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 (644 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 head of a long bone that is separated from the shaft by the epiphyseal plate until bone growth stops. At that time, the plate disappears and the head and shaft are united.
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: Epiphysis.
Where it fits in the MeSH classification
- Broader topics
- Bone and Bones
- Narrower topics
- Growth Plate
Research landscape
PubMed indexes 12,263 records tagged with the MeSH heading “Epiphyses” (counts retrieved 2026-10-31). 1,132 of them (9.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 6,760 records.
Reviews account for 853 records (7.0%) and meta-analyses for 19. Randomized controlled trials number 15 (0.1%) 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 | 6,760 |
| 2000-2009 | 1,938 |
| 2010-2019 | 2,433 |
| 2020 onward | 1,132 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 853 | 7.0% |
| Meta-analyses | 19 | 0.2% |
| Randomized controlled trials | 15 | 0.1% |
Method: PubMed query "Epiphyses"[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 |
|---|---|---|---|---|
| Growth Plate Chondrocytes: Skeletal Development, Growth and Beyond | 2019 | Review article Design not recorded in structured metadata | 134 | cc by PMID 31795305 · DOI · PMC6929081 |
| The Local CNP/GC-B system in growth plate is responsible for physiological endochondral bone growth | 2015 | Research article Design not recorded in structured metadata | 64 | cc by PMID 26014585 · DOI · PMC5395013 |
| Differential aging of growth plate cartilage underlies differences in bone length and thus helps determine skeletal proportions | 2018 | Research article Design not recorded in structured metadata | 59 | cc0 PMID 30036371 · DOI · PMC6056026 |
| Inherent tissue homeostasis of the juvenile metaphysis provides a foundation for osteosarcoma development | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42363015 · DOI · PMC13373234 |
Growth Plate Chondrocytes: Skeletal Development, Growth and Beyond [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Growth plate chondrocytes play central roles in the proper development and growth of endochondral bones.
- Closing excerpt
- Here, we discuss our current understanding of the molecular signatures defining growth plate chondrocytes.
- 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 (140 words)
Growth plate chondrocytes play central roles in the proper development and growth of endochondral bones. Particularly, a population of chondrocytes in the resting zone expressing parathyroid hormone-related protein (PTHrP) is now recognized as skeletal stem cells, defined by their ability to undergo self-renewal and clonally give rise to columnar chondrocytes in the postnatal growth plate. These chondrocytes also possess the ability to differentiate into a multitude of cell types including osteoblasts and bone marrow stromal cells during skeletal development. Using single-cell transcriptomic approaches and in vivo lineage tracing technology, it is now possible to further elucidate their molecular properties and cellular fate changes. By discovering the fundamental molecular characteristics of these cells, it may be possible to harness their functional characteristics for skeletal growth and regeneration. Here, we discuss our current understanding of the molecular signatures defining growth plate chondrocytes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31795305 · DOI · PMC6929081
The Local CNP/GC-B system in growth plate is responsible for physiological endochondral bone growth [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Recent studies revealed C-type natriuretic peptide (CNP) and its receptor, guanylyl cyclase-B (GC-B) are potent stimulators of endochondral bone growth.
- Closing excerpt
- The local CNP/GC-B system in growth plate is responsible for physiological endochondral bone growth and might further affect mortality via unknown mechanisms.
- 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)
Recent studies revealed C-type natriuretic peptide (CNP) and its receptor, guanylyl cyclase-B (GC-B) are potent stimulators of endochondral bone growth. As they exist ubiquitously in body, we investigated the physiological role of the local CNP/GC-B in the growth plate on bone growth using cartilage-specific knockout mice. Bones were severely shorter in cartilage-specific CNP or GC-B knockout mice and the extent was almost the same as that in respective systemic knockout mice. Cartilage-specific GC-B knockout mice were shorter than cartilage-specific CNP knockout mice. Hypertrophic chondrocyte layer of the growth plate was drastically reduced and proliferative chondrocyte layer, along with the proliferation of chondrocytes there, was moderately reduced in either cartilage-specific knockout mice. The survival rate of cartilage-specific CNP knockout mice was comparable to that of systemic CNP knockout mice. The local CNP/GC-B system in growth plate is responsible for physiological endochondral bone growth and might further affect mortality via unknown mechanisms.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26014585 · DOI · PMC5395013
Differential aging of growth plate cartilage underlies differences in bone length and thus helps determine skeletal proportions [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Bones at different anatomical locations vary dramatically in size.
- Closing excerpt
- Taken together, the findings reveal that the striking disparities in the lengths of different bones, which characterize normal mammalian skeletal proportions, is achieved in part by modulating the progression of growth plate senescence.
- 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 (204 words)
Bones at different anatomical locations vary dramatically in size. For example, human femurs are 20-fold longer than the phalanges in the fingers and toes. The mechanisms responsible for these size differences are poorly understood. Bone elongation occurs at the growth plates and advances rapidly in early life but then progressively slows due to a developmental program termed "growth plate senescence." This developmental program includes declines in cell proliferation and hypertrophy, depletion of cells in all growth plate zones, and extensive underlying changes in the expression of growth-regulating genes. Here, we show evidence that these functional, structural, and molecular senescent changes occur earlier in the growth plates of smaller bones (metacarpals, phalanges) than in the growth plates of larger bones (femurs, tibias) and that this differential aging contributes to the disparities in bone length. We also show evidence that the molecular mechanisms that underlie the differential aging between different bones involve modulation of critical paracrine regulatory pathways, including insulin-like growth factor (Igf), bone morphogenetic protein (Bmp), and Wingless and Int-1 (Wnt) signaling. Taken together, the findings reveal that the striking disparities in the lengths of different bones, which characterize normal mammalian skeletal proportions, is achieved in part by modulating the progression of growth plate senescence.
Abstract reproduced from the open-access article under the recorded cc0 licence; © the authors. PMID 30036371 · DOI · PMC6056026
Inherent tissue homeostasis of the juvenile metaphysis provides a foundation for osteosarcoma development [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Osteosarcomas preferentially arise in the metaphysis of juvenile long bones, near the growth plate, unlike most cancers, whose incidence increases with age.
- Closing excerpt
- These findings reveal juvenile metaphyseal tissue homeostasis as a potential basis for the age of onset, anatomical specificity, and mutational profile of human osteosarcomas.
- 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)
Osteosarcomas preferentially arise in the metaphysis of juvenile long bones, near the growth plate, unlike most cancers, whose incidence increases with age. Here, we show that p21, a negative regulator of the cell cycle, is induced in proliferating juvenile metaphyseal osteoblasts in response to DNA replication-associated damage. Single-cell RNA sequencing defines a differentiation hierarchy from multipotent progenitors to mature osteoblasts and identifies immature osteoblasts enriched for proliferation and replication stress responses. p21-positive metaphyseal osteoblasts associate with growth plate Indian hedgehog expression and decline after growth plate maturation or Hedgehog inhibition. c-Myc induction selectively promotes juvenile osteoblast proliferation despite p53 activation, but this proliferative response remains Hedgehog-dependent and ceases after growth plate maturation. By contrast, p53 inactivation enables sustained Hedgehog-independent proliferation of c-Myc-induced osteoblasts and lung metastasis. These findings reveal juvenile metaphyseal tissue homeostasis as a potential basis for the age of onset, anatomical specificity, and mutational profile of human osteosarcomas.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42363015 · DOI · PMC13373234
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 Developmental regulation of the growth plate [5]
- Research article Matrix vesicles and calcification [6]
- Research article The skeleton: a multi-functional complex organ: the growth plate chondrocyte and endochondral ossification [7]
- Research article Mechanism of longitudinal bone growth and its regulation by growth plate chondrocytes [8]
- Research article Angiogenesis and bone growth [9]
- Research article Growth plate mechanics and mechanobiology. A survey of present understanding [10]
References
- Hallett SA, Ono W, Ono N. Growth Plate Chondrocytes: Skeletal Development, Growth and Beyond. . 2019. PMID 31795305 · DOI · PMC6929081
- Nakao K, Osawa K, Yasoda A, Yamanaka S, Fujii T, Kondo E, et al.. The Local CNP/GC-B system in growth plate is responsible for physiological endochondral bone growth. . 2015. PMID 26014585 · DOI · PMC5395013
- Lui JC, Jee YH, Garrison P, Iben JR, Yue S, Ad M, et al.. Differential aging of growth plate cartilage underlies differences in bone length and thus helps determine skeletal proportions. . 2018. PMID 30036371 · DOI · PMC6056026
- Saito M, Nakasuka F, Sankoda N, Wang Y, Taguchi J, Ohta S, et al.. Inherent tissue homeostasis of the juvenile metaphysis provides a foundation for osteosarcoma development. . 2026. PMID 42363015 · DOI · PMC13373234
- Kronenberg HM. Developmental regulation of the growth plate. Nature. 2003. PMID 12748651 · DOI
- Anderson HC. Matrix vesicles and calcification. Curr Rheumatol Rep. 2003. PMID 12744815 · DOI
- Mackie EJ, Tatarczuch L, Mirams M. The skeleton: a multi-functional complex organ: the growth plate chondrocyte and endochondral ossification. J Endocrinol. 2011. PMID 21642379 · DOI
- Hunziker EB. Mechanism of longitudinal bone growth and its regulation by growth plate chondrocytes. Microsc Res Tech. 1994. PMID 7949396 · DOI
- Gerber HP, Ferrara N. Angiogenesis and bone growth. Trends Cardiovasc Med. 2000. PMID 11282299 · DOI
- Villemure I, Stokes IA. Growth plate mechanics and mechanobiology. A survey of present understanding. J Biomech. 2009. PMID 19540500 · DOI · PMC2739053
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.