Initiation of Adolescence

The first events of puberty occur in the brain, and although considerable research progress has been made in this area, the precise stimulus for their unfolding remains unknown. For whatever reason, apparently influenced both by an internal clock and external stimuli, brain cells in the hypothalamus begin to secrete substances called releasing factors. Both the cells and their method of action are somewhat unusual. These neuroendocrine cells look like typical neurons, but they secrete materials in the cell body, which are carried by cytoplasmic transport down the axon toward a richly vascular area at the base of the hypothalamus near the pituitary gland (Figure 4-1). The substances secreted by the nerve cells pass into capillaries in this vascular region and are carried the short distance to the pituitary by blood flow. It is unusual in the body for the venous return system to transport substances from one closely adjacent region to another, but here the special arrangement of the vessels seems made to order for this purpose. Accordingly, this special network of vessels, analogous to the venous supply to the liver but on a much smaller scale, is called the pituitary portal system.

In the anterior pituitary, the hypothalamic releasing factors stimulate pituitary cells to produce several related but different hormones called pituitary gonadotropins. Their function is to stimulate endocrine cells in both the adrenal glands and the developing sex organs to produce sex hormones. In every individual a mixture of male and female sex hormones is produced, and it is a biologic fact, as well as an everyday observation, that there are feminine males and masculine females. Presumably this represents the balance of the competing male and female hormones. In the male, different cell types in the testes produce both the male sex hormone testosterone and the female sex hormones. A different pituitary gonadotropin stimulates each of these cell types. In the female, the pituitary gonadotropins stimulate secretion of estrogen by the ovaries, and later progesterone by the same organ. In the female, male sex hormones are produced in the adrenal cortex, stimulated by still another pituitary hormone, and possibly some female hormones are produced in the male adrenal cortex.

Under the stimulation of the pituitary gonadotropins, sex hormones from the testes, ovaries, and adrenal cortex are released into the bloodstream in quantities sufficient to cause development of secondary sexual characteristics and accelerated growth of the genitalia. The increasing level of the sex hormones also causes other physiologic changes, including the acceleration in general body growth and shrinkage of lymphoid tissues seen in the classic growth curves described in Chapter 2. Neural growth is unaffected by the events of adolescence, since it is essentially complete by age 6. The changes in the growth curves for the jaws, general body, lymphoid, and genital tissues, however, can be considered the result of the hormonal changes that accompany sexual maturation (Figure 4-2).

The system by which a few neurons in the hypothalamus ultimately control the level of circulating sex hormones may seem curiously complex. The principle, however, is one utilized in control systems throughout the body and also in modern technology. Each of the steps in the control process results in an amplification of the control signal, in a way analogous to the amplification of a small musical signal between the signal source and speakers of a stereo system. The amount of pituitary gonadotropin produced is 100 to 1000 times greater than the amount of gonadotropin-releasing factors produced in the hypothalamus, and the amount of sex hormones produced is 1000 times greater than the amount of the pituitary hormones themselves. The system, then, is a three-stage amplifier. Rather than being a complex biologic curiosity, it is better viewed as a rational engineering design. A similar amplification of controlling signals from the brain is used, of course, in all body systems.

Timing of Puberty

There is a great deal of individual variation, but puberty and the adolescent growth spurt occur on the average nearly 2 years earlier in girls than in boys (Figure 4-3). Why this occurs is not known, but the phenomenon has an important impact on the timing of orthodontic treatment, which must be done earlier in girls than in boys to take advantage of the adolescent growth spurt. Because of the considerable individual variation, however, early-maturing boys will reach puberty ahead of slow-maturing girls, and it must be remembered that chronologic age is only a crude indicator of where an individual stands developmentally. The stage of development of secondary sexual characteristics provides a physiologic calendar of adolescence that correlates with the individual’s physical growth status. Not all the secondary sexual characteristics are readily visible, of course, but most can be evaluated in a normal fully clothed examination, such as would occur in a dental office.

Adolescence in girls can be divided into three stages, based on the extent of sexual development. The first stage, which occurs at about the beginning of the physical growth spurt, is the appearance of breast buds and early stages of the development of pubic hair. The peak velocity for physical growth occurs about 1 year after the initiation of stage I, and coincides with stage II of development of sexual characteristics (see Figure 4-3). At this time, there is noticeable breast development. Pubic hair is darker and more widespread, and hair appears in the armpits (axillary hair).

The third stage in girls occurs 1 to years after stage II and is marked by the onset of menstruation. By this time, the growth spurt is all but complete. At this stage, there is noticeable broadening of the hips with more adult fat distribution, and development of the breasts is complete.

The stages of sexual development in boys are more difficult to specifically define. Puberty begins later and extends over a longer period—about 5 years compared with years for girls (see Figure 4-3). In boys, four stages in development can be correlated with the curve of general body growth at adolescence.

The initial sign of sexual maturation in boys usually is the “fat spurt.” The maturing boy gains weight and becomes almost chubby, with a somewhat feminine fat distribution. This probably occurs because estrogen production by the Leydig cells in the testes is stimulated before the more abundant Sertoli cells begin to produce significant amounts of testosterone. During this stage, boys may appear obese and somewhat awkward physically. At this time also, the scrotum begins to increase in size and may show some increase or change in pigmentation.

At stage II, about 1 year after stage I, the spurt in height is just beginning. At this stage, there is a redistribution and relative decrease in subcutaneous fat, pubic hair begins to appear, and growth of the penis begins.

The third stage occurs 8 to 12 months after stage II and coincides with the peak velocity in gain in height. At this time, axillary hair appears and facial hair appears on the upper lip only. A spurt in muscle growth also occurs, along with a continued decrease in subcutaneous fat and an obviously harder and more angular body form. Pubic hair distribution appears more adult but has not yet spread to the medial of the thighs. The penis and scrotum are near adult size.

Stage IV for boys, which occurs anywhere from 15 to 24 months after stage III, is difficult to pinpoint. At this time, the spurt of growth in height ends. There is facial hair on the chin and the upper lip, adult distribution and color of pubic and axillary hair, and a further increase in muscular strength.

The timing of puberty makes an important difference in ultimate body size, in a way that may seem paradoxical at first: the earlier the onset of puberty, the smaller the adult size, and vice versa. Growth in height depends on endochondral bone growth at the epiphyseal plates of the long bones, and the impact of the sex hormones on endochondral bone growth is twofold. First, the sex hormones stimulate the cartilage to grow faster, and this produces the adolescent growth spurt. But the sex hormones also cause an increase in the rate of skeletal maturation, which for the long bones is the rate at which cartilage is transformed into bone. The acceleration in maturation is even greater than the acceleration in growth. Thus during the rapid growth at adolescence, the cartilage is used up faster than it is replaced. Toward the end of adolescence, the last of the cartilage is transformed into bone, and the epiphyseal plates close. At that point, of course, growth potential is lost and growth in height stops.

This early cessation of growth after early sexual maturation is particularly prominent in girls. It is responsible for much of the difference in adult size between men and women. Girls mature earlier on the average and finish their growth much sooner. Boys are not bigger than girls until they grow for a longer time at adolescence. The difference arises because there is slow but steady growth before the growth spurt, and so when the growth spurt occurs, for those who mature late, it takes off from a higher plateau. The epiphyseal plates close more slowly in males than in females, and therefore the cutoff in growth that accompanies the attainment of sexual maturity is also more complete in girls.

The timing of puberty seems to be affected by both genetic and environmental influences. There are early- and late-maturing families, and individuals in some racial and ethnic groups mature earlier than others. As Figure 4-4 shows, Dutch boys are about 5 cm taller than their American counterparts at age 10, and it is likely that both heredity and environment play a role in producing that considerable difference. In girls, it appears that the onset of menstruation requires the development of a certain amount of body fat. In girls of a slender body type, the onset of menstruation can be delayed until this level is reached. Athletic girls with low body fat often are slow to begin their menstrual periods, and highly trained female athletes whose body fat levels are quite low may stop menstruating, apparently in response to the low body fat levels.

Seasonal and cultural factors also can affect the overall rate of physical growth. For example, everything else being equal, growth tends to be faster in spring and summer than in fall and winter, and city children tend to mature faster than rural ones, especially in less developed countries. Such effects presumably are mediated via the hypothalamus and indicate that the rate of secretion of gonadotropin-releasing factors can be influenced by external stimuli.

In the description above, the stages of adolescent development were correlated with growth in height. Fortunately, growth of the jaws usually correlates with the physiologic events of puberty in about the same way as growth in height (Figure 4-5). There is an adolescent growth spurt in the length of the mandible, though not nearly as dramatic a spurt as that in body height, and a modest though discernible increase in growth at the sutures of the maxilla. The cephalocaudal gradient of growth, which is part of the normal pattern, is dramatically evident at puberty. More growth occurs in the lower extremity than in the upper, and within the face, more growth takes place in the lower jaw than in the upper. This produces an acceleration in mandibular growth relative to the maxilla and results in the differential jaw growth referred to previously. The maturing face becomes less convex as the mandible and chin become more prominent as a result of the differential jaw growth.

Although jaw growth follows the curve for general body growth, the correlation is not perfect. Longitudinal data from studies of craniofacial growth indicate that a significant number of individuals, especially among the girls, have a “juvenile acceleration” in jaw growth that occurs 1 to 2 years before the adolescent growth spurt (Figure 4-6).¹ This juvenile acceleration can equal or even exceed the jaw growth that accompanies secondary sexual maturation. In boys, if a juvenile spurt occurs, it is nearly always less intense than the growth acceleration at puberty.

Recent research has shown that sexual development really begins much earlier than previously thought.² Sex hormones produced by the adrenal glands first appear at age 6 in both sexes, primarily in the form of a weak androgen (dehydroepiandrosterone [DHEA]). This activation of the adrenal component of the system is referred to as adrenarche. DHEA reaches a critical level at about age 10 that correlates with the initiation of sexual attraction. It is likely that a juvenile acceleration in growth is related to the intensity of adrenarche and not surprising that a juvenile acceleration is more prominent in girls because of the greater adrenal component of their early sexual development.

This tendency for a clinically useful acceleration in jaw growth to precede the adolescent spurt, particularly in girls, is a major reason for careful assessment of physiologic age in planning orthodontic treatment. If treatment is delayed too long, the opportunity to utilize the growth spurt is missed. In early-maturing girls, the adolescent growth spurt often precedes the final transition of the dentition, so that by the time the second premolars and second molars erupt, physical growth is all but complete. The presence of a juvenile growth spurt in girls accentuates this tendency for significant acceleration of jaw growth in the mixed dentition. For many girls, if they are to receive orthodontic treatment while they are growing rapidly, the treatment must begin during the mixed dentition rather than after all succedaneous teeth have erupted.

In slow-maturing boys, on the other hand, the dentition can be relatively complete while a considerable amount of physical growth remains. In the timing of orthodontic treatment, clinicians have a tendency to treat girls too late and boys too soon, forgetting the considerable disparity in the rate of physiologic maturation.

Dimensional Changes