Puberty In Girls
Puberty is the process by which the immature individual will acquire the
physical and behavioral attributes that allow him or her to reproduce. In
girls, puberty is largely the response of the body to the widespread actions of
estrogens, secreted by the newly awakened plural-ovaries under the influence of
gonadotropins secreted by the anterior pituitary. While the progression of
pubertal changes is predictable, age of 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
pubertal onset.
In North American and European
girls, puberty visibly begins with breast development between the ages of 8 and
10. Other secondary sexual characteristics appear over the ensuing 2.5 years.
Puberty culminates with onset of menstruation. The average age of menarche in
Caucasian girls is 12.8 ± 1.2 years and, on average, 4–8 months earlier in
African-American girls.
The physical changes of puberty
in girls have been divided into five stages using a system developed by
Marshall and Tanner, who examined groups of English girls as they went through
sexual maturation (Fig. 12.1). 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.
Adrenarche
This describes the contribution
of the adrenal gland to puberty in both girls and boys. It is a developmentally
programmed increase in adrenal synthesis and secretion of the weak androgens:
androstenedione, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone
sulfate (DHEA-S). Adrenarche begins at about ages 6–8 years in girls. Secretion
of weak adrenal androgens precedes the visible onset of puberty by about 2
years. DHEA and DHEA-S are responsible for initiating growth of pubic and
axillary hair as well as growth of and secretion by axillary sebaceous glands. Axillary
and pubic hair appear in parallel with the beginning of breast development and
visibly mark the onset of puberty in girls.
The exact trigger for adrenarche
is not known. It is independent of adenocorticotropic hormone (ACTH) release,
gonadotropin release and ovarian function, and appears to be an
intrinsic, programmed event within the adrenal gland. Adrenarche is distinct
from the other events of puberty (pubarche) and either may occur in the absence
of its counterpart.
Breast development (thelarche)
The mammary gland, or breast, is
an ectodermal derivative. The breast tissues are remarkably sensitive to
hormones. Such hormonal effects are most notable during embryonic development
and after puberty. The basic structure of the breast is common to all mammals
although there exist wide variations in the number of mammary glands, their
size, location and shape. Each mammary gland comprises lobulated masses of
glandular tissue. Glandular tissues are embedded in adipose tissue and
separated by fibrous connective tissues. Each of the lobes contains lobules of
alveoli, blood vessels and lactiferous ducts. See Chapter 23 for a more
detailed description of the structure and function of the human breast.
At birth, the breasts consist
almost entirely of lactiferous ducts with few, if any, alveoli. These
rudimentary mammary glands are capable of a small degree of secretory function
(“witch’s milk”) within a few days of birth. Breast secretion in the neonatal
period occurs in response to the high prolactin levels in the newborn infant
following prior exposure of the fetal breast to high concentrations of
placental estrogen during gestation. After placental estrogens are cleared from
the neonatal circulation, the breast enters a dormant phase until puberty. With
the onset of puberty, ovarian estrogens induce growth of the lactiferous duct
system. The ducts branch as they grow and their ends form into small, solid,
spheroidal cell masses. These structures will form the lobular alveoli. The
breast and alveoli enlarge. With menarche, cyclic estrogen and progesterone
secretion begin and an extra phase of ductal and rudimentary lobular growth
will occur. Adrenal corticosteroids further enhance duct development. The
breasts continue to increase in size for some time after menarche due to
deposition of fat and additional connective tissue. Final breast
differentiation and growth will not occur
until pregnancy.
Secondary sexual characteristics
Ovarian estrogens also produce
the following changes in pubertal girls:
•
Pubic
hair.
•
Keratinization
(cornification) of the vaginal mucosa.
•
Enlargement
of labia minora and majora.
•
Uterine
enlargement.
•
Increased
fat deposition in hips and thighs.
Somatic growth
The pubertal growth spurt in
girls typically begins 2 years before it begins in boys, accounting for about
50% of the 12 cm difference in average height between men and women. The other
50% results from a slower rate of growth during the spurt in girls compared
with boys. The mechanisms by which sex steroids induce bone growth in girls are
the same as in boys (Chapter 11). Structural growth ceases at a median age of
17 years in girls.
Menarche
The term used to describe the
onset of menstrual cycles. It is the culmination of a complex sequence of
events that involves maturation of the hypothalamic–pituitary–ovarian (HPO)
axis to produce both mature ova and an endometrium that can support a zygote if
fertilization should occur. The three stages of maturation of the HPO axis
include: (i) an increase in the release of follicle-stimulating hormone
(FSH) and luteinizing hormone
(LH) from the pituitary gland; (ii) ovarian recognition of, and response to
these gonadotropins, allowing production of ovarian steroids (estrogen and
progesterone); (iii) establishment of positive feedback regulation of the
hypothalamus and pituitary gland by estrogens. The combination of these
maturational events permits ovulation.
Throughout childhood, FSH and LH
concentrations within the pituitary gland and plasma of boys and girls are low.
As described in Chapter 11, the pulse amplitude and frequency of FSH and LH
release are also low, suggesting the gonadotropin-releasing hormone (GnRH)
pulse generator is cycling slowly. This characteristic pattern has been called
the juvenile pause. The first endocrinologic manifestation of puberty is an
increase in FSH and LH pulse amplitude. At its initiation, this increase is
most notable during sleep, although the diurnal sleep– awake difference in FSH
and LH secretion is almost obliterated by the end of puberty.
The initiation of puberty remains
incompletely understood. Still, most agree it must be related to a release of
the hypothalamic GnRH pulse generator from CNS inhibition.
There has been much interest in
the observation that the age of menarche decreased by 2–3 months per decade
during the 150 years preceding World War II and then stabilized over the next
50 years. A decrease was again noted in recent studies, thought to represent
the influence of optimal nutrition. Onset of menarche is closely related to
attainment of a crucial percentage of body fat. Two metabolic signals have been
recently identified that can act centrally and may be causal in pubertal
events: insulin-like growth factor 1 (IGF-1) and leptin. Serum IGF-1 levels
increase during childhood and peak at puberty: the increase parallels that of
DHEA-S, the marker of adrenarche. Leptin, a hormone signaling satiety, inhibits
neuropeptide Y (NPY). NPY is a mediator of food intake, but also controls GnRH
neuronal activity in the hypothalamus. Serum leptin levels increase in both
sexes prior to onset of puberty. Rising leptin levels inhibit NPY. This, in
turn, releases GnRH from its prepubertal inhibition. Leptin levels continue
to rise throughout puberty among healthy females, but fall fairly rapidly after
pubertal initiation in males.
Maturation of the ovary at
puberty allows initiation of estrogen production by the granulosa cells
surrounding the ova. Waves of granulosa cells undergo development and sub sequentatresia as puberty progresses. Ova begin to mature under the
influence of ovarian estrogen produced by these granulosa cells. In addition to
oocyte maturation, estrogen from the granulosa cells will regulate production
of gonadotropins by the pituitary gland. With complete maturation of the HPO
axis, this estrogen will drive maturation of a dominant ovarian follicle,
culminating in ovulation. With ovulation of the first ovum, the collapsing
ovarian follicle reconfigures itself as a corpus luteum and begins to produce
progesterone. The endometrium responds to estrogen by proliferating and to
progesterone by converting to a secretory tissue capable of supporting embryo
implantation. In the first years after menarche many menstrual cycles will be
anovulatory, reflecting the incomplete maturation of the hypothalamic positive
feedback response to ovarian estrogen. The menstrual bleeding patterns often
encountered soon after menarche represent continuous exposure of the
endometrium to estrogen and sloughing of proliferative or hyperplastic
endometrium. Because no corpus luteum forms in the absence of ovulation, the
endometrium cannot exhibit the progesterone effect that makes menstruation a
self-limited phenomenon. This anovulatory bleeding can be very unpredictable
and quite heavy. By 5 years after onset of menarche, 90% of girls have regular, ovulatory
menstrual cycles.
