- 1 Definition of Puberty
- 2 Physiology of Normal Puberty
- 3 Disorders of Puberty
- 4 Conclusion
- 5 Related Posts
Definition of Puberty
Puberty is the period during which sexual maturity is reached, resulting in the capacity for reproduction. It involves the growth and maturation of the primary sexual characteristics (gonads and genitals) and the appearance of secondary sexual characteristics (including sexual hair and voice change).
A study of more than 17,000 healthy 3- to 12-year-old girls sponsored by the American Academy of Pediatrics suggests that puberty occurs at an earlier age today than in the past. Consequently, a change in the lower limit of puberty in girls (from eight to seven years of age in whites, and six years of age in African-Americans) was proposed recently by the Lawson Wilkins Pediatric Endocrine Society. On the other hand, two recent studies in boys did not show a distinct trend toward earlier maturation, and in one of them, the investigators did not find a significant difference in the timing of puberty based on race. Thus, puberty continues to be considered normal in boys if it starts after the age of 9 years and before the age of 13.5 years.
Physiology of Normal Puberty
Secondary Sexual Characteristics
The method described by Tanner (stages is the most utilized throughout the world for assessing sexual maturation. The stages are defined by physical measurements of development based on external primary and secondary sexual characteristics, such as the size of the breasts and genitalia, and the development of pubic hair. Although pubic hair is usually the first evidence of puberty in girls, increased testicular size is the first physical evidence of puberty in boys. In general, pubertal testicular enlargement has begun when the longitudinal measurement of a testis is greater than 2.5 cm (excluding the epididymis) or the volume is equal to or greater than 4 mL. The right testis is usually larger than the left, and the left testis is located lower in the scrotum than the right.
The phallus is more accurately measured in the stretched, flaccid state. The length of the erectile tissue (excluding the foreskin) increases from an average of 6.2 cm in the prepubertal stage to 12.4+2.7 cm in the white adult; in black men, the mean length is 14.6 cm, and in Asians, 10.6 cm.
During puberty, the male larynx, cricothyroid cartilage, and laryngeal muscles enlarge; the voice breaks at approximately 13.9 years and the adult voice is achieved by 15 years of age.
Pubertal Growth Spurt
The pubertal growth spurt can be divided into three stages: the stage of minimal growth velocity just before the spurt (takeoff velocity), the stage of most rapid growth, or peak height velocity, and the stage of decreased velocity and cessation of growth at epiphyseal fusion. Boys reach peak height velocity approximately two years later than girls and are taller at takeoff; peak height velocity occurs at stages three to four of puberty in most boys and is completed by stage five in more than 95% of boys. The mean takeoff age is 11 years, and the peak height velocity occurs at a mean age of 13.5 years in boys. The total height gain in boys between takeoff and cessation of growth is approximately 31 cm. The mean height difference (boys taller than girls) between adult-height men and women is 12.5 cm.
Bone Age and Body Composition
Skeletal maturation is assessed by comparing radiographs of the hand, the knee, or the elbow with standards of maturation in a normal population. In normal children, bone age, an index of physiological maturation, does not have a well-defined relationship to the onset of puberty and is as variable as the chronologic age; however, in boys with delayed puberty, bone age correlates better with the onset of secondary sexual characteristics than does chronologic age.
There are dramatic changes during puberty in males, including increases in lean body mass, skeletal mass, bone-mineral density, and body water, and decreases in percentage fat mass. In boys, bone-mineral density reaches a peak early in the third decade of life, well after the peak height velocity. The growth spurt at a time well before peak bone mass may be a factor that results in a period of increased fragility and susceptibility to trauma.
Before puberty, the pulse amplitude of gonadorropin release [luteinizing hormone (luteinizing hormone) and follicle-stimulating hormone (follicle-stimulating hormone)] is low and occurs infrequently. The onset of pubertal hormonal changes is first evident in dramatic episodes of luteinizing hormone release of short duration that first occurs during sleep. With maturity, this release occurs regularly throughout the day. The intermittent release of gonadotropin is reflective of the episodic release of gonadorropin-releasing hormone (gonadotropin-releasing hormone). The increased sex hormone production by the testes (predominantly testosterone) results from increased luteinizing hormone stimulation; follicle-stimulating hormone stimulates the Sertoli cells, which, in conjunction with testosterone, stimulate maturation of spermatogenesis.
Prepubertal boys have plasma testosterone concentrations of less than 0.3 nmol / L (0.1 ng / mL), except during the first three to five months of life, when pubertal levels are found. Nighttime elevations of serum testosterone are detectable in the male before the onset of physical signs of puberty and during early puberty after the development of sleep-entrained secretion of luteinizing hormone. In the daytime, testosterone levels begin to increase at approximately 11 years of age, after the testis volume is at least 4 mL, and continue to increase throughout puberty. The steepest increment in testosterone levels occurs between pubertal stages two and three.
In the male, approximately 75% or more of estradiol is derived from extraglandular aromarization of testosterone and (indirectly) androstenedione, and the remainder is secreted by the testes. Many actions of testosterone on growth, skeletal maturation, and accretion of bone mass are, to a great extent, the result of its aromarization to estrogen.
In boys, low levels of estradiol are present before puberty and rise throughout puberty until the pubertal growth spurt occurs, and decrease thereafter.
There is a progressive increase in plasma levels of dehydroepiandrosterone (DHEA) and its sulfated form (DHEAS) in both boys and girls beginning at the age of seven or eight years and continuing throughout early adulthood. The increase in the secretion of adrenal androgens and its precursors is known as “adrenarche.” Dissociation of adrenarche and gonadarche (maturation of the gonads) occurs in several disorders of sexual maturation, including premature adrenarche (onset of pubic or axillary hair before the age of eight years) and central precocious puberty (CPP).
Serum growth hormone (GH) levels rise during pubertal development in both boys and girls as a result of increased gonadal steroid secretion. Basal GH secretion is evident before puberty; the amplitude and mass of GH secretion, but not secretory episodes, are increased during pubertal development. This increase in pubertal GH secretion is characterized by a concomitant rise in plasma insulin-like growth factor-1 concentration.
The aromatization of testosterone to estradiol accounts for a significant portion of the effect of testosterone on GH secretion. Treatment of late pubertal boys with the estrogen antagonist tamoxifen leads to smaller GH secretory peaks and, to a lesser degree, fewer GH secretory episodes, supporting the critical role of estrogens in regulating GH secretion.
Disorders of Puberty
During the last decade, intensive basic and clinical research has enhanced the understanding of the normal physiology of puberty. Using this knowledge, it is essential to determine which patients should undergo an in-depth evaluation and which conditions should be considered normal variants.
Most boys with CDGP will undergo normal puberty without intervention; however, androgen therapy may have beneficial effects on bone-mineral density and body composition, in addition to its psychological benefits.
Delayed puberty may be secondary to insufficient pulsatile secretion of gonadotropin-releasing hormone (hypogonadotropic hypogonadism) or testicular failure despite high levels of gonadotropins (hypergonadorropic hypogonadism). In both conditions, testosterone treatment is indicated to induce and / or maintain sexual maturation and to maximize linear growth.
Precocious puberty can be central (Gn RH-dependent) or peripheral (gonadotropin-releasing hormone-independent). Gonadotropin-releasing hormone agonist therapy is effective in the treatment of CPP. On the other hand, treatment of PPP is directed toward the specific pathophysiologic process.