Arch Gynecol Obstet (2006) 273: 195–202
DOI 10.1007/s00404-005-0079-x
R EV IE W
Miranda Farage Æ Howard Maibach
Lifetime changes in the vulva and vagina
Received: 28 June 2005 / Accepted: 1 September 2005 / Published online: 6 October 2005
Ó Springer-Verlag 2005
Abstract The morphology and physiology of the vulva
and vagina change over a lifetime. The most salient
changes are linked to puberty, the menstrual cycle,
pregnancy, and menopause. The cutaneous epithelia of
the mons pubis, labia, and clitoris originate from the
embryonic ectoderm and exhibit a keratinized, stratified
structure similar to the skin at other sites. The mucosa of
the vulvar vestibule, which originates from the embry-
onic endoderm, is non-keratinized. The vagina, derived
from the embryonic mesoderm, is responsive to estrogen
cycling. At birth, the vulva and vagina exhibit the effects
of residual maternal estrogens. During puberty, the
vulva and vagina acquire mature characteristics in a
sequential fashion in response to adrenal and gonadal
maturation. A trend to earlier pubertal onset has been
observed in Western developed countries. In women of
reproductive age, the vaginal mucosa responds to steroid
hormone cycling, exhibiting maximal thickness and
intracellular glycogen content at mid-cycle. Vulvar skin
thickness remains unchanged but menstrual cycle-asso-
ciated changes in ortho- and parakeratosis occur at the
cytological level. The vulva and vagina further adapt to
the needs of pregnancy and delivery. After menopause,
tissue atrophy ensues. Post-menopausal changes in skin
barrier function, skin hydration, and irritant suscepti-
bility have been observed on exposed skin but not on the
vulva. Nevertheless, older women with incontinence are
at increased risk for developing incontinence dermatitis.
A combination of factors, such as tissue atrophy, slower
M. Farage (&)
The Procter & Gamble Company, Feminine Care Clinical Sciences,
Winton Hill Technical Center, 6110 Center Hill Rd,
Box 136, Cincinnati, OH 45224, USA
E-mail: farage.m@pg.com
Tel.: +1-513-6345594
Fax: +1-513-6347634
H. Maibach
Dermatology Department, University of California School of
Medicine, San Francisco, CA, USA
dissipation of excess skin hydration, shear forces
associated with limited mobility, and lower tissue
regeneration capacity increase the risk of morbidity
from incontinence dermatitis in older women.
Key words Vulva Æ Vagina Æ Puberty Æ Reproductive
age Æ Menopause
Introduction
The vulva and vagina change over a lifetime. The most
salient changes are hormonally mediated, being linked
to the onset of puberty, the menstrual cycle, pregnancy,
and menopause. This article reviews the morphology
and physiology of the vulva and the vagina from infancy
to old age (Table 1).
Embryonic derivation and epithelial structure
The lower urogenital tract is the only portion of the
female anatomy derived from all three embryologic
layers (ectoderm, endoderm, and mesoderm) [1]. Like
skin at other anatomical sites, the skin of the mons
pubis, the labia, the clitoris, and the perineum, derived
from the embryonic ectoderm, has a keratinized, strati-
fied squamous structure with sweat glands, sebaceous
glands, and hair follicles (Fig. 1a). Cutaneous thickness
and degree of keratinization is relatively high on the
mons pubis and labia majora, but decreases over the
anterior portions of the clitoris and in going from the
outer surface to the inner surface of the labia minora [2].
The mucosa of the vulvar vestibule is the only portion of
the female genital tract of endodermal origin [3]. Its
superficial stratum is non-keratinized and differentiation
of the inner layers is indistinct: loosely packed, polyhe-
dral cells alter in size and organelle density as they
migrate upward from the generative basal layer, but do
not form clearly demarcated strata as observed in the
skin (Fig. 1b). The vagina, of mesodermal origin, has
196
Table 1 The vulva and vagina from infancy to old age

Life stage Pertinent physiology Vulvar characteristics Vaginal features

Newborn Effects of residual, Plump labia majora Stratified squamous epithelium

trans-placental maternal
estrogens Well-developed labia minora
Immature hair follicles
and sebaceous glands
Early Lack of stimulation Mons pubis and labia majora lose fat
childhood by adrenal or gonadal
steroid hormones
Benign labial adhesions, if present,
normalize without treatment [11]
Puberty Adrenal and gonadal Subcutaneous fat is deposited in the
maturation ensues. mons pubis and labia majora
Secondary sex characteristics
are acquired and The vulvar epithelium thickens
menstruation begins [5]
The labia minora and clitoris
become more prominent
Pubic hair emerges
Reproductive The menstrual cycle The morphology of the vulva is mature
years
Vulvar skin thickness and
remains constant
throughout the menstrual cycle [4]
Parakeratosis of the vulvar stratum
corneum rises at mid-cycle [4, 34]
Pregnancy Blood volume increases. Hair may darken along the
The menstrual cycle ceases mid line of the abdomen
during gestation Increased blood flow heightens
vulvar coloration
Susceptibility to vulvar varicose
veins increases [38]
Flattening of the fourchette and
perineal trauma occur during delivery
Postmenopause Follicular function and the menstrual Pubic hair becomes sparse
cycle ceases. The prevalence of urinary Subcutaneous fat is lost
and fecal incontinence rises.
Physical health, immune function, Vulvar tissue atrophies
tissue regeneration capacity,
and cognition may be compromised The risk of perineal dermatitis rises
with increasing age in older women with incontinence
high in glycogen content
Lactic acid-producing
microbes colonize the vagina
shortly after birth
White or blood-tinged vaginal
discharge may be present [7]
The vaginal epithelium
thins, is less stratified,
and has a low glycogen content
Vaginal pH is neutral
or alkaline
Prevalence of lactic
acid-producing microbes
decreases [9]
The vaginal
epithelium thickens
and stratifies
Cyclical changes
in intracellular glycogen
content ensue
Cervico-vaginal secretions
are produced
Prevalence of
lactic acid-producing
microbes rises [9]
Vaginal epithelial
thickness, parakeratosis,
and glycogen content rise
at mid-cycle [4, 34]
Lactic acid-producing microbes
are numerically dominant in
healthy women [36, 37]
Menstrual cycle becomes
established [14, 15]
Cervico-vaginal secretions
become thicker, clearer and
more elastic prior to ovulation
Connective tissue relaxes and
vaginal muscle fibers thicken
The risk of Candida infection
increases [39]
Following delivery, the
morphology and dimensions
of the vaginal tract are
re-established
The vaginal epithelium atrophies
Cervico-vaginal secretions
become sparse
Vaginal pH rises; colonization
by enteric microflora may rise
Atrophic vaginitis is common

non-keratinized squamous epithelium that is responsive
to ovarian steroid hormone cycling [4].
Infancy and early childhood
The vulva and vagina of the newborn exhibit the effects
of residual maternal estrogens. At birth, the labia ma-
jora appear plump and the labia minora are well
developed. The vaginal introitus is visible, but the
urethral opening is less easily discerned. The vaginal
mucosa is rich in glycogen. It becomes colonized with
lactic acid-producing microbes, such as Lactobacillus
species, within the first 24 h of birth [5]. A physiologic,
white, mucoid vaginal discharge is present, which may
become tinged by slight withdrawal endometrial bleed-
ing as the concentration of residual maternal estrogen
falls [6, 7].
These estrogenic effects dissipate by the fourth post-
natal week. The vaginal epithelium loses its stratification

Fig. 1 Vulvar epithelial
structure. a vulvar skin; b
vulvar vestibule Adapted with
permission from Ref. [58]
and glycogen content, becoming much thinner. The
vaginal pH becomes neutral or alkaline, presumably
because of a relative deficiency of acid-producing vagi-
nal microbes [8, 9]. Vulvar skin thickness drops, [2, 10]
and the mons pubis and labia majora subcutaneous fat.
Although the full complement of vulvar hair follicles
and sebaceous glands is thought to be present from
birth, these structures do not mature until the adrenal
glands are activated at puberty. The prepubescent labia
minora have barely discernible vellus hair follicles that
are lost at puberty when the follicles of the labia majora
and mons pubis terminally differentiate [10].
Labial adhesions may occur between the ages of 2
months and 2 years, creating a flat vulvar appearance.
197
This benign condition is due to a lack of estrogen and
normalizes without treatment. Should the condition
interfere with urinary flow, topical estrogen treatment
promotes separation of the labia [11].
Puberty
Pubertal changes in the vulva and vagina are induced by
adrenal and gonadal maturation. Puberty generally be-
gins between the ages of 8 and 13 years. Physical changes
associated with puberty are an accelerated growth rate,
the appearance of pubic hair (pubarche), the appearance
of axillary hair, breast development (telarche), and the
198

onset of menstruation (menarche). The timing and stages of breast changes, typically sometime between the ages
of development of secondary sex characteristics were first of 11 and 15 years [5]. The mean age of menarche
defined in Marshall and Tanner’s seminal study of 192 world-wide lies between 12 and 13 years [13]. The se-
girls in a British orphanage [12]. quence from first appearance of pubic hair through
Maturation of the adrenal glands and androgen breast development and menarche takes about 4 years.
secretion (adrenarche) begin at about age six, approxi- Normative menstrual cycle length is established by the
mately 2 years before pituitary-gonadal maturation and sixth gynecologic year (i.e., the sixth year following
the production of ovarian steroid hormones (gonadar- menarche), usually at a chronologic age of 19 or 20
che). Because adrenarche and gonadarche proceed [14, 15].
independently, the appearance of pubic hair does not
provide information about pituitary-ovarian matura-
tion. Pubic hair development, elicited by androgens, Idiopathic precocious puberty
proceeds in five stages [12] (Fig. 2):
Historically, puberty had been defined as precocious in
– Stage 1: no pubic hair.
girls when secondary sex characteristics (particularly
– Stage 2: sparse hair appears on the labia majora and
breast development) appeared prior to the age of 8.
the mons pubis along the midline.
However, an apparent advance in the age of onset of
– Stage 3: the thickness and coarseness of the hair in-
pubertal changes has been observed in the United States
creases, with coverage of the lobes of the labia majora
and in girls from developing countries who have mi-
and increased lateral growth from the midline of the
grated to Western Europe for foreign adoption (re-
mons pubis.
viewed in [16]). Two large studies in the U.S. found that
– Stage 4: hair growth increases such that only the
pubertal signs may appear before the age of 8, especially
upper lateral corners of the mature triangular con-
in African-American compared to Caucasian girls (Ta-
figuration are deficient.
ble. 2, 3) [17–19]. Between the 1970 s and 1990 s, the
– Stage 5: adult pattern, attained between the ages of 12
average age of menarche in the U.S. fell from 12.75 y to
and 17 years, with a characteristic horizontal upper
12.54 years [17].
margin on the mons pubis just above the limit of the
Controversy surrounds the clinical significance of
genitofemoral folds, and hair coverage extending from
these findings. Most of the cases of early pubertal
the labia to the upper aspects of the thighs.
development are idiopathic [20, 21] and probably do not
represent precocious puberty unless bone maturation
Gonadal maturation usually occurs during the 2 years
and developmental characteristics are so accelerated that
preceding menarche. During the maturation process,
diminished adult height is likely [20]. However, because
follicular development causes estrogen production to
true endocrine pathology may be overlooked if early
rise. The vaginal epithelium thickens and intracellular
pubertal signs are dismissed, vigilant longitudinal follow
glycogen production begins. The cervix and vagina
up of girls with early pubertal onset is advised [22].
increase in size, the vaginal fornices develop, cervico-
Several risk factors, including genetics [23], low birth
vaginal secretions are produced, and vaginal fluid be-
weight [24, 25], higher body mass index [17, 26–29], and
comes acidic.
exposure to endocrine disruptors [30–33], have been
Vulvar morphology also matures at this time. Fat
statistically linked to early onset of pubertal signs.
deposition occurs in the mons pubis and labia majora.
However, the causative biological mechanisms for this
The vulvar epithelium increases in thickness [2], labial
phenomenon are unknown.
skin becomes rugose, the clitoris becomes more promi-
nent, the vestibular glands become active, the introitus
increases in diameter, and the urethral orifice is more
discernible. Reproductive years
Breast development, influenced by estrogens, is also
described by five Tanner stages, from no development Changes in the vulva and vagina during the repro-
(Stage 1) to the mature adult breast (Stage 5) [12]. ductive years are linked to the menstrual cycle and
Menarche occurs near the end of the Tanner sequence pregnancy.

Fig. 2 Tanner stages of pubic hair development

 199

indicate that lactic acid-producing species such as

Table 2 Mean onset of secondary sex characteristics (Tanner stage 2) Atopobium, Megasphaera, and Leptotrichia, rather than
[12]) and menarche in Caucasian and African-American girls from
North American suburban medical practices [18]
Lactobacillus, are numerically dominant in some women
[37]. Consequently, genera besides Lactobacillus may
Ethnicity Mean age of onset Percentage of contribute to the acidity of the vaginal tract, but the
(years) subjects with impact of the menstrual cycle on these genera has not
pubertal
Menarche Breast Pubic signs by
been studied.
development hair age 8

African-American 12.16 8.87 8.78 48.3 Effects of pregnancy and delivery

(SD 1.21) (SD 1.93) (SD 2.00)
Caucasian 12.88 9.96 10.52 14.7
(SD 1.20) (SD 1.82) (SD 1.67)
SD standard deviation
Vulvar and vaginal effects of the menstrual cycle
Vulvar epithelial thickness is at its highest in the
reproductive years. Vulvar skin thickness remains con-
stant over the menstrual cycle, but its surface cells are
predominantly orthokeratotic (lacking nuclei) at the
beginning and end of the cycle, and increasingly para-
keratotic (bearing a degenerated nucleus) at mid-cycle
[34]. These cytological changes are thought to be medi-
ated by estrogen: for example, parakeratosis of vulvar
epithelial cells is rare in post-menopausal women, but
rises dramatically in this group in response to systemic
estrogen supplementation [34].
The vaginal mucosa is sensitive to ovarian steroid
hormone cycling. Estrogen stimulation causes the
thickness, glycogen content, and parakeratosis of the
vaginal epithelium to peak at approximately mid-cycle
[4].
Vaginal pH rises during menstruation [35], but the
impact of the menstrual cycle on the microbial ecology
of the vagina is not well understood. Studies using tra-
ditional culture techniques suggest that Lactobacillus
species predominate in the vaginal flora of healthy wo-
men and that their cell densities remain relatively con-
stant over the menstrual cycle [36]. However, culture
techniques typically identify only the most readily cul-
tivated microbial populations, which may represent but
a subset of the extant community. Emerging data ob-
tained by analysis of total microbial community DNA
During pregnancy, an increase in total blood volume
heightens the coloration of the vulva and vagina. The
connective tissue of the vulva, vagina, and perineum
relaxes, and the muscle fibers of the vaginal wall increase
in size in preparation for delivery. Progesterone elevates
venous distensibility, which may cause varicose veins in
the vulva [38]. Pregnancy is associated with a 10- to 20-
fold increase in the prevalence of vulvo-vaginal candi-
diasis [39].
During delivery, the perineal and vaginal musculature
relaxes and the vaginal rugae flatten to allow expansion
of the vaginal tract, accommodating passage of the
newborn infant. Injury to the perineum may occur
spontaneously or because of episiotomy. After delivery,
the vaginal introitus is wider and the fourchette appears
more flattened. Over the next 6–12 weeks, the typical
morphology and dimensions of the vaginal tract are re-
established.
Menopause and older age
Menopause is the permanent cessation of menstruation
due to the loss of follicular activity. A constellation of
symptoms emerges during the peri-menopause (the
transition period to menopause). The most notable is
menstrual cycle irregularity, reflecting an increase in the
number of anovulatory cycles and cycles with a pro-
longed follicular phase. Some women experience
cramps, bloating, or breast tenderness; symptoms of
estrogen depletion, such as vasomotor symptoms (‘‘hot
flashes’’), migraine, and vaginal dryness, may ensue. The
peri-menopause typically commences after the age of 45
and lasts for about 4 years. Menstruation ceases at a
median age of 50 years in Western industrialized socie-

Table 3 Mean age of menarche and median age of onset of secondary sex characteristics (Tanner stage 2 [12]) by race from the U.S. Third
National Health and Nutrition Examination Survey (NHANES III) (1988–1994)

Ethnicity Age (years)

Menarchea Breast developmentb Pubic Hairb

African-American 12.14 (SE: 11.87–12.39) 9.48 (FL: 9.14–9.76) 9.43 (FL: 9.05–9.74)
Caucasian 12.60 (SE: 12.48–12.71) 10.38 (FL: 10.11–10.65) 10.57 (FL: 10.29–10.85)
a
Mean age of menarche.Anderson et al [17]
b
Median age at which 50% of the sample entered Stage 2 of pubertal development. FL = fiducial limit based on probit analysis for
multiple race comparisons at the 95% confidence level. Sun et al. [19]
200

ties [40]. Menopause is considered established 1 year
after the final menstrual period [41].
Following menopause, pubic hair grays and be-
comes sparse, the labia majora lose subcutaneous fat,
and the labia minora, vestibule, and vaginal mucosa
atrophy [2, 42]. At the cytological level, estrogen-in-
duced parakeratosis of vulvar stratum corneum is
highest in the third decade of life, but rarely seen by the
eighth decade [43].
Post-menopausal atrophic vulvovaginitis is a virtu-
ally universal condition. Vaginal secretions decrease,
reducing lubrication and increasing coital discomfort.
Thinned tissue is more easily irritated and may be more
susceptible to infection. The vaginal pH rises and the
prevalence of colonization by enteric organisms associ-
ated with urinary tract infections increases [44]. Besides
these physiologically induced changes, certain vulvar
dermatoses, such as lichen sclerosus, are most prevalent
in peri- and post-menopausal women [45].
Vulvar skin differs from exposed skin in the charac-
teristics of skin hydration, friction, permeability, and
visually discernible irritation (reviewed in Ref. [46]). It is
commonly assumed that aged skin is intrinsically less
hydrated, less elastic, more permeable, and more sus-
ceptible to irritation. However, assessments of the vulvar
skin of pre- and post-menopausal women, using bioen-
gineering techniques, did not reveal large age-related
changes in these characteristics (Table 4).
For example, the skin of the labia majora is more
hydrated than forearm skin as measured by trans-epi-
dermal water loss [47] and its coefficient of friction is
higher [48]. Although small age-related changes in these
parameters were measured on the forearm of pre- and
post-menopausal women, the impact of the menopause
on the water barrier function and friction coefficient of
vulvar skin was negligible [48].
Vulvar skin is more permeable to hydrocortisone
than forearm skin, but comparable testosterone pene-
tration rates have been measured at both sites. In post-
menopausal women, skin permeability to hydrocorti-
sone drops on the forearm but not on the vulva, and no
age-related differences in testosterone penetration were
found on either sites [49].
Exposed forearm skin was more susceptible than
vulvar skin to the model irritant, aqueous sodium lauryl
sulfate (SLS; 1% w/v). This agent caused more intense
erythema on the forearms of pre-menopausal women,
but no visually discernable response on the vulva in ei-
ther pre- or post-menopausal women [50].
Although large age-related differences in vulvar skin
permeability and intrinsic susceptibility to irritants have
not been demonstrated, dermatitis of the vulva, peri-
neum, and buttocks is nevertheless a significant problem
in older people with incontinence. Studies of inconti-
nence dermatitis in infants have elucidated a multi-fac-
torial etiology. In brief, exposure to urinary moisture
under occlusion makes the skin more susceptible to
friction damage; urinary ammonia elevates the local pH,
which alters skin barrier function [51] and activates fecal
enzymes; these enzymes further compromise skin integ-
rity and increase skin susceptibility to microbial infec-
tion [52–56].

Table 4 Physiologic skin parameters in pre- and post-menopausal women

Parameter Site Age groupa Measured value Significanceb Reference

Water barrier function (TEWL, g/m2 h) Forearm Pre-menopausal 3.7 ± 0.4 p < 0.05 [48]
Post-menopausal 2.6 ± 0.3
Vulva Pre-menopausal 14.8 ± 1.5 n.s. [48]
Post-menopausal 13.5 ± 1.8
Skin hydration (capacitance, AU) Forearm Pre-menopausal 93.3 ± 2.3 n.s. [48]
Post-menopausal 91.9 ± 2.8
Vulva Pre-menopausal 116.8 ± 4.1 n.s. [48]
Post-menopausal 118.0 ± 8.2
Friction coefficient, ± Forearm Pre-menopausal 0.49 ± 0.02 p < 0.05 [48]
Post-menopausal 0.45 ± 0.01
Vulva Pre-menopausal 0.60 ± 0.04 n.s. [48]
Post-menopausal 0.60 ± 0.06
Hydrocortisone penetration (percent dose absorbed) Forearm Pre-menopausal 2.8 ± 2.4 n.s. [49]
Post-menopausal 1.5 ± 1.1
Vulva Pre-menopausal 8.1 ± 4.1 p < 0.01 [49]
Post-menopausal 4.4 ± 2.8
Testosterone penetration (percent dose absorbed) Forearm Pre-menopausal 20.2 ± 8.1 n.s. [49]
Post-menopausal 14.7 ± 4.2
Vulva Pre-menopausal 26.7 ± 8.0 n.s. [49]
Post-menopausal 24.6 ± 5.5
Visual erythema scores (scored on day 2 after Forearm Pre-menopausal 9 p=0.03 [50]
24 h post-exposure to 1% SLS) Post-menopausal 5
Vulva Pre-menopausal 0 n.s. [50]
Post-menopausal 0
a
Group sizes (water barrier function, skin hydration and friction parameters): premenopausal 34 subjects, post menopausal 10 subjects.
Group sizes (hydrocortisone and testosterone penetration): 9 subjects in each age group visual erythema score to sodium lauryl sulfate
(SLS) application: 10 subjects per age group
b
Level of statistical significance of age-group differences; ns not significant

Perineal dermatitis is particularly debilitating to older
people with incontinence, because urine and feces exert
their effects against a background of atrophied tissue,
immobility, a potentially weakened immune response,
and often compromised physical health and cognition.
Several factors exacerbate the deleterious effects of skin
wetness, occlusion, and fecal enzyme action in elders.
Although the baseline skin wetness level does not differ
significantly in aged skin, the excess hydration induced
by occlusion is significantly greater and dissipated more
slowly in older than in young skin [57]. Although the
coefficient of vulvar skin friction is unchanged in older
women, due to reduced mobility that atrophied genital
tissue to higher shear forces than those encountered by
infants. Moreover, atrophied genital tissue may be more
susceptible to pH changes and enzymatic action, while
immune function and tissue regeneration capacity also
may be compromised. Finally, elders may not receive the
same degree of attentiveness as infants, and those with
impaired cognition may be unable to alert caregivers to
incontinent episodes. These factors underscore the need
for vigilant care and proper hygiene to help maintain
healthy urogenital skin in older women with inconti-
nence.
In summary, the vulva and vagina undergo charac-
teristic age-related changes over a lifetime. At birth,
these tissues exhibit the effects of residual maternal
estrogens. During puberty, the vulva and vagina mature
under the influence of adrenal and gonadal steroid
hormones. During the reproductive years, the vagina
responds to ovarian steroid hormone cycling and both
tissues adapt to the needs of pregnancy and delivery.
Following menopause, the vulva and vagina atrophy. A
rise in the prevalence of incontinence among older wo-
men increases the risk of vulvar and perineal dermatitis.
Vigilant care is needed to avoid dermatitis in the older
person with incontinence, as the condition is particularly
debilitating at this stage of life.
Acknowledgements The authors are grateful to Paula J. Adams
Hillard, MD for her technical review of this manuscript and to
Deborah Hutchins, Ph.D., of Hutchins and Associates, LLC
(Cincinnati, OH), for her technical input.
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