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Dwarfism

Rare and Inherited Diseases · NLM MeSH · updated 2026-10-29 · version 1

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

A genetic or pathological condition that is characterized by short stature and undersize.

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 (863 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 genetic or pathological condition that is characterized by short stature and undersize. Abnormal skeletal growth usually results in an adult who is significantly below the average height.

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: Nanism.

Where it fits in the MeSH classification

Broader topics
Bone Diseases, Developmental; Genetic Diseases, Inborn; Endocrine System Diseases
Narrower topics
Achondroplasia; Cockayne Syndrome; Congenital Hypothyroidism; Dwarfism, Pituitary; Laron Syndrome; Mulibrey Nanism; Weill-Marchesani Syndrome; Silver-Russell Syndrome

Research landscape

PubMed indexes 18,675 records tagged with the MeSH heading “Dwarfism” (counts retrieved 2026-10-29). 2,535 of them (13.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 10,059 records.

Reviews account for 2,142 records (11.5%) and meta-analyses for 35. Randomized controlled trials number 92 (0.5%) 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: 10,059 records; 2000-2009: 2,575 records; 2010-2019: 3,506 records; 2020 onward: 2,535 records10,059through 19992,5752000-20093,5062010-20192,5352020 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 199910,059
2000-20092,575
2010-20193,506
2020 onward2,535
Share of records by publication typeReviews: 11.5 percent; Meta-analyses: 0.2 percent; Randomized controlled trials: 0.5 percentReviews11.5% (2,142)Meta-analyses0.2% (35)Randomized controlled trials0.5% (92)
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 18,675 PubMed records
TypeRecordsShare
Reviews2,14211.5%
Meta-analyses350.2%
Randomized controlled trials920.5%

Method: PubMed query "Dwarfism"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.

Reading the evidence in rare and inherited diseases

Rare conditions are difficult to study: few patients means small studies, case reports and registries are common, and randomized trials are the exception. Small samples limit precision and can exaggerate effects, and cases reported in the literature may be the most severe or unusual. Evidence from many small studies is best read together. Check how patients were identified, how many were included and how long they were followed.

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
Transcription-coupled repair of DNA-protein cross-links depends on CSA and CSB
Carnie CJ, Acampora AC, Bader AS, Erdenebat C, Zhao S, Bitensky E, et al.
2024Research article
Design not recorded in structured metadata
60cc by
PMID 38600235 · DOI · PMC11098753
Novel therapeutic perspectives in Noonan syndrome and RASopathies
Saint-Laurent C, Mazeyrie L, Yart A, Edouard T
2024Review article
Design not recorded in structured metadata
36cc by
PMID 37863846 · DOI · PMC10951041
Deeplasia: deep learning for bone age assessment validated on skeletal dysplasias
Rassmann S, Keller A, Skaf K, Hustinx A, Gausche R, Ibarra-Arrelano MA, et al.
2024Research article
Design not recorded in structured metadata
27cc by
PMID 37953411 · DOI · PMC10776485
An overview of the International Consensus Statement on achondroplasia
Alves I, Fredwall SO, Hughes M, Ireland PJ, Kaisermann MC, Savarirayan R
2026Review article
Design not recorded in structured metadata
2cc by
PMID 41559786 · DOI · PMC12857165

Transcription-coupled repair of DNA-protein cross-links depends on CSA and CSB [1]

Research article Carnie CJ, Acampora AC, Bader AS, Erdenebat C, Zhao S, Bitensky E, et al. · · 2024 · cited 60 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Covalent DNA-protein cross-links (DPCs) are toxic DNA lesions that block replication and require repair by multiple pathways.
Closing excerpt
Our study describes a transcription-coupled DPC repair pathway and suggests that defects in this pathway may contribute to the unique neurological features of CS.
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 (151 words)

Covalent DNA-protein cross-links (DPCs) are toxic DNA lesions that block replication and require repair by multiple pathways. Whether transcription blockage contributes to the toxicity of DPCs and how cells respond when RNA polymerases stall at DPCs is unknown. Here we find that DPC formation arrests transcription and induces ubiquitylation and degradation of RNA polymerase II. Using genetic screens and a method for the genome-wide mapping of DNA-protein adducts, DPC sequencing, we discover that Cockayne syndrome (CS) proteins CSB and CSA provide resistance to DPC-inducing agents by promoting DPC repair in actively transcribed genes. Consequently, CSB- or CSA-deficient cells fail to efficiently restart transcription after induction of DPCs. In contrast, nucleotide excision repair factors that act downstream of CSB and CSA at ultraviolet light-induced DNA lesions are dispensable. Our study describes a transcription-coupled DPC repair pathway and suggests that defects in this pathway may contribute to the unique neurological features of CS.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38600235 · DOI · PMC11098753

Novel therapeutic perspectives in Noonan syndrome and RASopathies [2]

Review article Saint-Laurent C, Mazeyrie L, Yart A, Edouard T · · 2024 · cited 36 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Noonan syndrome belongs to the family of RASopathies, a group of multiple congenital anomaly disorders caused by pathogenic variants in genes encoding components or regulators of the RAS/mitogen-activated protein kinase (MAPK) signalling pathway.
Closing excerpt
C-type natriuretic peptide analogues in achondroplasia or statins in hypercholesterolaemia) represents a challenging approach to the treatment of RASopathies.
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 (260 words)

Noonan syndrome belongs to the family of RASopathies, a group of multiple congenital anomaly disorders caused by pathogenic variants in genes encoding components or regulators of the RAS/mitogen-activated protein kinase (MAPK) signalling pathway. Collectively, all these pathogenic variants lead to increased RAS/MAPK activation. The better understanding of the molecular mechanisms underlying the different manifestations of NS and RASopathies has led to the identification of molecular targets for specific pharmacological interventions. Many specific agents (e.g. SHP2 and MEK inhibitors) have already been developed for the treatment of RAS/MAPK-driven malignancies. In addition, other molecules with the property of modulating RAS/MAPK activation are indicated in non-malignant diseases (e.g. C-type natriuretic peptide analogues in achondroplasia or statins in hypercholesterolemia). Conclusion: Drug repositioning of these molecules represents a challenging approach to treat or prevent medical complications associated with RASopathies. What is Known: • Noonan syndrome and related disorders are caused by pathogenic variants in genes encoding components or regulators of the RAS/mitogen-activated protein kinase (MAPK) signalling pathway, resulting in increased activation of this pathway. • This group of disorders is now known as RASopathies and represents one of the largest groups of multiple congenital anomaly diseases known. What is New: • The identification of pathophysiological mechanisms provides new insights into the development of specific therapeutic strategies, in particular treatment aimed at reducing RAS/MAPK hyperactivation. • Drug repositioning of specific agents already developed for the treatment of malignant (e.g. SHP2 and MEK inhibitors) or non-malignant diseases (e.g. C-type natriuretic peptide analogues in achondroplasia or statins in hypercholesterolaemia) represents a challenging approach to the treatment of RASopathies.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37863846 · DOI · PMC10951041

Deeplasia: deep learning for bone age assessment validated on skeletal dysplasias [3]

Research article Rassmann S, Keller A, Skaf K, Hustinx A, Gausche R, Ibarra-Arrelano MA, et al. · · 2024 · cited 27 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundSkeletal dysplasias collectively affect a large number of patients worldwide.
Closing excerpt
ConclusionWe demonstrated that Deeplasia is competent in assessing the age and monitoring the development of both normal and dysplastic bones.
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 (300 words)

BackgroundSkeletal dysplasias collectively affect a large number of patients worldwide. Most of these disorders cause growth anomalies. Hence, evaluating skeletal maturity via the determination of bone age (BA) is a useful tool. Moreover, consecutive BA measurements are crucial for monitoring the growth of patients with such disorders, especially for timing hormonal treatment or orthopedic interventions. However, manual BA assessment is time-consuming and suffers from high intra- and inter-rater variability. This is further exacerbated by genetic disorders causing severe skeletal malformations. While numerous approaches to automate BA assessment have been proposed, few are validated for BA assessment on children with skeletal dysplasias.ObjectiveWe present Deeplasia, an open-source prior-free deep-learning approach designed for BA assessment specifically validated on patients with skeletal dysplasias.Materials and methodsWe trained multiple convolutional neural network models under various conditions and selected three to build a precise model ensemble. We utilized the public BA dataset from the Radiological Society of North America (RSNA) consisting of training, validation, and test subsets containing 12,611, 1,425, and 200 hand and wrist radiographs, respectively. For testing the performance of our model ensemble on dysplastic hands, we retrospectively collected 568 radiographs from 189 patients with molecularly confirmed diagnoses of seven different genetic bone disorders including achondroplasia and hypochondroplasia. A subset of the dysplastic cohort (149 images) was used to estimate the test-retest precision of our model ensemble on longitudinal data.ResultsThe mean absolute difference of Deeplasia for the RSNA test set (based on the average of six different reference ratings) and dysplastic set (based on the average of two different reference ratings) were 3.87 and 5.84 months, respectively. The test-retest precision of Deeplasia on longitudinal data (2.74 months) is estimated to be similar to a human expert.ConclusionWe demonstrated that Deeplasia is competent in assessing the age and monitoring the development of both normal and dysplastic bones.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37953411 · DOI · PMC10776485

An overview of the International Consensus Statement on achondroplasia [4]

Review article Alves I, Fredwall SO, Hughes M, Ireland PJ, Kaisermann MC, Savarirayan R · · 2026 · cited 2 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Achondroplasia is the most common form of short-limbed short stature of genetic origin.
Closing excerpt
We provide commentary on the recommendations from the perspective of both patients and physicians through addressing medical/developmental considerations, the healthcare system, and psychosocial considerations.
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 (152 words)

Achondroplasia is the most common form of short-limbed short stature of genetic origin. Most people with achondroplasia live fully independent, productive, and socially engaged lives. However, the condition is associated with several potential medical complications. Individuals with achondroplasia may experience medical, functional, and psychosocial challenges at different times in their life. The goal for lifelong care of individuals with achondroplasia is to optimize their physical and mental health through provision of individualized care and to promote participation and inclusion in society. In this article, as a tool for individuals with achondroplasia, their families, and their healthcare team, we provide a guided overview of the 2022 International Consensus Statement for management and care of individuals with achondroplasia. The International Consensus Statement recommendations are based on current, best available knowledge. We provide commentary on the recommendations from the perspective of both patients and physicians through addressing medical/developmental considerations, the healthcare system, and psychosocial considerations.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41559786 · DOI · PMC12857165

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 Diagnosis and management of Silver-Russell syndrome: first international consensus statement [5]
    Wakeling EL, Brioude F, Lokulo-Sodipe O, O'Connell SM, Salem J, Bliek J, et al. · Nat Rev Endocrinol · 2017 · cited 365 times (Europe PMC)
  • Research article Congenital Hypothyroidism: A 2020-2021 Consensus Guidelines Update-An ENDO-European Reference Network Initiative Endorsed by the European Society for Pediatric Endocrinology and the European Society for Endocrinology [6]
    van Trotsenburg P, Stoupa A, Léger J, Rohrer T, Peters C, Fugazzola L, et al. · Thyroid · 2021 · cited 328 times (Europe PMC)
  • Research article Achondroplasia: a comprehensive clinical review [7]
    Pauli RM · Orphanet J Rare Dis · 2019 · cited 291 times (Europe PMC)
  • Research article European Society for Paediatric Endocrinology consensus guidelines on screening, diagnosis, and management of congenital hypothyroidism [8]
    Léger J, Olivieri A, Donaldson M, Torresani T, Krude H, van Vliet G, et al. · J Clin Endocrinol Metab · 2014 · cited 272 times (Europe PMC)
  • Research article Cockayne syndrome: Clinical features, model systems and pathways [9]
    Karikkineth AC, Scheibye-Knudsen M, Fivenson E, Croteau DL, Bohr VA · Ageing Res Rev · 2017 · cited 204 times (Europe PMC)
  • Research article Cartilage oligomeric matrix protein: COMPopathies and beyond [10]
    Posey KL, Coustry F, Hecht JT · Matrix Biol · 2018 · cited 182 times (Europe PMC)

References

  1. Carnie CJ, Acampora AC, Bader AS, Erdenebat C, Zhao S, Bitensky E, et al.. Transcription-coupled repair of DNA-protein cross-links depends on CSA and CSB. . 2024. PMID 38600235 · DOI · PMC11098753
  2. Saint-Laurent C, Mazeyrie L, Yart A, Edouard T. Novel therapeutic perspectives in Noonan syndrome and RASopathies. . 2024. PMID 37863846 · DOI · PMC10951041
  3. Rassmann S, Keller A, Skaf K, Hustinx A, Gausche R, Ibarra-Arrelano MA, et al.. Deeplasia: deep learning for bone age assessment validated on skeletal dysplasias. . 2024. PMID 37953411 · DOI · PMC10776485
  4. Alves I, Fredwall SO, Hughes M, Ireland PJ, Kaisermann MC, Savarirayan R. An overview of the International Consensus Statement on achondroplasia. . 2026. PMID 41559786 · DOI · PMC12857165
  5. Wakeling EL, Brioude F, Lokulo-Sodipe O, O'Connell SM, Salem J, Bliek J, et al.. Diagnosis and management of Silver-Russell syndrome: first international consensus statement. Nat Rev Endocrinol. 2017. PMID 27585961 · DOI
  6. van Trotsenburg P, Stoupa A, Léger J, Rohrer T, Peters C, Fugazzola L, et al.. Congenital Hypothyroidism: A 2020-2021 Consensus Guidelines Update-An ENDO-European Reference Network Initiative Endorsed by the European Society for Pediatric Endocrinology and the European Society for Endocrinology. Thyroid. 2021. PMID 33272083 · DOI · PMC8001676
  7. Pauli RM. Achondroplasia: a comprehensive clinical review. Orphanet J Rare Dis. 2019. PMID 30606190 · DOI · PMC6318916
  8. Léger J, Olivieri A, Donaldson M, Torresani T, Krude H, van Vliet G, et al.. European Society for Paediatric Endocrinology consensus guidelines on screening, diagnosis, and management of congenital hypothyroidism. J Clin Endocrinol Metab. 2014. PMID 24446653 · DOI · PMC4207909
  9. Karikkineth AC, Scheibye-Knudsen M, Fivenson E, Croteau DL, Bohr VA. Cockayne syndrome: Clinical features, model systems and pathways. Ageing Res Rev. 2017. PMID 27507608 · DOI · PMC5195851
  10. Posey KL, Coustry F, Hecht JT. Cartilage oligomeric matrix protein: COMPopathies and beyond. Matrix Biol. 2018. PMID 29530484 · DOI · PMC6129439

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 2026-10-29.

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At a glance

18,675
PubMed records on this heading
14%
published since 2020
2,142
review articles
92
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

Related topics See all →

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