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 (844 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 period in the human life in which the development of the hypothalamic-pituitary-gonadal system takes place and reaches full maturity. The onset of synchronized endocrine events in puberty lead to the capacity for reproduction (fertility), development of secondary sex characteristics, and other changes seen in adolescent development.
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: Puberties.
Where it fits in the MeSH classification
- Broader topics
- Reproductive Physiological Phenomena; Sexual Development
- Narrower topics
- Adrenarche; Menarche
- See also
- Sexual Maturation
Related concepts
- Fertility
- Sex Characteristics
- Adolescent Development
Research landscape
PubMed indexes 20,354 records tagged with the MeSH heading “Puberty” (counts retrieved 2026-10-31). 2,675 of them (13.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 9,114 records.
Reviews account for 2,659 records (13.1%) and meta-analyses for 148. Randomized controlled trials number 316 (1.6%) 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 | 9,114 |
| 2000-2009 | 4,002 |
| 2010-2019 | 4,563 |
| 2020 onward | 2,675 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,659 | 13.1% |
| Meta-analyses | 148 | 0.7% |
| Randomized controlled trials | 316 | 1.6% |
Method: PubMed query "Puberty"[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 |
|---|---|---|---|---|
| Understanding the genetic complexity of puberty timing across the allele frequency spectrum | 2024 | Research article Design not recorded in structured metadata | 62 | cc by PMID 38951643 · DOI · PMC11250262 |
| Factors affecting prepubertal and pubertal bone age progression | 2022 | Review article Design not recorded in structured metadata | 28 | cc by PMID 36072933 · DOI · PMC9441639 |
| The Dynamic Interplay Between Puberty and Structural Brain Development as a Predictor of Mental Health Difficulties in Adolescence: A Systematic Review | 2024 | Systematic review Design not recorded in structured metadata | 22 | cc by PMID 38925264 · DOI · PMC11794195 |
| Hypothalamic control of puberty: from neuronal circuits to mechanisms for its metabolic regulation | 2026 | Review article Design not recorded in structured metadata | 11 | cc by PMID 41108362 · DOI · PMC13246832 |
Understanding the genetic complexity of puberty timing across the allele frequency spectrum [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Pubertal timing varies considerably and is associated with later health outcomes.
- Closing excerpt
- We also highlight body size-dependent and independent mechanisms that potentially link reproductive timing to later life disease.
- 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)
Pubertal timing varies considerably and is associated with later health outcomes. We performed multi-ancestry genetic analyses on ~800,000 women, identifying 1,080 signals for age at menarche. Collectively, these explained 11% of trait variance in an independent sample. Women at the top and bottom 1% of polygenic risk exhibited ~11 and ~14-fold higher risks of delayed and precocious puberty, respectively. We identified several genes harboring rare loss-of-function variants in ~200,000 women, including variants in ZNF483, which abolished the impact of polygenic risk. Variant-to-gene mapping approaches and mouse gonadotropin-releasing hormone neuron RNA sequencing implicated 665 genes, including an uncharacterized G-protein-coupled receptor, GPR83, which amplified the signaling of MC3R, a key nutritional sensor. Shared signals with menopause timing at genes involved in DNA damage response suggest that the ovarian reserve might signal centrally to trigger puberty. We also highlight body size-dependent and independent mechanisms that potentially link reproductive timing to later life disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38951643 · DOI · PMC11250262
Factors affecting prepubertal and pubertal bone age progression [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Bone age (BA) is a clinical marker of bone maturation which indicates the developmental stage of endochondral ossification at the epiphysis and the growth plate.
- Closing excerpt
- In the present study, we aimed to review the factors affecting prepubertal and pubertal BA progression, BA progression in children with hypogonadism, and bone maturation and deformities in children with Turner syndrome.
- 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 (170 words)
Bone age (BA) is a clinical marker of bone maturation which indicates the developmental stage of endochondral ossification at the epiphysis and the growth plate. Hormones that promote the endochondral ossification process include growth hormone, insulin-like growth factor-1, thyroid hormone, estrogens, and androgens. In particular, estrogens are essential for growth plate fusion and closure in both sexes. Bone maturation in female children is more advanced than in male children of all ages. The promotion of bone maturation seen in females before the onset of puberty is thought to be an effect of estrogen because estrogen levels are higher in females than in males before puberty. Sex hormones are essential for bone maturation during puberty. Since females have their pubertal onset about two years earlier than males, bone maturation in females is more advanced than in males during puberty. In the present study, we aimed to review the factors affecting prepubertal and pubertal BA progression, BA progression in children with hypogonadism, and bone maturation and deformities in children with Turner syndrome.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36072933 · DOI · PMC9441639
The Dynamic Interplay Between Puberty and Structural Brain Development as a Predictor of Mental Health Difficulties in Adolescence: A Systematic Review [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Puberty is a time of intense reorganization of brain structure and a high-risk period for the onset of mental health problems, with variations in pubertal timing and tempo intensifying this risk.
- Closing excerpt
- Social processes may be more relevant than biological ones to the link between puberty and mental health problems and represent an important target for educational 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 (238 words)
Puberty is a time of intense reorganization of brain structure and a high-risk period for the onset of mental health problems, with variations in pubertal timing and tempo intensifying this risk. We conducted 2 systematic reviews of articles published up to February 1, 2024, focusing on 1) the role of brain structure in the relationship between puberty and mental health, and 2) precision psychiatry research evaluating the utility of puberty in making individualized predictions of mental health outcomes in young people. The first review provides inconsistent evidence about whether and how pubertal and psychopathological processes may interact in relation to brain development. While most studies found an association between early puberty and mental health difficulties in adolescents, evidence on whether brain structure mediates this relationship is mixed. The pituitary gland was found to be associated with mental health status during this time, possibly through its central role in regulating puberty and its function in the hypothalamic-pituitary-gonadal and hypothalamic-pituitary-adrenal axes. In the second review, the design of studies that have explored puberty in predictive models did not allow for a quantification of its predictive power. However, when puberty was evaluated through physically observable characteristics rather than hormonal measures, it was more commonly identified as a predictor of depression, anxiety, and suicidality in adolescence. Social processes may be more relevant than biological ones to the link between puberty and mental health problems and represent an important target for educational strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38925264 · DOI · PMC11794195
Hypothalamic control of puberty: from neuronal circuits to mechanisms for its metabolic regulation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- The hypothalamus is a singular brain region with essential roles in the control of a wide diversity of vegetative functions, from growth and energy balance to reproduction.
- Closing excerpt
- While characterization of these regulatory circuits is still uncomplete, this review aims to provide a synoptic and updated view of our current knowledge of the essential elements responsible for the hypothalamic control of puberty, also as a means to understand the putative basis for acquired pubertal disorders, including those linked to metabolic perturbations, such as early-onset obesity or undernutrition.
- 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 (286 words)
The hypothalamus is a singular brain region with essential roles in the control of a wide diversity of vegetative functions, from growth and energy balance to reproduction. These processes are governed by interconnected neuroendocrine pathways that enable proper adjustment of fundamental biological programs to internal and external cues along the lifespan. Puberty is a key maturational phenomenon that permits full sexual and somatic maturation, and attainment of reproductive capacity, together with important psychological changes. Puberty is to a large extent, a brain-driven phenomenon, with the hypothalamus playing a major role as the essential hub for the integration of central and peripheral signals, responsible for driving puberty onset and its modulation by endogenous and environmental factors. Our understanding of the hypothalamic circuits governing puberty has expanded enormously in the last decades, as exemplified by the discovery and later characterization of the roles of neurons producing kisspeptins, aka Kiss1 neurons, as major gatekeepers of puberty onset, mainly through their role as indispensable upstream activators of GnRH neurons. In recent years, the intimate molecular programs and co-players of Kiss1 neurons that participate in pubertal control have been partially exposed. In addition, given the paramount importance of metabolic signals in the modulation of puberty, the nature and mechanisms of action of different factors, converging at the hypothalamus, that participate in pubertal modulation by the metabolic and nutritional status have been disclosed. While characterization of these regulatory circuits is still uncomplete, this review aims to provide a synoptic and updated view of our current knowledge of the essential elements responsible for the hypothalamic control of puberty, also as a means to understand the putative basis for acquired pubertal disorders, including those linked to metabolic perturbations, such as early-onset obesity or undernutrition.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41108362 · DOI · PMC13246832
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 Pubertal development and regulation [5]
- Research article Control of puberty onset and fertility by gonadotropin-releasing hormone neurons [6]
- Research article Worldwide Secular Trends in Age at Pubertal Onset Assessed by Breast Development Among Girls: A Systematic Review and Meta-analysis [7]
- Research article Puberty and the human brain: Insights into adolescent development [8]
- Research article Puberty Initiates Cascading Relationships Between Neurodevelopmental, Social, and Internalizing Processes Across Adolescence [9]
- Research article Recent secular trends in pubertal timing: implications for evaluation and diagnosis of precocious puberty [10]
References
- Kentistou KA, Kaisinger LR, Stankovic S, Vaudel M, Mendes de Oliveira E, Messina A, et al.. Understanding the genetic complexity of puberty timing across the allele frequency spectrum. . 2024. PMID 38951643 · DOI · PMC11250262
- Satoh M, Hasegawa Y. Factors affecting prepubertal and pubertal bone age progression. . 2022. PMID 36072933 · DOI · PMC9441639
- Kretzer S, Lawrence AJ, Pollard R, Ma X, Chen PJ, Amasi-Hartoonian N, et al.. The Dynamic Interplay Between Puberty and Structural Brain Development as a Predictor of Mental Health Difficulties in Adolescence: A Systematic Review. . 2024. PMID 38925264 · DOI · PMC11794195
- Jimenez-Puyer M, Sobrino V, Colledge WH, Jones S, Tena-Sempere M. Hypothalamic control of puberty: from neuronal circuits to mechanisms for its metabolic regulation. . 2026. PMID 41108362 · DOI · PMC13246832
- Abreu AP, Kaiser UB. Pubertal development and regulation. Lancet Diabetes Endocrinol. 2016. PMID 26852256 · DOI · PMC5192018
- Herbison AE. Control of puberty onset and fertility by gonadotropin-releasing hormone neurons. Nat Rev Endocrinol. 2016. PMID 27199290 · DOI
- Eckert-Lind C, Busch AS, Petersen JH, Biro FM, Butler G, Bräuner EV, et al.. Worldwide Secular Trends in Age at Pubertal Onset Assessed by Breast Development Among Girls: A Systematic Review and Meta-analysis. JAMA Pediatr. 2020. PMID 32040143 · DOI · PMC7042934
- Vijayakumar N, Op de Macks Z, Shirtcliff EA, Pfeifer JH. Puberty and the human brain: Insights into adolescent development. Neurosci Biobehav Rev. 2018. PMID 29972766 · DOI · PMC6234123
- Pfeifer JH, Allen NB. Puberty Initiates Cascading Relationships Between Neurodevelopmental, Social, and Internalizing Processes Across Adolescence. Biol Psychiatry. 2021. PMID 33334434 · DOI · PMC8494463
- Sørensen K, Mouritsen A, Aksglaede L, Hagen CP, Mogensen SS, Juul A. Recent secular trends in pubertal timing: implications for evaluation and diagnosis of precocious puberty. Horm Res Paediatr. 2012. PMID 22508036 · 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.