Initiated in late childhood via endocrine changes that lead to sexual maturation and reproductive capability.
A normal process of growth and development towards sexual maturity.
Requires an intact hypothalamic-pituitary-gonadal axis ( HPG).
Manifested by the reemergence of gonadotropin-releasing hormone (GnRH) from its relative quiescence during childhood.
GnRH stimulates secretion of luteinizing hormone and follicle stimulating hormone, which then stimulate gonadal maturation and sex steroid production.
Accompanied by physical growth and significant brain maturational changes.
Propels individuals into adolescence with peaks in strength and fitness.
Triggers emotional, cognitive, and behavioral changes.
Associated with increased mortality and morbidity from accidents, injuries, mental disorders, substance abuse, eating disorders, and suicide.
Begins with complex neuroendocrine network which has been quiescent since neonatal life.
Gonadarche (sexual maturation) is initiated with pulsatile nocturnal release of gonadotropin releasing hormone from specialized hypothalamic neurons that leads to the pituitary release of follicle stimulating hormone and lutenizing hormone.
Gonadal growth and production of gonadal sex steroids cause the development of secondary sexual characteristics.
In girls process of growth and sexual maturity lead to noticeable changes in breast growth as well as development of axillary and pubic hair, while growth of internal genital organs of the ovaries, uterus, and vagina also occur but are not visible.
In middle childhood the pituitary secretes Luteinizing Hormone (LH) in girls which trigger puberty.
The adrenal androgens increase from around 6-8 years in a process called adrenarche, with development of axillary and pubic hair and contribute to acne.
Tanner stages are utilized to evaluate pubertal development: in girls breast development is rated from 1-5 from preadolescent to mature with stage 2 the appearance of the breast bud marking the onset of pubertal development, in boys and girls pubic hair is rated from 1-5, preadolescent with no hair to adult and stage 2 marking onset of pubic hair, in boys genital development rated from 1-5, preadolescent to adult with stage 2 marked by enlargement of the scrotum and testes and by change in scrotal reddening and texture.
Stage 2 public hair develops an average of 12-20 months after stage 2 genital development.
Onset of puberty Tanner stage 2 noted by breast development in girls and testicular enlargement with a volume of greater than 4 ml or testicular length greater than 25 mm.
Normal age range for Tanner stage 2 development refers to the age at which 95% of children attain pubertal onset and it is between 8 and 13 years in girls and 9 years 6 months and 13 years 6 months in boys.
Exposure to chemicals in toothpaste, cosmetics, and mothballs could be one of the reasons girls are entering puberty an early age: suggesting endocrine disrupting chemicals could be contributing to the phenomenon of early puberty.
Delayed puberty is defined as the absence of testicular enlargement in boys or breast development in girls at an age that is 2-2.5 standard deviations later than the population mean.
Mean age of puberty for males is 14 years and for girls is 13 years.
There has been a downward trend in the timing of puberty in the United States and other countries.
The onset of puberty has changed among racial and ethnic groups as well.
Pubic hair development is usually not considered in the definition of delayed puberty because pubarche may result from maturation of the adrenal glands and the onset of pubic hair can be independent of HPG-axis activation.
Delaying puberty can affect psychological well-being.
Delayed puberty can affect adult stature, but on average is only slightly below the genetic target.
Delayed puberty in boys that is an extreme of the normal spectrum of pubertal timing, referred to as a constitutional delay of growth and puberty (CDGP).
Downward trend in pubertal timing in US and many other countries.
Approximately 65% of boys and 30% of girls with delayed puberty have CDGP (Sedlimeyer IL et al).
CDGP can be diagnosed after underlying conditions have been ruled out.
CDGP cause is unknown, but has a genetic relationship such that 50-80% of variation in the timing of puberty is due to such factors and , and 50-75% of patients with from the GG have a family history of delayed puberty.
CDGP inheritance is variable, but is most commonly autosomal dominant, with or without complete penetrance.
CDGP Is not sex specific.
CDGP is the single most common cause of delayed puberty in both sexes, but it can be diagnosed after underlying conditions have been ruled out.
CDGP cause is unknown.
CDGP management includes observation or therapy with low dose sex steroids.
CDGP treatment goal is to induce the appearance of secondary sexual characteristics or acceleration of growth, and to mitigate psychosocial difficulties associated with pubertal delay and short stature.
Routine use of growth hormone, anabolic steroids, or aromatase inhibitors is not recommended.
Causes of early puberty are still somewhat unclear.
Girls who have a high-fat diet and are not physically active and who are obese are more likely to physically mature earlier.
Obese girls, defined as at least 10 kilograms (22 pounds) overweight, had an 80 percent chance of developing breasts before their ninth birthday and starting menstruation before age 12.
Exposure to chemicals that mimic estrogen is another possible cause of early puberty in girls.
There is a higher prevalence of early puberty in black versus white girls.
While more girls are increasingly entering puberty at younger ages, new research indicates that some boys are actually starting later.
Increasing rates of obese and overweight children in the United States may be contributing to a later onset of puberty in boys.