Puberty In Boys - pediagenosis
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Monday, October 8, 2018

Puberty In Boys

Puberty In Boys
Puberty is the process by which the immature individual will acquire the physical and behavioral attributes that allow him or her to repro- duce. In males, puberty is largely the response of the body to the wide- spread actions of androgens. These are secreted by the newly awakened testes, under the influence of gonadotropins secreted by the anterior pituitary. While the progression of pubertal changes is predictable, the age of their onset differs dramatically in different areas of the world and even among children of different ethnic backgrounds within a particular region. Economic disparities may also be reflected in the age of onset.

Physical changes of puberty
In North America and Europe, puberty in males visibly begins with testes enlargement between ages 9 and 14. Secondary sexual characteristics progressively appear over the ensuing 2–2.5 years, and facial hair, the last to appear, will not be fully mature until 20–25 years.
The physical changes of male puberty have been divided into five stages using a system developed by Marshall and Tanner, who examined groups of English boys as they went through sexual maturation (Fig. 11.1). They then classified the relative and absolute changes in the sexual characteristics of the participants. Although they did not regard their findings as universal, their system has been widely used to describe the timing and progression of typical pubertal changes. Their descriptions must be recognized as specific to the demographics of their study population and to the years covered by the study. Pat- terns persist, but the characteristics and timing of these changes are affected by race, nutrition and other genetic and environmental factors.

This describes the contribution of the adrenal gland to puberty. It is characterized by an increase in adrenal synthesis and secretion of the relatively weak androgens: androstenedione, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S). Although the adrenal gland contributes only 5% of the total circulating androgen pool in boys, these adrenal androgens are responsible for initiating axillary and pubic hair growth. They are converted in the periphery to the more potent androgens: testosterone and dihydrotestosterone (DHT). Testosterone and DHT then stimulate pubic and axillary hair growth as well as growth of, and secretion by, the axillary sebaceous glands. Axillary and pubic hair typically appear in parallel with increasing testicular size and visibly mark the onset of puberty.
The exact trigger for adrenarche is unknown. The best evidence indicates it is an intrinsic, programmed event within the adrenal gland independent of adrenocorticotropic hormone (ACTH). Adrenarche is distinct from pubarche and either may occur in the absence of its counterpart.

Testicular maturation
Testicular maturation at puberty involves initiation of androgen production by the Leydig cells, growth of the seminiferous tubules and initiation of spermatogenesis. The gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) control all three events. Throughout childhood, FSH and LH concentrations in both the pituitary gland and plasma are low. Pulse amplitude and frequency of both hormones are also low, suggesting that the gonadotropin-releasing hormone (GnRH) pulse generator is cycling slowly. This characteristic of the gonadotropin–pituitary axis has been called the juvenile pause. About a year before testicular enlargement occurs, the release of pulsatile FSH and LH begins to increase in both amplitude and concentration. When this begins, it is most notable during sleep. This marked diurnal rhythm in FSH and LH secretion is the first endocrinologic manifestation of puberty. While these diurnal variations may be striking during early and mid-puberty, they are almost obliterated by the end of puberty.
The initiation of puberty is thought to reflect the release of the hypothalamic GnRH pulse generator from CNS inhibition. The site and exact mechanism of this inhibitory release are unknown. While much evidence indicates that the source of the trigger also resides in the CNS, there is growing interest in the role of leptin, a hormone produced by fat cells, in the initiation and progression of puberty. Leptin has been shown to be one of the many factors that influence the maturation of the GnRH pulse generator. Individuals who lack the hypothalamic GnRH pulse generator do not undergo puberty (Kallmann syndrome; Chapter 29) and tumors or surgery in the region of the median basal hypothalamus can be linked with delayed or absent puberty.
The increase in size of the testes with onset of puberty is largely the result of increasing mass of the seminiferous tubules and initiation of spermatogenesis. Leydig cell stimulation results in a 10-fold increase in testosterone production over the course of puberty but accounts for only a small proportion of the change in testicular size. The Leydig cells occupy less than 10% of the total testicular mass.

Secondary sexual characteristics Testosterone and its metabolites cause the following somatic changes in pubertal boys:
               Increased laryngeal size.
               Deepening of the voice.
               Increased bone mass.
               Increased mass and strength of skeletal muscle.
               Thickened skin.
               Increased and thickened hair on the trunk, pubis, axillae and face.

Somatic growth
Somatic growth at puberty is the result of a complex interaction between gonadal sex steroids, growth hormone (GH) and insulin-like growth factor 1 (IGF-1). Insulin and thyroxine are also necessary for optimal growth. The absence of GH, IGF-1 or IGF-1 receptor will lead to somatic dwarfism, even in the presence of normal plasma sex steroid concentrations.
Concomitant with the changes in the pulse frequency of LH that signal the beginning of puberty is a change in the amplitude of GH secretion. This appears to be the result of estrogen stimulation in both boys and girls. In boys, while the increase in GH can be initiated and maintained by testosterone, it does not occur with the administration of DHT. Further, GH secretion in the presence of testosterone can be blocked by the administration of tamoxifen, which blocks the estrogen receptor. In contrast, even miniscule doses of estrogen substantially increase GH concentrations. These findings suggest that the effect of testosterone on bone growth is indirect and probably secondary to aromatization of testosterone to estradiol. This is in stark contrast to the action of testosterone on muscle, where androgens act directly to increase muscle mass.
Bone growth occurs when testosterone, aromatized to estradiol, increases GH levels. This causes a parallel rise in IGF-1, a potent anabolic hormone that mediates many metabolic actions of GH, including trabecular bone formation. Normally, GH stimulates IGF-1 synthesis, and IGF-1 suppresses GH release in a negative feedback loop. At puberty, however, GH continues to rise despite high levels of circulating IGF-1. This allows for maximum linear bone growth during puberty. Outside of puberty, this combination of an increase in both GH and IGF-1 is seen only in acromegaly, a disease state characterized by autonomous GH secretion. Peak growth velocity in boys occurs when plasma testosterone levels reach 50% of adult male levels, and growth will continue until epiphyseal fusion occurs in the long bones. The sex steroids (perhaps via estrogen activity) are responsible for epiphyseal closure, which occurs at a median age of 21 in young men. The determinants of final adult height are many and include genetic predisposition, body mass index at the onset of puberty, nutrition and length of puberty. Genetic determinants of bone growth appear to be carried on the distal short arm of the X chromosome. This locus does not appear to undergo X inactivation. Therefore, this locus, and any homologous loci on the Y chromosome, will direct final adult height. The effects of this genetic control pattern are apparent among men with the sex chromosome disorder Klinefelter syndrome; they have a 47XXY karyotype and are unusually tall, presumably because of the double dose of X-linked stature determinants.
Higher body mass indices in late childhood affect final height in both boys and girls. Children with increased body fat tend to enter puberty earlier. They begin their growth spurt after a shorter period of prepubertal growth and hence may not reach the full genetically pre- determined adult height. Boys enter puberty later than girls and so have a longer period of prepubertal growth. Boys also experience a greater peak linear growth velocity during adolescence than girls. For both reasons, men tend to be taller than women.
Androgens have a direct anabolic effect on muscle mass. The increase in androgen secretion during puberty increases muscle mass in both boys and girls. Reflecting the higher levels of circulating androgens, this effect is more dramatic in boys.

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