blood and immune cell production in postnatal life.
- Closing excerpt
- comBOs offer a physiologically faithful bone marrow platform for disease modeling and therapeutic discovery in translational hematology and immunology.
- 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 (153 words)
The bone marrow is the primary site of blood and immune cell production in postnatal life. Current human models do not capture lympho-myeloid hematopoiesis and the stromal diversity needed for lifelong blood and immune maintenance. Here, we introduce comBO (combined bone and lympho-myeloid bone marrow organoid), a scalable induced pluripotent stem cell (iPSC)-derived system that generates osteolineage, vascular, lymphoid, and myeloid compartments within a single organoid. Developed under physioxia in granular microgel scaffolds, comBOs improve scalability and reproducibility and sustain long-term lympho-myeloid potential in serial organoid re-seeding assays. Incorporating healthy or malignant donor cells produces "chimeroids" that model physiological and pathological states. Using multiple myeloma as an exemplar, comBOs recapitulate niche remodeling and identify macrophage inhibitory factor (MIF) signaling as a disease driver. MIF inhibition reduces inflammation and myeloma proliferation, highlighting its therapeutic potential. comBOs offer a physiologically faithful bone marrow platform for disease modeling and therapeutic discovery in translational hematology and immunology.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41734765 · DOI · PMC7618947
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 Macrophages in health and disease [5]
- Research article Sources and Clinical Applications of Mesenchymal Stem Cells: State-of-the-art review [6]
- Research article SF3B1-mutant MDS as a distinct disease subtype: a proposal from the International Working Group for the Prognosis of MDS [7]
- Research article Niches that regulate stem cells and hematopoiesis in adult bone marrow [8]
- Research article The relationship between bone marrow adipose tissue and bone metabolism in postmenopausal osteoporosis [9]
- Research article Clinical implications of bone marrow adiposity [10]
References
- Lutz R, Poos AM, Solé-Boldo L, John L, Wagner J, Prokoph N, et al.. Bone marrow breakout lesions act as key sites for tumor-immune cell diversification in multiple myeloma. . 2025. PMID 39919199 · DOI · PMC7619224
- Prummel KD, Woods K, Kholmatov M, Schmitt EC, Vlachou EP, Labyadh M, et al.. Inflammatory stromal and T cells mediate human bone marrow niche remodeling in clonal hematopoiesis and myelodysplasia. . 2025. PMID 41253811 · DOI · PMC12627676
- Gui G, Bingham MA, Herzog JR, Wong-Rolle A, Dillon LW, Goswami M, et al.. Single-cell spatial transcriptomics reveals immunotherapy-driven bone marrow niche remodeling in AML. . 2025. PMID 40632867 · DOI · PMC12239967
- Shen Y, Benlabiod C, Watson E, Gurashi K, Fower A, Rodriguez-Romera A, et al.. comBO: A combined human bone and lympho-myeloid bone marrow organoid for preclinical modeling of hematopoietic disorders. . 2026. PMID 41734765 · DOI · PMC7618947
- Park MD, Silvin A, Ginhoux F, Merad M. Macrophages in health and disease. Cell. 2022. PMID 36368305 · DOI · PMC9908006
- Berebichez-Fridman R, Montero-Olvera PR. Sources and Clinical Applications of Mesenchymal Stem Cells: State-of-the-art review. Sultan Qaboos Univ Med J. 2018. PMID 30607265 · DOI · PMC6307657
- Malcovati L, Stevenson K, Papaemmanuil E, Neuberg D, Bejar R, Boultwood J, et al.. SF3B1-mutant MDS as a distinct disease subtype: a proposal from the International Working Group for the Prognosis of MDS. Blood. 2020. PMID 32347921 · DOI · PMC7362582
- Comazzetto S, Shen B, Morrison SJ. Niches that regulate stem cells and hematopoiesis in adult bone marrow. Dev Cell. 2021. PMID 34146467 · DOI · PMC8282762
- Li J, Chen X, Lu L, Yu X. The relationship between bone marrow adipose tissue and bone metabolism in postmenopausal osteoporosis. Cytokine Growth Factor Rev. 2020. PMID 32081538 · DOI
- Veldhuis-Vlug AG, Rosen CJ. Clinical implications of bone marrow adiposity. J Intern Med. 2018. PMID 29211319 · DOI · PMC5847297
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.