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: 3 complete abstracts (592 words), 9 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 growth and development of bones from fetus to adult. It includes two principal mechanisms of bone growth: growth in length of long bones at the epiphyseal cartilages and growth in thickness by depositing new bone (osteogenesis) with the actions of osteoblasts and osteoclasts.
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 Growth.
Where it fits in the MeSH classification
- Broader topics
- Biomineralization
- Narrower topics
- Calcification, Physiologic; Maxillofacial Development; Osteogenesis
Related concepts
- Osteogenesis
- Osteoblasts
- Osteoclasts
Research landscape
PubMed indexes 82,795 records tagged with the MeSH heading “Bone Development” (counts retrieved 2026-10-31). 20,143 of them (24.3%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 25,860 records.
Reviews account for 7,678 records (9.3%) and meta-analyses for 146. Randomized controlled trials number 740 (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 | 23,631 |
| 2000-2009 | 13,161 |
| 2010-2019 | 25,860 |
| 2020 onward | 20,143 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 7,678 | 9.3% |
| Meta-analyses | 146 | 0.2% |
| Randomized controlled trials | 740 | 0.9% |
Method: PubMed query "Bone Development"[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 |
|---|---|---|---|---|
| Effects of Periodontal-Specific Exosomes and rhBMP2 on Osteogenic Behaviour and Differentiation of BMSCs | 2026 | Research article Design not recorded in structured metadata | 8 | cc by PMID 41606422 · DOI · PMC12852057 |
| Sensory Nerve-Derived CGRP Controls Osteoclastogenesis by Limiting Macrophage Bioenergetics in Bone Repair | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41764371 · DOI · PMC13067781 |
| Atrophic Skeletal Muscle-Derived Extracellular Vesicles Transfer miR-125a-5p to Inhibit Bone Formation in Osteoporosis during Aging | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41747076 · DOI · PMC13137847 |
Effects of Periodontal-Specific Exosomes and rhBMP2 on Osteogenic Behaviour and Differentiation of BMSCs [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Growth factors, including recombinant human bone morphogenetic protein-2 (rhBMP2), have been clinically utilised for large bone augmentation with good outcomes.
- Closing excerpt
- Overall, Px significantly enhanced BMSC osteogenesis compared to rhBMP2, highlighting their potential as a cell-free nanotherapeutic in bone tissue engineering.
- 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 (200 words)
Growth factors, including recombinant human bone morphogenetic protein-2 (rhBMP2), have been clinically utilised for large bone augmentation with good outcomes. Nevertheless, long-term healing, swelling, safety concerns, and high cost limit their use. Exosomes, nanoscale extracellular vesicles, have emerged as promising regenerative alternatives. This study assessed the osteogenic potential of periodontal-specific exosomes (Px) on bone marrow mesenchymal stem cells (BMSCs) compared to rhBMP2. Px were morphologically characterised by TEM and quantified via BCA assay. BMSCs were treated with Px at 1:10, 1:50, and 1:100 dilutions (100, 20, and 10 μg/mL) and compared to rhBMP2 (100 ng/mL). Px uptake was evaluated using PKH26 labeling. Functional assays included viability, migration, alkaline phosphatase (ALP) activity, alizarin red (ARS) mineralization, collagen, osteocalcin secretion, and RT-PCR analysis of osteogenic genes. Px exhibited spheroidal to cup-shaped morphology and internalisation in BMSCs up to 18 days. Compared to rhBMP2, Px promoted viability (1.14-fold), migration (1.78-fold) up to 1.14 and 1.78-fold, ALP (1.48-, 4.11-fold), ARS (1.43-, 14.71-fold), collagen (1.40-, 3.58-fold), and osteocalcin (1.86-, 5.2-fold). Gene expression demonstrated significant upregulation of ALP (1.73-fold), RUNX2 (1.70-fold), OCN (1.36-fold), and OPN (1.35-fold). Overall, Px significantly enhanced BMSC osteogenesis compared to rhBMP2, highlighting their potential as a cell-free nanotherapeutic in bone tissue engineering.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41606422 · DOI · PMC12852057
Sensory Nerve-Derived CGRP Controls Osteoclastogenesis by Limiting Macrophage Bioenergetics in Bone Repair [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Bone healing is a tightly orchestrated, multiphase process that requires coordinated interactions between immune cells and skeletal cells.
- Closing excerpt
- It emphasizes the potential of incorporating sensory signals into therapeutic strategies, particularly those targeting immunometabolism in bone regeneration.
- 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 (193 words)
Bone healing is a tightly orchestrated, multiphase process that requires coordinated interactions between immune cells and skeletal cells. Sensory nerves act as intrinsic effectors of the inflammatory response, whose role in osteoimmunology during healing remains poorly defined. Using a bone healing model with sensory denervation, it's shown that sensory nerves protect bone repair by suppressing excessive osteoclastogenesis. During the acute inflammatory phase, sensory nerves are upstream regulators of macrophage activation. At the molecular level, calcitonin gene-related peptide (CGRP), a sensory neuron-derived neuropeptide, is identified to modulate macrophage activation by restricting key functions such as migration, phagocytosis, and pro-inflammatory cytokine production. Importantly, CGRP rapidly constrains adenosine triphosphate (ATP) synthesis and mitochondrial respiration in activating macrophages, accompanied by downregulation of genes associated with oxidative phosphorylation and mitochondrial complex components. Following the metabolic alterations, macrophages exposed to CGRP show attenuated osteoclastogenic capacity, with decreased secretion of multiple key factors that support osteoclast differentiation and survival. Together, these findings indicate a neuro-immune-metabolic axis in bone healing, where sensory nerve-derived CGRP influences macrophage bioenergetics and thereby contributes to osteoimmunoligical regulation. It emphasizes the potential of incorporating sensory signals into therapeutic strategies, particularly those targeting immunometabolism in bone regeneration.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41764371 · DOI · PMC13067781
Atrophic Skeletal Muscle-Derived Extracellular Vesicles Transfer miR-125a-5p to Inhibit Bone Formation in Osteoporosis during Aging [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Understanding how skeletal muscle influences bone formation is essential for uncovering the mechanisms of muscle-bone communication and developing therapies for osteoporosis.
- Closing excerpt
- Our findings reveal a novel endocrine pathway from muscle to bone mediated by EV-associated miRNA and highlight miR-125a-5p as a promising therapeutic target for sarcopenia-related osteoporosis.
- 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 (199 words)
Understanding how skeletal muscle influences bone formation is essential for uncovering the mechanisms of muscle-bone communication and developing therapies for osteoporosis. Here, we demonstrate that extracellular vesicles (EVs) derived from atrophic skeletal muscle (Aged-SKM-EVs) inhibit bone formation during aging. Utilizing a muscle-specific EV tracking transgenic mouse model, we found that Aged-SKM-EVs were significantly increased and taken up by osteoblasts in bone during aging. Notably, pharmacological blockade of muscle EV generation via a skeletal muscle-targeted delivery of GW4869 significantly restored osteoblast activity and alleviated bone loss in aged mice. Functional studies revealed that Aged-SKM-EVs suppressed bone formation and inhibited osteogenic differentiation both in vivo and in vitro. Mechanistically, we identified miR-125a-5p as a key cargo enriched in EVs from sarcopenic patients and aged mice. Muscle-specific overexpression of miR-125a-5p inhibited osteogenesis and exacerbated muscle atrophy and bone loss, whereas silencing miR-125a-5p in skeletal muscle effectively reversed these effects. Further investigation demonstrated that miR-125a-5p inhibits osteogenic differentiation by directly targeting Sirt7 in preosteoblasts, thereby disrupting SIRT7-mediated histone deacetylation at the Sp7 promoter and suppressing Sp7 transcription. Our findings reveal a novel endocrine pathway from muscle to bone mediated by EV-associated miRNA and highlight miR-125a-5p as a promising therapeutic target for sarcopenia-related osteoporosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41747076 · DOI · PMC13137847
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 Mechanisms of bone development and repair [4]
- Research article Wnt/β-catenin signaling components and mechanisms in bone formation, homeostasis, and disease [5]
- Research article Regulation of Osteoblast Differentiation by Cytokine Networks [6]
- Research article The endothelium-bone axis in development, homeostasis and bone and joint disease [7]
- Research article The osteocyte as a signaling cell [8]
- Research article Making and shaping endochondral and intramembranous bones [9]
References
- Ahmad P, Siddiqui DA, Bianchi-Smak J, Farshidfar N, Estrin N, Miron RJ, et al.. Effects of Periodontal-Specific Exosomes and rhBMP2 on Osteogenic Behaviour and Differentiation of BMSCs. . 2026. PMID 41606422 · DOI · PMC12852057
- Liu J, Zhang T, Mu Y, Li L, Jin J, Dudley KJ, et al.. Sensory Nerve-Derived CGRP Controls Osteoclastogenesis by Limiting Macrophage Bioenergetics in Bone Repair. . 2026. PMID 41764371 · DOI · PMC13067781
- Shao X, Zhang P, Fan Z, Lin J, Chen X, Liu N, et al.. Atrophic Skeletal Muscle-Derived Extracellular Vesicles Transfer miR-125a-5p to Inhibit Bone Formation in Osteoporosis during Aging. . 2026. PMID 41747076 · DOI · PMC13137847
- Salhotra A, Shah HN, Levi B, Longaker MT. Mechanisms of bone development and repair. Nat Rev Mol Cell Biol. 2020. PMID 32901139 · DOI · PMC7699981
- Hu L, Chen W, Qian A, Li YP. Wnt/β-catenin signaling components and mechanisms in bone formation, homeostasis, and disease. Bone Res. 2024. PMID 38987555 · DOI · PMC11237130
- Amarasekara DS, Kim S, Rho J. Regulation of Osteoblast Differentiation by Cytokine Networks. Int J Mol Sci. 2021. PMID 33799644 · DOI · PMC7998677
- Tuckermann J, Adams RH. The endothelium-bone axis in development, homeostasis and bone and joint disease. Nat Rev Rheumatol. 2021. PMID 34480164 · DOI · PMC7612477
- Delgado-Calle J, Bellido T. The osteocyte as a signaling cell. Physiol Rev. 2022. PMID 34337974 · DOI · PMC8858675
- Galea GL, Zein MR, Allen S, Francis-West P. Making and shaping endochondral and intramembranous bones. Dev Dyn. 2021. PMID 33314394 · DOI · PMC7986209
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.