Delayed puberty is absence of sexual maturation at the expected time (breast development by age 13 in girls and testicular enlargement by age 14 in boys). Diagnosis is by measurement of gonadal hormones (testosterone and/or estradiol), luteinizing hormone, and follicle-stimulating hormone; imaging studies; and genetic testing. Treatment, when necessary, usually involves specific hormone replacement.
Delayed puberty may result from constitutional delay, which often occurs in adolescents with a family history of delayed growth, or from other causes. (See also puberty in males, puberty in females, and Physical Growth and Sexual Maturation in Adolescents.)
Constitutional delay of puberty
Constitutional delay of pubertyis a self-limiting form of normal development in which puberty is delayed but begins spontaneously and normally albeit later than in peers; it is more common among boys. Many children have a family history of delayed sexual development in a parent or sibling. Typically, stature is usually short during childhood, adolescence, or both but ultimately reaches the normal range. Growth velocity is in low- normal range, and growth pattern parallels the lower percentile curves of the growth chart. The pubertal growth spurt is delayed, and at the expected time of puberty, height percentile begins to drop, which may contribute to psychosocial difficulties for some children. Skeletal age is delayed, often by 2 or more years, and is most consistent with the child's height age (age at which a child's height is at the 50th percentile) rather than chronologic age. Sexual maturation is delayed but normal. Because of delayed skeletal growth, growth lasts longer than peers, and most reach a normal adult height. Constitutional delay of growth and puberty is a diagnosis of exclusion and must be differentiated from other causes of delayed puberty (e.g. hypogonadotropic hypogonadism) or growth hormone deficiency.
Other causes of delayed puberty
Other causes of delayed puberty include (1):
Genetic disorders (Turner syndrome in girls, Klinefelter syndrome in boys)
Central nervous system (CNS) disorders (eg, hypothalamic or pituitary tumors that reduce gonadotropin secretion)
Other causes of hypogonadism
Testicular disorders such as injury (eg, testicular torsion) or infection (eg, mumps) in boys
CNS radiation
Certain chronic disorders (eg, poorly controlled diabetes mellitus, inflammatory bowel disorders, renal disorders, cystic fibrosis, anemia)
Autoimmune disorders (eg, Hashimoto thyroiditis, primary adrenal insufficiency, and some disorders that directly affect the ovaries such as autoimmune oophoritis and autoimmune polyglandular syndromes)
Undernutrition/eating disorders, which cause functional gonadotropin deficiency
Excess physical activity, especially in girls
General reference
1. Howard SR, Dunkel L. The genetic basis of delayed puberty. Neuroendocrinology. 2018;106(3):283-291. doi: 10.1159/000481569
Symptoms and Signs of Delayed Puberty
In girls, breast development, pubic hair growth, and/or menarche do not occur.
In boys, genital development and/or pubic hair growth are absent.
Short stature, decreased growth velocity, or both may indicate delayed puberty in either sex.
Adolescents with delayed puberty may be teased or bullied, and often need help in coping with and managing social concerns (1, 2). Boys are more likely than girls to feel psychological stress and embarrassment because of short stature and delayed puberty (3), but both boys and girls may perceive an effect on school and social performance.
Manifestations of possible causes of delayed puberty
Signs of possible underlying chronic disease include an abrupt change in growth, undernutrition, discordant development (eg, pubic hair without breast development), or stalled pubertal development (ie, puberty starts then fails to progress).
Neurologic symptoms (eg, headaches, vision problems), polydipsia, and/or galactorrhea could suggest a CNS disorder. Hyposmia or anosmia could indicate Kallman syndrome.
Gastrointestinal symptoms could suggest an inflammatory bowel disorder.
An abnormal body image (eg, false belief in being overweight) suggests the need to evaluate for an eating disorder.
Primary amenorrhea could suggest Turner syndrome.
Symptoms and signs references
1. Bigelow JC, Chaku N. Appearance-Related Victimization and Pubertal Asynchrony: Identifying Sex-Specific Vulnerabilities. J Youth Adolesc. 2025;54(4):821-836. doi:10.1007/s10964-024-02099-z
2. Palmert MR, Dunkel L. Clinical practice. Delayed puberty. N Engl J Med. 2012;366(5):443-453. doi:10.1056/NEJMcp1109290
3. Quitmann JH, Bullinger M, Sommer R, Rohenkohl AC, Bernardino Da Silva NM. Associations between Psychological Problems and Quality of Life in Pediatric Short Stature from Patients' and Parents' Perspectives. PLoS One. 2016;11(4):e0153953. doi:10.1371/journal.pone.0153953
Diagnosis of Delayed Puberty
History and physical examination
Family history of delayed puberty
Clinical criteria
Measurement of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone or estradiol
Bone age radiograph
Sometimes additional imaging studies
Sometimes karyotype or other genetic testing
The initial evaluation of delayed puberty should consist of a complete history and physical examination to evaluate pubertal development, nutritional status, and growth. Depending on findings, laboratory tests for other causes of slow growth should be considered:
Hypothyroidism (eg, thyroid-stimulating hormone, thyroxine [T4])
Renal disorders (eg, electrolytes, creatinine levels)
Inflammatory and immune conditions (eg, tissue transglutaminase antibodies, C-reactive protein)
Hematologic disorders (eg, complete blood count with differential)
Criteria for delayed puberty
Although many children seem to be starting puberty earlier than in past years, there are no indications that the criteria for delayed puberty should change.
In girls, delayed puberty is diagnosed if 1 of the following occurs:
No breast development by age 13 years
> 3 years elapsed between the beginning of breast growth and menarche
Menstruation does not occur by age 15 (in the presence of normal secondary sexual characteristics)
In boys, delayed puberty is diagnosed if 1 of the following occurs:
No testicular enlargement by age 14 years
> 4 years elapsed between initial and complete growth of the genitals
Onset of pubic hair is not included in the definition of delayed puberty because it is a sign of adrenarche as opposed to true puberty.
Children who have no evidence of pubertal progression (referred to as stalled or interrupted puberty) for a sustained period of time (typically > 1 year) can be evaluated sooner, even if before the established age threshold for delayed puberty.
Hormonal testing
LH and FSH are measured, and testosterone in boys or estradiol in girls is measured. LH and FSH are gonadotropins secreted by the pituitary, which stimulate production of sex hormones. LH and FSH levels are the most useful initial tests (see also algorithm ). FSH is most helpful for establishing evidence of gonadal failure, whereas LH is helpful for determining the onset of puberty. Testing should be performed in the morning and requires pediatric-specific assays (often labeled as ultrasensitive or immunochemiluminometric [ICMA]).
Elevated serum LH and FSH levels indicate:
Gonadal failure caused by defects of the gonads themselves (primary hypogonadism [hypergonadotropic hypogonadism])
FSH measurement is particularly important for the diagnosis of primary hypogonadism because FSH has a longer half life, is more sensitive, and shows less variability than LH. FSH levels > 20 mIU/mL (> 20 units/L) suggest probable gonadal dysfunction.
Assays for testosterone and estradiol levels do not always distinguish early pubertal from prepubertal levels.
In children who have elevated serum LH and FSH levels, karyotype analysis should be performed to investigate for Klinefelter syndrome in boys and Turner syndrome in girls. If karyotype is normal, girls with severe pubertal delay should be further investigated for other causes of primary ovarian insufficiency.
Low or normal FSH and LH levels along with low testosterone and/or estradiol levels in children with short stature and delayed pubertal development may indicate:
Constitutional delay
Secondary hypogonadism (hypogonadotropic hypogonadism)
Functional hypogonadotropic hypogonadism (caused by hypothyroidism, inflammatory conditions, undernutrition, or excessive exercise)
Constitutional delay of puberty is more commonly diagnosed in boys, partly because adolescent boys may be more distressed if they do not mature or grow at the same rate as their peers and are thus more likely to present for evaluation (1, 2). In addition to FSH, LH, and testosterone, inhibin B and anti-müllerian hormone (AMH) may be helpful markers of gonadal function (see Diagnosis of Male Hypogonadism in Children) (3, 4) to distinguish constitutional delay of puberty from permanent causes of hypogonadotropic hypogonadism.
Chronic disorders that cause inadequate nutrition can delay puberty by impairing gonadotropin-releasing hormone release.
Permanent forms of hypogonadotropic hypogonadism are more likely if endogenous LH and testosterone production does not significantly increase after 1 or 2 short courses of testosterone therapy have been completed. If a pituitary disorder is suspected, levels of other pituitary hormones should be measured because, in addition to being isolated, hypogonadotropic hypogonadism can be associated with other hormone deficiencies.
Imaging studies
When growth is abnormal, bone age radiograph should be the first test. Bone age is determined from a radiograph of the left hand (by convention) and can provide an estimate of remaining growth potential and help predict adult height.
This radiograph is of the hand and wrist of a 10-year-old girl who has constitutional growth delay. Her bone development is typical of that of a 7-year-old child with wider gaps between bones in the hand and the wrist compared to those in a bone x-ray of a 10-year-old, which shows narrower epiphyses (growth plates).
DR P. MARAZZI/SCIENCE PHOTO LIBRARY
Evaluating the pituitary gland with MRI may be indicated to exclude tumors and structural anomalies in suspected hypogonadotropic hypogonadism.
For girls with primary amenorrhea, a pelvic ultrasound can be performed to identify the presence of a uterus. If the uterus is absent, a karyotype and testosterone level are performed to evaluate for chromosomal abnormalities. A 46,XY karyotype may indicate 5-alpha-reductase deficiency or complete androgen insensitivity syndrome (with clinical phenotype as well as testosterone and dihydrotestosterone levels distinguishing further); and a 46,XX karyotype may indicate müllerian agenesis. If the uterus and breast development are present, an outflow tract obstruction is more likely.
Genetic testing
About half of cases of hypogonadotropic hypogonadism are genetic (5), and Kallman syndrome is the most common cause (see Secondary hypogonadism). If other pituitary hormone deficiencies are noted, specific genetic abnormalities may be present (eg, PROP1).
Diagnosis references
1. Jonsdottir-Lewis E, Feld A, Ciarlo R, Denhoff E, Feldman HA, Chan YM. Timing of Pubertal Onset in Girls and Boys With Constitutional Delay. J Clin Endocrinol Metab. 2021;106(9):e3693-e3703. doi:10.1210/clinem/dgab270
2. Quitmann JH, Bullinger M, Sommer R, Rohenkohl AC, Bernardino Da Silva NM. Associations between Psychological Problems and Quality of Life in Pediatric Short Stature from Patients' and Parents' Perspectives. PLoS One. 2016;11(4):e0153953. Published 2016 Apr 20. doi:10.1371/journal.pone.0153953
3. Varimo T, Miettinen PJ, Känsäkoski J, et al. Congenital hypogonadotropic hypogonadism, functional hypogonadotropism or constitutional delay of growth and puberty? An analysis of a large patient series from a single tertiary center. Hum Reprod. 2017;32(1):147-153. doi: 10.1093/humrep/dew294
4. Rohayem J, Nieschlag E, Kliesch S, Zitzmann M. Inhibin B, AMH, but not INSL3, IGF1 or DHEAS support differentiation between constitutional delay of growth and puberty and hypogonadotropic hypogonadism. Andrology. 2015;3(5):882-887. doi: 10.1111/andr.12088
5. Louden ED, Poch A, Kim HG, Ben-Mahmoud A, Kim SH, Layman LC. Genetics of hypogonadotropic Hypogonadism-Human and mouse genes, inheritance, oligogenicity, and genetic counseling. Mol Cell Endocrinol. 2021;534:111334. doi:10.1016/j.mce.2021.111334
Treatment of Delayed Puberty
Hormone therapy
If boys show no sign of pubertal development by age 14 years, they may be given a 4- to 6-month course of low-dose testosterone (eg, cypionate, enanthate) once per month. These low doses induce puberty with some degree of virilization and do not jeopardize adult height potential. Testosterone has traditionally been given by intramuscular injections during short courses, but it can also be given subcutaneously to "jump start" puberty. Transdermal preparations are reserved for in older males (≥ 18 years) (1).
After the course is complete, treatment is stopped, and testosterone levels are measured several weeks or months later to differentiate temporary from permanent deficiency; an increase to pubertal levels suggests the deficiency was temporary rather than permanent. If testosterone levels are not higher than the initial value and/or pubertal development does not continue after completion of treatment, a second course of low-dose treatment can be given.
If endogenous puberty has not begun after 2 courses of treatment, the likelihood of permanent deficiency is higher, and patients need to be reevaluated for other causes of hypogonadism. For permanent forms of hypogonadism, the testosterone dose is increased over an 18- to 24-month period towards adult replacement doses (see treatment of male hypogonadism in children). Testosterone has also been the traditional treatment for permanent hypogonadotropic hypogonadism. It promotes virilization but not testicular growth or spermatogenesis. Gonadotropin therapy, typically FSH in combination with human chorionic gonadotropin (hCG), may help with testicular development and spermatogenesis, but consensus is lacking on the use of these medications in this age group for pubertal induction or completion (2).
Testosterone therapy is used for hypergonadotropic hypogonadism, constitutional growth delay (when reassurance is not sufficient), and in some cases of permanent hypergonadotropic hypogonadism (3).
In girls, depending on the cause, hormone therapy may be used to induce puberty or, in some cases (eg, Turner syndrome), may be needed for long-term replacement. Estrogen replacement is given orally or transdermally, and the dose is increased over an 18- to 24-month period (3). Doses are lower than those used in adults, and transdermal patches are generally preferred over pills. Girls can be transitioned to transdermal estrogen patches with cyclic progestin (often given orally on days 1 to 10 of the calendar month either as medroxyprogesterone or micronized progesterone) or to combined estrogen-progestin oral contraceptive preparations for long-term treatment.
Treatment references
1. Chioma L, Cappa M. Hypogonadism in Male Infants and Adolescents: New Androgen Formulations. Horm Res Paediatr. 2023;96(6):581-589. doi:10.1159/000521455
2. Alexander EC, Faruqi D, Farquhar R, et al. Gonadotropins for pubertal induction in males with hypogonadotropic hypogonadism: systematic review and meta-analysis. Eur J Endocrinol. 2024;190(1):S1-S11. doi:10.1093/ejendo/lvad166
3. Harrington J, Palmert MR. An Approach to the Patient With Delayed Puberty. J Clin Endocrinol Metab. 2022;107(6):1739-1750. doi:10.1210/clinem/dgac054
Key Points
Delayed puberty may represent constitutional delay or be caused by a variety of genetic or acquired disorders.
Measure levels of testosterone or estradiol, luteinizing hormone, and follicle-stimulating hormone.
Do a bone age radiograph as part of initial evaluation.
Pituitary imaging, pelvic ultrasound in girls, and genetic testing may be performed to diagnose cause.
Hormone therapy may be indicated to induce puberty or as long-term replacement.
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