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Original Author(s): Charlotte Reay and Dr James Greening
Last updated: 16th October 2021
Revisions: 8

Original Author(s): Charlotte Reay and Dr James Greening
Last updated: 16th October 2021
Revisions: 8

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Introduction

Puberty defines the period in a child’s life when they undergo various physiological changes, leading to sexual maturity and giving them the ability to reproduce.

As well as changes in physical and physiological characteristics, puberty can also lead to changes in mood and emotions.

The mechanism behind the onset of puberty is via the HPA axis. Gonadotrophin-releasing hormone (GnRH) is released from the hypothalamus, stimulating the synthesis and release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These in turn stimulate the gonads to produce oestrogen or testosterone.

Normal puberty usually occurs at an earlier age in girls than boys. Some changes occur across both sexes, whilst others are unique to one.

Clinical Features

Pubertal changes on average begin at 10 ½ in girls and 11 ½ in boys, although full development may not be complete until years after onset.

Precocious puberty is defined as being 2-2 ½ SDS from the mean. This means that pubertal changes before the age of 8 in girls and 9 in boys are described as early-onset, or precocious. If physical changes (breast and testicular development) have not begun before the age of 14 then this is described as late-onset puberty.

There are many stages to puberty and although there is an age range for the onset of puberty, the order of characteristics’ development typically follows a set sequence for both boys and girls. This is known as consonant puberty. This sequence can be staged using the Tanner Stages of Sexual Development.

The end of puberty is linked to the fusion of the epiphyseal growth plates of the long bones. This means once puberty has occurred, you speed up your growth rate but this also heralds the cessation of growth within a fixed timeframe. Pubertal hormones are required to stop growth.

Puberty in girls

Adrenarche – Increased production of androgens by the adrenal glands, converted to oestrogens by the liver, ovaries and peripheral fats. This leads to:

  • Increased sebaceous gland activity ± acne
  • Sweating
  • Hair growth (pubic hair follows axillary hair)
  • Body odour

Thelarche – breast bud development is usually the first feature of puberty, but after onset, it can continue for another 5-6 years. Breasts begin as breast buds and continue to a mature breast contour. This can be assessed using Tanner’s classification.

Menarche – This is when menstruation begins. It usually coincides with Tanner’s stage 3 of breast development. The average age of menarche is 12.9 in the UK.

Growth – increased vertical height. Girls typically grow between 5-10 cm from the date of menarche.

The Tanner Stages of a female, showing thelarche and pubic hair growth

Puberty in boys

Adrenarche – Increased androgen production leads to:

  • Increased axillary, pubic and facial hair
  • Deepened voice
  • The ability to ejaculate developing

Testicular development – 

  1. Testicular enlargement. This can be measured using an orchidometer, which is a string with 12 different sized beads, corresponding to stages of testicle growth.
  2. Increased pigmentation.
  3. Scrotal thickening.
  4. Penile growth and thickening.

Growth – increased body size and muscle bulk. Peak growth usually occurs between 14-17 years of age.

The Tanner Stages of a male, showing penile and testicular growth

Complications of puberty

Acne

Pathophysiology: Linked to increased sebaceous gland activity and the production of free fatty acids. The inflammation and consequent pustule formation around the sebaceous glands occur as a result of colonisation by microorganisms.

Clinical features: Multiple skin lesions consisting of whiteheads (closed comedones), blackheads (open comedones) and pustules, which may be interspersed with scar tissue. Lesions most often affect the face, arms, chest and upper back.

NOTE: adolescents become preoccupied with their appearance throughout puberty, so having acne can be of significant distress for a young person. Acne can begin to rule their lives and be detrimental to their mental health.

Gynecomastia (breast development in boys)

This is a very common side effect of puberty. It is caused by an initial imbalance of oestrogen and androgens at puberty onset, with oestrogen initially raised, causing breast tissue growth. Reassurance is usually all that is required.

Disorders of puberty

Early-Onset (Precocious) Puberty

In girls, this is usually idiopathic and familial. In boys, you should have a high suspicion for underlying pathology such as a tumour or trauma. Precocious puberty may be classed as either true or false:

  • True precocious puberty- due to early activation of the Hypothalamic-Pituitary axis.
  • False precocious puberty- gonadotrophin independent. Usually presents with the isolated development of one pubertal characteristic.

Causes of true gonadotrophin dependent precocious puberty

  • Central malformation or damage e.g. hydrocephalus, neurofibromatosis
  • Acquired- post-sepsis, surgery, radiotherapy, trauma, birth anoxia
  • Brain tumours

Causes of false gonadotrophin-dependent precocious puberty

  • Increased adrenal activity- congenital adrenal hyperplasia
  • Exogenous sex steroids
  • Gonadal tumour- ovarian/testicular tumours
  • Hypothyroidism
  • McCune Albright syndrome- polyostotic fibrous dysplasia

Atypical Patterns of Puberty

  • Isolated breast development (thelarche variant)
  • Adrenarche: adrenal hormonal source:
  • CAH
  • Cushing’s
  • PCOS
  • Adrenal tumours
  • Isolated menarche
  • Ovarian cyst and secondary oestrogen

Consequences of early puberty

  • Short stature: early onset of puberty means a child loses 2-3 yrs of typical growth hormone-dependent growth (20cm in females and 30 cm in males)
  • Psychological disturbance: child treated as older than their age, deprived of their childhood.
  • Early menarche: particularly a practical consideration with onset in primary school-age – children where the school isn’t set up for it.
  • Safeguarding concerns of early development, particularly in vulnerable special educational needs children

Late-Onset Puberty

Diagnosis of late-onset puberty is made if there are no signs seen by the age of 13 ½  in boys and 13 in girls. It can also be diagnosed in girls who have not had their first menstrual period by the age of 16. There are a variety of causes of delayed puberty. Causes of delayed puberty in both sexes are:

  • Maturational delay- commonly runs in families
  • Gonadal failure- hypogonadotropic hypogonadism (high LH and FSH)
    • XXY, XO, XY/XO and variants (Turners/Klinefelters)
    • Abnormal gonad development (genes SRY, SF-1, WT-1 etc)
  • Hypothalamic Pituitary dysfunction (hypogonadotropic hypogonadism (low FSH and LH)
    • Tumours, infection, trauma
    • Genetic e.g. Kallmann Syndrome
  • Chronic and severe disease
  • Chemo/radiotherapy
  • Metabolic: Glycogen storage disorders, galactosaemia

Some causes of delayed puberty only seen in girls are:

  • Turner’s Syndrome- the absence of one of the X chromosomes
  • Anorexia Nervosa
  • Low body weight/athletic lifestyle
  • Autoimmune failure- premature ovarian failure

References

No. Reference
1 Rudolf M, Miall L, Smith D. Paediatrics at a glance. Oxford: Wiley-Blackwell; 2012.
2 Hull D, Johnston DI. Essential paediatrics. Edinburgh: Churchill Livingstone; 1993.
3 Rudolf M, Levene MI, Lee TJ. Paediatrics and child health. Oxford: Wiley-Blackwell; 2011.
4 Kapoor R, Barnes K. Paediatrics. 4th ed. Edinburgh: Mosby Elsevier; 2013.
5 Butler G, Kirk J. Paediatric endocrinology and diabetes. Oxford: Oxford University Press; 2011.
6 Hamilton-Fairley D. Lecture notes: obstetrics and gynaecology. Chichester: Wiley-Blackwell; 2008.
7 Brook c, Dattani M:  handbook of clinical pediatric endocrinology.wiley-blackwell 2012

 

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