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Robert W. Rebar Arasen A. V. Paupoo
Normal pubertal development occurs in a predictable orderly sequence over a definite time frame.
The major causes of delayed puberty include anatomic genital tract abnormalities and hypo-and hypergonadotropic amenorrhea.
When pubertal development occurs asynchronously with development of breasts in the absence of significant pubic and axillary hair, the diagnosis is usually androgen insensitivity.
The most common cause of precocious puberty is constitutional (idiopathic), but more serious causes must be ruled out and therapy geared toward optimizing adult height.
The most common cause of heterosexual development at the expected age of puberty is polycystic ovary syndrome.
Puberty is the period during which secondary sexual characteristics develop and the capability of sexual reproduction is attained. The physical changes accompanying pubertal development result directly or indirectly from maturation of the hypothalamus, stimulation of the sex organs, and secretion of sex steroids. Hormonally, puberty in humans is characterized by the resetting of the classic negative gonadal steroid feedback loop, alterations in circadian and ultradian (frequent) gonadotropin rhythms, and the acquisition in the woman of a positive estrogen feedback loop, which controls the monthly rhythm as an interdependent expression of gonadotropins and ovarian steroids.
The ability to evaluate and treat aberrations of pubertal development requires an understanding of the normal hormonal and physical changes that occur at puberty. An understanding of these changes is important in evaluating young women with amenorrhea.
Factors Affecting Time of Onset
The major determinant of the timing of the onset of puberty is no doubt genetic, but a number of other factors appear to inﬂuence both the age at onset and the progression of pubertal development. Among these inﬂuences are nutritional state, general health, geographic location, exposure to light, and psychological state (1). The concordance of the age of menarche in mother–daughter pairs and between sisters and in ethnic populations illustrates the importance of genetic factors (1). Typically, the age of menarche is earlier than average in children with moderate obesity (up to 30% above normal weight for age), whereas delayed menarche is common in those with severe malnutrition. Children who live in urban settings, closer to the equator, and at lower altitudes typically begin puberty earlier than those who live in rural areas, farther from the equator, and at higher elevations. The risk of earlier onset of puberty is 10 to 20 times greater after international adoption for unclear reasons (2). Other risk factors implicated for precocious puberty include exposure to estrogenic endocrine-disrupting chemicals and the absence of a father in the home (3,4). Blind girls apparently undergo menarche earlier than sighted girls, suggesting some inﬂuence of light (5).
In Western Europe, the age of menarche declined 4 months each decade between 1850 and 1960 (1). Data suggest that the trend toward earlier pubertal development may be continuing among girls (but not boys) who live in the United States (6). It is presumed that these changes represent improved nutritional status and healthier living conditions.