Normal puberty

04/03/15 20:29

Official reprint from UpToDate

www.uptodate.com 2015 UpToDate

Normal puberty
Author
Frank M Biro, MD

Section Editors
Amy B Middleman, MD, MPH, MS Ed
Teresa K Duryea, MD
Peter J Snyder, MD
Mitchell Geffner, MD

Deputy Editor
Alison G Hoppin, MD

Disclosures: Frank M Biro, MD Nothing to disclose. Amy B Middleman, MD, MPH, MS Ed Grant/Research Support: Novartis
[immunizations; developing student curricula]. Teresa K Duryea, MD Nothing to disclose. Peter J Snyder, MD Grant/Research/Clinical Trial
Support: AbbVie [hypogonadism (Testosterone gel 1% and 1.62%)]; Novo Nordisk [GH deficiency (norditropin)]; Ipsen [Acromegaly

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2015. | This topic last updated: Nov 05, 2013.
INTRODUCTION Adolescents experience several types of maturation, including cognitive (the development of formal
operational thought), psychosocial (the stages of adolescence), and biological. The complex series of biological transitions
are known as puberty, and these changes may impact psychosocial factors.
The most visible changes during puberty are growth in stature and development of secondary sexual characteristics.
Equally profound are changes in body composition; the achievement of fertility; and changes in most body systems, such
as the neuroendocrine axis, bone size, and mineralization; and the cardiovascular system. As an example, puberty is
associated with cardiovascular changes, including greater aerobic power reserve, electrocardiographic changes, and blood
pressure changes.
The normal sequence of pubertal events and perils of puberty are reviewed here. Precocious and delayed puberty are
discussed separately. (See "Definition, etiology, and evaluation of precocious puberty" and "Diagnosis and treatment of
delayed puberty".)
DEFINITIONS Puberty is the general term for biological maturation into sexual maturity. A number of other terms
describe specific antecedents or components of puberty:
Adrenarche is the activation of the adrenal cortex for the production of adrenal androgens, and typically occurs before
the onset of puberty. This process is discussed in detail separately. (See "Normal adrenarche" and "Premature
adrenarche".)
Gonadarche is the activation of the gonads by the pituitary hormones follicle-stimulating hormone (FSH) and
luteinizing hormone (LH)
Pubarche is the appearance of pubic hair
Thelarche is the appearance of breast tissue
Menarche is the age of onset of the first menstrual period
Spermarche is the age at first ejaculation (heralded by nocturnal sperm emissions and appearance of sperm in the
urine) [1]
Precocious puberty is usually defined as the onset of secondary sexual development before the age of eight years in girls
and nine years in boys. These limits are chosen to be 2.5 to 3 standard deviations (SD) below the mean age of onset of
puberty. (See "Definition, etiology, and evaluation of precocious puberty".)
Delayed puberty is defined as the absence or incomplete development of secondary sexual characteristics by an age at

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which 95 percent of children of that sex and culture have initiated sexual maturation. In the United States this corresponds
to an upper limit of 12 years for girls (breast development), and of 14 years for boys (for testicular enlargement). (See
"Diagnosis and treatment of delayed puberty".)
PUBERTAL CHANGES
Sexual maturity rating (Tanner stages) Puberty consists of a series of predictable events that usually proceed in a
predictable pattern, with some variation in timing of onset, sequence, and tempo (figure 1A-B).
The staging system utilized most frequently is that of sexual maturity ratings (SMR). These are also known as "Tanner
stages" because they were initially published by Marshall and Tanner [2,3]. These consist of systematized descriptions of
the development of secondary sexual characteristics, consisting of breast changes in females, pubic hair changes in both
males and females, and genital changes in males. SMR for pubic hair, breast, and genitalia consists of five categories, with
stage one representing prepuberty and stage five representing adult development (table 1). The stages are illustrated by
the figure in boys (picture 1) and in girls (picture 2A-B). In girls, estrogen stimulation of the vaginal mucosa causes a
physiologic leukorrhea, which is a thin white non foul-smelling vaginal discharge that typically begins 6 to 12 months before
menarche. (See "The pediatric physical examination: The perineum", section on 'Preadolescent and adolescent females'.)
As is discussed below, the timing of pubertal maturation has an important influence on self-esteem, behavior, growth, and
weight. As an example, early maturation is associated with slightly shorter adult stature [4,5] and with greater adult
ponderosity and adiposity [5,6]. Details of the physiological changes expected during puberty are discussed below. (See
'Sequence of pubertal maturation' below.)
Growth spurt Approximately 17 to 18 percent of adult height accrues during puberty [7]. The timing of the growth spurt
(peak height velocity) varies by gender, occurring approximately two years earlier in girls than in boys. In girls, peak height
velocity occurs, on average, 0.5 years prior to menarche [8]. The increase in height affects both axial (trunk) and
appendicular (limbs) components [9]. The limbs accelerate before the trunk, with the distal portions of the limbs
accelerating before the proximal portions; thus, the adolescent in early puberty is "all hands and feet." In later puberty,
however, the growth spurt is primarily truncal [9].
Height velocity can be plotted and compared with norms using height velocity growth charts. The most commonly used
charts are those published by Tanner and Davies (figure 1A-B) [10]. Although these are used for longitudinal tracking and
acknowledge the variation between early, average and late maturers, their accuracy is limited because they were prepared
from cross-sectional rather than longitudinal data. Other growth charts were generated from longitudinal data, such as the
series of charts published by the Harvard Six-Cities study, but are less widely available [11].
The disparity in mean adult height of men and women results from the timing and peak of the growth spurt in boys and
girls. On average, boys are 2 cm taller at the age girls begin their peak height velocity and continue to accrue 3 to 4 cm per
year for an additional one to two years, until they enter puberty. Boys experience a greater peak height velocity than do
girls (10.3 versus 9.0 cm/year) (figure 2A-B). When calculated over a 12-month span rather than a shorter period of peak
growth, these values fall to 9.5 and 8.3 cm, respectively. When evaluating growth, the clinician should look at whole-year
changes because of seasonal variability; greater growth typically occurs in spring, although the time of year may vary when
a given individual has a seasonal peak.
Extremely early onset of puberty (precocious puberty) and earlier peak height velocity is associated with reduced adult
height, due to early epiphyseal closure (see "Treatment of precocious puberty", section on 'Decision to treat'). Whether
pubertal onset that is early but within the normal range is associated with reduced adult stature is less clear. In girls, early
menarche was associated with greater peak height velocity but shorter adult stature, while early thelarche had no effect on
adult stature [12]. In boys, those who mature relatively early but within the normal range have a modest reduction in adult
height [13]. The diminished adult height is attributable to shorter leg length; sitting height is not reduced. Body weight
appears to influence these results: in the same study, boys who were underweight during childhood tended to have longer
leg length and no change in adult height. It is probably not appropriate to extrapolate these results to girls, because obesity
is sometimes associated with earlier onset of puberty in girls, and obesity may have the opposite effect in boys. (See
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"Comorbidities and complications of obesity in children and adolescents", section on 'Growth and puberty'.)
Bone growth Bone growth accelerates during puberty, in concert with height velocity, but bone mineralization lags
behind. As examples, bone mineralization peaks around the age of menarche in girls, which occurs approximately 9 to 12
months later than peak height velocity [14,15]. Bone growth occurs first in length, followed by width, then mineral content,
then bone density [16]. The disparity in the timing of bone growth and mineralization may place the growing adolescent at
increased risk for fracture. (See 'Musculoskeletal injuries' below.)
Of total body calcium, approximately one-half is laid down during puberty in females, and one-half to two-thirds in males
[16,17]; by the end of puberty, males have nearly 50 percent more total body calcium than do females. The increase in
bone density during puberty is greater in African-American females than in Caucasian females [18].
The risk for osteoporosis during adulthood may be related to both specific "insults" and the timing of factors impacting bone
deposition during puberty [9]. These data suggest that the window of opportunity to maximize peak bone mass may be
limited [16]. (See "Prevention of osteoporosis", section on 'Maximizing peak bone mass'.)
Weight and body composition Puberty is associated with significant changes in body weight and alterations in body
composition, especially in lean body mass and the proportion of body fat (adiposity), with different patterns in girls as
compared with boys. Growth curves for Body Mass Index (BMI) describe the typical increase in body mass that occurs
during puberty (figure 3A-B), but do not reflect the differences between early-maturing and late-maturing children, nor do
they distinguish between changes in lean body mass versus adipose tissue.
In early puberty, the annual increase in BMI is driven primarily by changes in lean body mass. Later, the increase in BMI
tends to be driven by increases in fat mass [19]. This general pattern diverges between the genders: boys tend to have a
decrease in body fat in early puberty, and then proceed to a substantial increase in lean body mass. Girls tend to have a
higher proportion of fat mass than boys at each phase, and after 16 years of age, the annual increase in BMI is largely
because of increases in fat mass [19,20]. These general patterns are altered by the individuals nutritional status; either
boys or girls may experience an ongoing increase in body fat, regardless of gender or pubertal stage, reflecting developing
or worsening obesity. Obesity tracks from adolescence to adulthood, and earlier onset of obesity is associated with
increased cardiovascular morbidity and mortality [21-23]. (See "Clinical evaluation of the obese child and adolescent".)
SEQUENCE OF PUBERTAL MATURATION Some variability occurs in a given individual's timing, sequence, or tempo
of pubertal maturation. However, most adolescents follow a predictable path through pubertal maturation.
Girls The earliest secondary sexual characteristic in most girls is breast/areolar development (thelarche) (picture 2A),
although a substantial minority have pubic hair as the initial manifestation (pubarche) (picture 2B) [24]. Maternal
preeclampsia increased threefold the likelihood of pubarche as the initial manifestation of puberty; the likelihood was
directly related to the severity of preeclampsia [25,26]. Menarche occurs, on average, 2.6 years after the onset of puberty
(figure 1A) [2,8,15].
The initial manifestation predicts body morphology and composition throughout pubertal maturation into early adulthood.
As an example, girls with breast development as the initial manifestation of puberty have both an earlier age of menarche
and greater body mass index (BMI) throughout puberty and as adults [27]. When menarche occurs before the individual
reaches the age of 12 years, it is associated with increases in weight and BMI [28-30]. In addition, girls who mature early
are at an increased risk for obesity when compared with late maturers [6].
Boys The earliest stage of male maturation, which has a mean duration of six months, is an increase in testicular
volume (figure 4). Almost all boys have an increase in testicular volume (3 mL) prior to the appearance of penile growth
and pubic hair (picture 1) [24,31]. Thus, if one considers only pubic hair in the assessment of early male puberty,
misclassification and unnecessary testing may result. The appearance of sperm in the urine and the onset of nocturnal
sperm emissions occur shortly after the attainment of peak height velocity; many consider these events the male
equivalent of menarche (figure 1B).
Testicular volume is typically measured using the Prader orchidometer, a series of three-dimensional ellipsoids with a
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volume from 1 to 25 mL or more. Penile length is measured from the pubic ramus to the tip of the glans while compressing
the suprapubic fat pad and applying gentle traction. Mean stretched penile stretch length (measured from the pubis
symphysis to the tip of the non-erect penis excluding foreskin) is approximately 3.75 cm ( 0.54 cm) at 1 year of age and
gradually increases to 4.84 cm by late childhood, then increases sharply to about 9.5 cm ( 1.12 cm) by late puberty
(according to measurements from a predominantly white population) [32]. This measurement is rarely used for monitoring
of pubertal progress.
In some clinical contexts (eg, when one is concerned about endogenous or exogenous androgens), it is helpful to consider
whether a given testicular volume is appropriate for a pubic hair stage. The following figure allows the clinician to evaluate
the relationship between testicular volume and pubic hair (figure 4) [31].
TIMING OF PUBERTAL ONSET The mean age of onset of puberty is about 10.5 years of age in girls and 11.5 years in
boys. The normal range for pubertal onset is between 8 and 12 years in girls, and 9 to 14 years in boys. (See 'Definitions'
above.)
Trends in pubertal timing Pubertal onset in girls has been trending earlier in the United States and in most other
developed countries, as illustrated by the following observations:
The average age of menarche in the United States declined from 12.53 to 12.34 years (a decline of 2.3 months)
between the late 1980s and the early 2000s [33]. In addition, there was an overall decline of 4.9 months since the
1960s through the early 2000s [33,34]. In non-Hispanic White girls, the age of menarche decreased from 12.57 to
12.52 years, non-Hispanic Blacks 12.09 to 12.06 years, and for Mexican Americans 12.23 to 12.09. Changes in the
population distribution of race/ethnicity and anthropometric changes in body weight and height may, in part, explain
the larger change seen in the overall group compared with changes within each ethnic group.
In a 1997 study from the United States and Puerto Rico, the mean ages for the onset of breast development were 8.9
years in African-American girls and 8.8 years in white girls; the mean age for pubic hair growth was 10.0 years in
African-American girls and 10.5 years in White girls (figure 5) [35]. In this study, the earliest signs of puberty were at
ages considerably younger than had been reported previously, and striking racial differences in timing were found.
Pubertal onset in boys also appears to be occurring earlier in the United States. In a study including more than 4000
healthy boys, the mean age for entering puberty (SMR for genital development stage 2) was 10.14 years for white boys,
10.04 years for Hispanic boys, and 9.14 years for African American boys [36]. These thresholds are 1.5 to 2 years earlier
than historical norms. Similar trends have been reported from several European and Scandinavian countries and China
[37-41]. The relationship between pubertal onset and obesity in boys is not clear. Some studies suggest that being
overweight or obese is associated with later onset of puberty in boys, in contrast to findings in girls [31,42-44]. Conversely,
other studies report that increased body mass index (BMI) and fat mass is associated with earlier puberty in boys, similar to
findings in girls [36,37,45,46]. However, several studies are inconclusive or demonstrate no relationship [28,47].
The earlier onset of puberty has had important implications for the diagnosis of precocious puberty. Precocious puberty
usually has been defined as pubertal onset prior to eight years of age in girls and nine years in boys. Because of the earlier
onset of puberty in the United States, it has been suggested that a threshold of seven years in White girls, and six years in
African-American girls be used as a threshold for evaluation for precocious puberty [4]. Following these suggestions may
lead to under-diagnosis of endocrine disorders, the appropriate threshold for evaluation remains controversial and probably
varies among populations [48]. (See "Definition, etiology, and evaluation of precocious puberty".)
Determinants of pubertal timing Genetics accounts for the majority of the variability in the timing of pubertal onset.
The timing of puberty and menarche in a girl is best predicted by the timing of menarche in her mother. Other factors that
influence pubertal onset include overall health, social environment (such as family stress or the presence of an adult
nonbiologically-related male) [49-51], and possibly environmental exposures, such as endocrine disruptors (environmental
contaminants that may affect endocrine processes) [52]. Studies have suggested an interaction between genetics and the
environment. As an example, age of menarche decreased to a greater extent in Black girls as compared with White girls
from the 1970s to the 1990s [53]. The influence of environmental factors, including endocrine disruptors, on timing of
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pubertal maturation is a subject of active research [54]. (See 'Trends in pubertal timing' above.)
Pubertal timing varies substantially between race/ethnic groups. In a 2001 study in the United States, the rates of early
maturation (menarche 11 years) were 7.8 percent for White, 12.3 percent for Black, 13.6 percent for Hispanic, and 5.2
percent for Asian girls [55]. The frequency of late maturation (menarche 14 years) ranged from 15.2 percent among White
girls to 27 percent among Asian girls. This relationship appears to be primarily mediated by differences in rates of
overweight; within each race/ethnic group, early maturing girls were approximately twice as likely to be overweight as
compared with those maturing at an average age. The data in this study did not establish whether the relationship between
age of menarche and obesity varies among racial and ethnic groups. (See 'Body fat and leptin' below.)
Genetic contributors Common genetic variants have been identified that appear to be associated with variation in
age at menarche.
In a meta-analysis of 32 genome-wide association studies that included more than 85,000 women, 32 common variants or
single nucleotide polymorphisms (SNPs) associated with age at menarche were identified [56].
One of the genes in the 6q21 region, LIN28B, has emerged as an important candidate for mediating variation in age at
menarche. Genetic variation in this region was also associated with age at menarche in several different human
populations and was analyzed in a meta-analysis [57,58]. A study employing direct genotyping of LIN28B confirmed that
variations in a particular region of this gene were associated with earlier puberty in both boys and girls [59]. LIN28B is a
regulator of microRNA processing involved in developmental timing in C. elegans; a common variant in this gene was
previously associated with reduced adult height.
A few other genetic variants associated with adult height also were associated with age at menarche [56-58]. These
observations suggest a genetic basis for previously observed associations between age at menarche and height; in some
cases, this association might be mediated by earlier epiphyseal closure caused by earlier exposure to estrogens. Similarly,
several genes that are associated with childhood obesity, including FTO (fat mass and obesity associated gene), SEC16B,
TRA2B, TMEM18, and NEGR1 (neuronal growth regulator 1), were also associated with earlier age at menarche [56,57].
(See "Pathogenesis of obesity", section on 'Common obesity'.)
One of the studies cited above also identified genetic variants associated with age at natural menopause [60]. (See
"Ovarian development and failure (menopause) in normal women", section on 'Genetics' and "Clinical manifestations and
diagnosis of menopause".)
The GPR54 gene on chromosome 19p13.3, which encodes a G-protein coupled receptor, appears to have an important
role in the initiation of puberty via its effect on hypothalamic GnRH [61]. Its ligand, kisspeptin, appears to modulate the
negative feedback on GnRH secretion exerted by sex steroids. Loss-of-function mutations in GPR54 cause autosomal
recessive idiopathic hypogonadotropic hypogonadism in humans and in a GPR54 knockout mouse model. Conversely,
gain-of-function mutations in the GPR54 gene are associated with a form of central precocious puberty [62]. Thus, the
GPR54-kisspeptin complex, appears to be an important gatekeeper for the onset of puberty and normal reproductive
function. (See "Congenital gonadotropin-releasing hormone deficiency (idiopathic hypogonadotropic hypogonadism)".)
Body fat and leptin It has been proposed that a critical body weight [63] or body composition [64] is the most salient
issue in the development and maintenance of pubertal events [28,63-65]. However, body weight alone probably is not a
sufficient explanation. The overall earlier onset of puberty among the general population has been attributed to the
increasing prevalence of obesity. (See 'Trends in pubertal timing' above.)
Leptin has been proposed as the hormone responsible for the initiation and progression of puberty. Leptin is produced
largely in adipocytes; large fat cells produce more leptin than do small ones, and serum leptin concentrations are highly
correlated with body fat content. The potential importance of leptin is illustrated by the observation that mice deficient in
leptin fail to undergo pubertal development, whereas the administration of leptin to such animals results in pubertal onset
[66]. Furthermore, higher serum leptin concentrations in girls are associated with increased body fat and an earlier onset of
puberty [67]. In this study, a 1 ng/mL increase in serum leptin lowered the age at menarche by one month, and a gain in

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body fat of 1 kg lowered the timing of menarche by 13 days. (See "Physiology of leptin".)
Leptin appears to be one of several factors that influence the maturation of the gonadotropin-releasing hormone (GnRH)
pulse generator, probably as a signal of the availability of metabolic fuel [68]. Serum leptin concentrations increase
immediately before puberty in both genders but differ after the initiation of puberty. In males, serum leptin falls after the
onset of puberty, returning to baseline 30 to 40 months later [69]. In females, leptin values rise throughout puberty and may
be influenced by many factors. In one study, leptin values in pubertal girls were correlated with the sum of skinfolds
(abdominal subcutaneous more than abdominal visceral more than peripheral subcutaneous fat), as well as serum free
testosterone and free estrogen; these three factors accounted for 74 percent of the variance in leptin levels [70].
PERILS OF PUBERTY Puberty is associated with a number of complications that present challenges to the patient and
family. These "perils of puberty" include anemia, gynecomastia, acne, psychological correlates of puberty, certain types of
sports-related injuries, myopia, scoliosis, and dysfunctional uterine bleeding.
Anemia Anemia and iron deficiency are common among adolescent girls as compared with adolescent boys or to
school-aged children. The Third National Health and Nutrition Examination Survey (NHANES III) found a 9 percent
incidence of iron deficiency and a 2 percent incidence of anemia among American girls between the ages of 12 and 15
years; the respective values were less than 2 percent for boys in this age group (table 2) [71]. Hemoglobin and serum
ferritin concentrations increase with advancing pubertal stage in males, but not in females [72,73]. The gender differences
are thought to result from biological differences (perhaps androgens), in addition to menstrual bleeding and insufficient iron
intake in girls [73]. (See "Iron requirements and iron deficiency in adolescents".)
Gynecomastia Pubertal gynecomastia (in contrast to neonatal or senescence gynecomastia) occurs in approximately
one-half of teenage boys at an average age of 13 years, and it persists for 6 to 18 months [74]. Boys with persistent
gynecomastia (ie, lasting two years or more) have a diameter of palpable tissue 2 cm during the first year (odds ratio 8.7)
[75]. Although the underlying diagnosis usually is "idiopathic pubertal gynecomastia," a variety of other etiologies including
drugs, hypogonadism, testicular tumors, and hyperthyroidism, must be considered. The underlying mechanisms
presumably reflect an imbalance in the effective estrogenic-to-androgenic stimulation, because of an increase in the
production or action of estrogens or estrogen-like agents, a decrease in the production or action of androgens, or
enhanced breast tissue sensitivity to these hormones [75]. (See "Epidemiology, pathophysiology, and causes of
gynecomastia" and "Clinical features, diagnosis, and evaluation of gynecomastia".)
Acne Acne, a disorder of the pilosebaceous unit, is characterized by follicular occlusion and inflammation caused by
androgenic stimulation. If the opening of the comedone is widely dilated, oxidation of keratinous material leads to the
development of a blackhead without inflammatory acne. With a small opening, a closed comedo (whitehead) forms and
may lead to inflammatory acne if the comedo ruptures into the dermis. With pubertal maturation in both boys and girls, the
number of acne lesions increases, with a greater number of comedones than inflammatory lesions at all stages [76]. In
girls, the severity of acne in later puberty is associated with higher serum levels of dehydroepiandrosterone sulfate
(DHEAS) and a greater number of acne lesions in early puberty [77]. Although acne is common during puberty, moderate
or severe acne in early puberty, usually with other signs of androgen excess, should alert the clinician to the possibility of
an endocrinologic disorder, such as non-classical congenital adrenal hyperplasia. (See "Pathogenesis, clinical
manifestations, and diagnosis of acne vulgaris".)
Psychological changes Pubertal maturation has an impact on psychological and social issues [78]. Puberty does not
affect cognitive development [79], although the timing of pubertal maturation may affect psychosocial functioning.
Prior to adolescence, no gender differences in depression occur; during adolescence, however, the prevalence of
depression is twice as great in girls compared with boys [80]. As puberty progresses, boys develop a more positive selfimage and mood. By contrast, girls tend to become less satisfied with their physical appearance, and this tendency is more
pronounced in Caucasian as compared with African-American girls. Caucasian girls also exhibit diminished self-worth as
they pass from early to mid-adolescence [81].
Pubertal development may have an especially negative impact when a lack of synchrony between the timing of pubertal
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development and chronologic age exists. For example, the early-maturing girl may experience a greater decrease in selfesteem and body satisfaction when compared with on-time or late-maturing girls [82]. In a large cross-sectional study, girls
who were early-maturing and boys who were late-maturing were more likely to have psychopathology. Girls who matured
early were more likely to have a lifetime history of disruptive behavior (attention-deficit, hyperactivity, oppositional, or
conduct disorders) and suicide attempts, whereas boys who were late-maturing were more likely to have internalizing
behaviors and emotional reliance on others [83]. Girls with early maturation are more likely to have older friends [84] and to
be more vulnerable to peer pressures [85].
Certain cognitive characteristics have long been observed in adolescents, in which they make very different decisions
when under the influence of strong emotions ("hot" cognition) as compared with decisions made under conditions of low
emotional arousal ("cool" cognition) [86]. Recent observations suggest that adolescents display these cognitive
characteristics because the dorsolateral prefrontal cortex, an area of the brain involved in impulse control, matures later
than the remainder of the brain [87]. Thus, in times of stress, the brain of the adolescent may be less able to modulate the
affective component as compared with adults.
Musculoskeletal injuries Pubertal status may help predict the specific type of musculoskeletal injuries that adolescents
may encounter during participation in sports [88]. The greatest risk of damage to epiphyseal growth plates occurs during
periods of peak height velocity, which also is the time of greatest change in bone mineral content [14] (see 'Bone growth'
above). The asynchronous growth of body parts may result in a limited range of motion of some joints; when combined with
the increase in muscle mass that occurs shortly after peak height velocity, the limited range of motion may lead to sprains
or strains. (See 'Growth spurt' above.)
A common overuse injury in teens is Osgood-Schlatter disease, which is an inflammation of the tibial tubercle apophysis.
Not surprisingly, the age of peak incidence of distal radius fractures matches the age of peak height velocity in both boys
and girls [89]. (See "Osgood-Schlatter disease (tibial tuberosity avulsion)".)
Gynecologic consequences Once a girl reaches menarche, rapid maturation of the reproductive axis ensues. By one
year after menarche, 65 percent of girls have regular menstrual cycles, with 10 or more periods per year [90]. Girls with
later onset of menarche progress more slowly to regular ovulatory cycles; when menarche occurs after the age of 13, only
one-half will ovulate regularly within 4.5 years [91].
Dysfunctional uterine bleeding (DUB) refers to excessive, prolonged, and/or irregular endometrial bleeding. In adolescents,
anovulation accounts for approximately 80 percent of cases of DUB. With anovulatory cycles, unopposed estrogen
stimulates the endometrium, leading to a sustained proliferative phase rather than maturing to a secretory endometrium.
Estrogen levels ultimately cannot sustain the hyperplastic endometrial lining, leading to irregular, sometimes heavy,
menstrual bleeding. (See "Abnormal uterine bleeding in adolescents: Definition and evaluation", section on 'Abnormal
uterine bleeding (AUB) in adolescents' and "Abnormal uterine bleeding in adolescents: Management".)
Myopia The greatest incidence of myopia occurs during puberty and is caused by growth in the axial diameter of the
eye [92]. (See "Refractive errors in children", section on 'Refractive errors'.)
Scoliosis Accelerated progression of the degree of scoliosis occurs during puberty because of growth in the axial
skeleton. (See "Adolescent idiopathic scoliosis: Clinical features, evaluation, and diagnosis", section on 'Natural history'.)
Sexually transmitted disease Sexually active adolescents represent the highest-risk age group for nearly all sexually
transmitted diseases [93]. Both behavioral and biological factors are important. (See "Adolescent sexuality", section on
'Adolescent development' and "Sexually transmitted diseases: Overview of issues specific to adolescents", section on
'Epidemiology'.)
Behavioral issues that increase risk for sexually transmitted diseases include younger age at onset of intercourse, the
number of lifetime partners, and the perceived prevalence of sexually transmitted infections [94].
Biological factors include age of menarche (which influences behavioral factors) and gynecologic maturation. In the first
year or two after menarche, a persistence of both columnar epithelial cells on the exocervix (cervical ectopy) and the
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transformation zone of columnar to squamous epithelial cells on the exocervix occur. These factors may enhance infection
with Chlamydia [95] and genital human papillomavirus [96,97].
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best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to
your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the
keyword(s) of interest.)
Basics topics (see "Patient information: Normal sexual development (puberty) (The Basics)" and "Patient information:
Early puberty (The Basics)" and "Patient information: Late puberty (The Basics)")
SUMMARY Puberty consists of a series of predictable events that usually proceed in a predictable pattern, with some
variation in timing of onset, sequence, and tempo.
The mean age for the first signs of puberty is about 10.5 years of age in girls, with a range from 8 to 12 years, In
boys, the mean age of pubertal onset is 11.5 years, with a range from 9 to 14 years. Precocious puberty is usually
defined as the onset of secondary sexual development before the age of eight years in girls and nine years in boys.
(See 'Timing of pubertal onset' above.)
Sexual maturity ratings (Tanner stages) for pubic hair, breast, and genitalia consists of five categories, with stage one
representing prepuberty and stage five representing adult development (table 1). These stages are illustrated by the
figure in boys (picture 1) and in girls (picture 2A-B). (See 'Sexual maturity rating (Tanner stages)' above.)
The timing of the growth spurt (peak height velocity) occurs approximately two years earlier in girls than in boys
(figure 1A-B). Extremely early onset of puberty (precocious puberty) and earlier peak height velocity is associated
with reduced adult height, due to early epiphyseal closure. Whether pubertal onset that is early but within the normal
range is associated with reduced adult stature is less clear. (See 'Growth spurt' above.)
In most girls, the earliest secondary sexual characteristic is breast/areolar development (thelarche) (picture 2A),
although a substantial minority have pubic hair as the initial manifestation (picture 2B). Menarche occurs, on average,
2.6 years after the onset of puberty and 0.5 years after peak height velocity (figure 1A). (See 'Girls' above.)
In boys, the earliest stage of maturation is an increase in testicular volume, followed by penile growth and the
appearance of pubic hair (picture 1). The appearance of sperm in the urine and the onset of nocturnal sperm
emissions occur shortly after the attainment of peak height velocity; many consider these events the male equivalent
of menarche (figure 1B). (See 'Boys' above.)
In the United States and most other developed countries, the average age of onset of puberty has declined during the
past four decades. Between 5 and 12 percent of girls have menarche younger than 11 years of age; this rate varies
by race/ethnic group and weight status. (See 'Trends in pubertal timing' above.)
The age at onset of puberty and the age of menarche are influenced by several factors. Genetics accounts for the
majority of the variability; other factors include overall health, body weight, and possibly environmental exposures,
such as endocrine disruptors. (See 'Body fat and leptin' above and 'Genetic contributors' above.)
Typical thresholds for evaluating children for precocious puberty are signs of pubertal development before age eight
years in girls and nine years in boys. Given the increasing frequency of earlier pubertal onset, some authorities
suggest that these thresholds are too high. (See 'Trends in pubertal timing' above.)

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Puberty is associated with a variety of physiologic changes which may come to medical attention, including acne and
scoliosis, gynecomastia in boys, and anemia and dysfunctional uterine bleeding in girls. Psychological and emotional
changes are common, with increased rates of depression and risk-taking behaviors. (See 'Perils of puberty' above.)
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