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Embryology of the

female genital tract

Pranab Chatterjee
Medical College, Kolkata
Embryology of the
female genital tract
The urogenital system (U.G.S)
develops from

the mesoderm of the urogenital sinus (the

intermediate cell anterior part of the cloaca(
mass (genital ridge)

medial part middle part lateral part

give rise to the

give rise to lower 1/4 of the
give rise to
undergo fallopian tubes, vagina and vulva
the ovaries
atrophy in uterus & upper
female 3/4 of vagina
Development of the ovaries
 The ovaries developed from the medial part of the
genital ridge
 At about 4 week gestation, primordial germ cells (that
give rise to the ova) originate from the primitive
hindgut (yolk sac) then migrate to the genital ridge
 Failure of its migration give rise to streak gonads
 At 12 weeks: Formation of the the mesentery of the
ovary)→ as a result of projection of the ovary into
coelomic cavity
).Development of the ovaries )cont
 The ovary descends in the abdominal cavity with
development of 2 ligaments
 The 1st is the suspensory ligament attached to
the cephalic pole →infundibulopelvic ligament.
 The other ligament is called the gubernaculum
(tractor) which is attached to the caudal end of
the ovary and to the abdominal parities at the
inguinal region.→ attached to the developing
uterus forming the future:
 round ligament in its distal part
 while its proximal part form the ovarian ligament.
Development of the fallopian tubes

They develop from

the upper parts of the
mullarian ducts after
their canalization
Development of the uterus
 The uterus develops from the
middle part of the mullarian ducts
after their fusion and canalization.
N.B: Failure of fusion or canalization
or disappearance of the formed
septum to become a single organ
give rise to many of congenital
uterine anomalies.
Development of the vagina
 The upper ¾ to 4/5 of vagina develops from the fused & canalized
parts of the caudal ends of mullarian ducts while the lower ¼ or 1/5
formed from the urogenital sinus
 Congenital malformation occurs when Mullerian ducts fail to
develop → (congenital absence of vagina) or fail to fuse (septate
vagina) or fail to canalize (atresia of vagina).
 The caudal ends are closed by a septum which is complete at 1st
but later become excavated centrally to form the hymen. At least,
the distal end of the vagina is formed from urogenital sinus
 The urogenital fold : is present in early embryo and contains the
origins of the wolffian and Mullerian duct i.e. the primordia of both
urinary and genital tract.
So, if there is genital tract malformation, look for associated
malformation in the urinary tract and vice versa.
In summary
 In females, Mullerian ducts give: f.
tubes + uterus (body + cx) + upper 3/4
to 4/5 of vagina.
 In males, at 6 weeks, the future testis
secretes Mullerian inhibitory factor
(MIF), which inhibits Mullerian ducts
development and secrets testosterone
which stimulates differentiation of
external genitalia
Development of the external
Up to 10 weeks development is the same in male and female i.e. neutral
primordium. Then differentiation occurs:
 In female: testicular androgen is absent (androgen insensitivity), the
following occur:
 The bladder and urethra from → vesical portion of UGS
 The vestibule→ from the pelvic and phallic potions of UGS
 The clitoris→ from the genital tubercle which enlarges only slightly
 The labia minora: develop from the genital folds which remain
 The labia majora: develop from the genital swellings
 Greater vestibular gland& lesser vestibular gland →arise from the
vestibular endoderm
Development of the external
In male: with androgen secretion, the following
 Genital tubercle: greater enlargement to form
the penis.
 Genital folds: fuse over a deep groove formed
between them to become the penile part of
male urethra.
 Genital swellings enlarge and fuse to form
Genital homologues in males and

Female Male
G. ridge Ovary Testis
G. swelling Labia majora Scrotum
G. fold Labia minora Penile urethra
Gubernaculum Round lig. & ov. ligament Gubernaculum testis
Mesonephric Duct Gartener duct Vas deferens
Pelvic UGS Skene's gland Prostate
The Wolffian remnants in the female
 in female, the wolffian ducts
undergo atrophy leaving remnants
between two layers of B.L. and in
the anterolateral wall of the vagina
 These remnants are:
 Hydated cyst of morgagni: lateral
to the tube
 Koblet's tubules: in the outer part
of B.L.
 Epoophoron: between the ovary
and F.T
 Paroophoron: between the ovary
and uterus.
 Gartener's duct: may undergo
cystic dilatation in the B.L. gives
rise to paraovarian cyst or in the
anterolateral wall of the vagina,
gives rise to Gartener's cyst
Congenital anomalies of
reproductive tract
 The Mullerian and wolffian ducts are closely related
embryologically, so, the association between the
genital & urinary system anomalies is common.
 Malformations of genital tract may be represented by:
aplasia ‑ atresia ‑ hypoplasia ­-fusion defects or
duplication of accessory organs.
 Complete formation and differentiation of the
mullerian ducts into the segments of the female
reproductive tract depend on completion of 3 phases
of development as follows:
 Organogenesis
 Fusion
 Septal resorption
Congenital anomalies of
).reproductive tract )cont
 Organogenesis: One or both Mulllerian ducts may not develop fully,
resulting in abnormalities such as uterine agenesis or hypoplasia
(bilateral) or unicornuate uterus
 Fusion:
 The process during which the lower segments of the paired
Mullerian ducts fuse to form the uterus, cervix, and upper vagina is
termed lateral fusion. Failure of fusion →bicornuate or didelphys
 The term vertical fusion occasionally is used to refer to fusion of the
ascending sinovaginal bulb with the descending Mullerian system
(ie, fusion of the lower 1/4and upper ¾ of the vagina). Complete
vertical fusion forms a normal patent vagina, while incomplete
vertical fusion results in an imperforate hymen.
 Septal resorption: after the lower Mullerian ducts fuse, a central
septum is present, which subsequently must be resorbed to form a
single uterine cavity and cervix.
 Failure of resorption is the cause of septate uterus.
Internal structures anomalies
 Mullerian duct anomalies are categorized
most commonly into 7 classes according to
the American Fertility Society (AFS)
Classification Scheme (1988) as follows:
Class I (hypoplasia/agenesis):
 Uterine/Cervical agenesis or hypoplasia.
 The most common form is the
Mayer‑Rokitansky‑Kuster­ Hauser syndrome,
which is combined agenesis of the uterus,
cervix, and upper portion of the vagina.
 Patients have no reproductive potential.
)Class II )unicornuate uterus
 Complete, or almost complete,
arrest of development of one
Mullerian duct. If the arrest is
incomplete, as in 90% of patients, a
rudimentary horn with or without
functioning endometrium is present.
If the rudimentary horn is obstructed,
it may come to surgical attention
when presenting as an enlarging
pelvic mass. If the contralateral
healthy horn is almost fully
developed, a full‑term pregnancy is
believed to be possible
)Class III )didelphys uterus
 Results from complete non-
fusion of both Mullerian ducts
 The individual horns are fully
developed and almost normal in
 Two cervices are inevitably
 A longitudinal or transverse
vaginal septum may be noted as
 Since each horn is almost a fully
developed uterus, patients have
been known to carry pregnancies
to full term.
Class IV))bicornuate uterus
 Results from partial non fusion of the
Mullerian ducts .
 The central myometrium may extend to the
level of the internal cervical os (bicornuate
unicollis) or ex ternal cervical os (bicornuate
bicollis). The latter is distinguished from
didelphys uterus because it demonstrates
some degree of fusion between the two
horns, while in classic didelphys uterus, the
two horns and cervices are separated
 In addition, the horns of the bicornuate uteri
are not fully developed; typically, they are
smaller than those bicornuate
 Some patients are surgical candidates for
metroplasty of didelphys uteri
Class V))septate uterus
 A septate uterus results from failure of resorption
of the septum between the two uterine horns.
 The septum can be partial or complete, in which
case it extends to the internal cervical os
 Histologically, the septum may be composed of
myometrium or fibrous tissue.
 The uterine fundus is typically convex but may be
flat or slightly concave (<1cm fundal cleft).
 Women with septate uterus have the highest
incidence of reproductive complications.
 Differentiation between a septate and a
bicornuate uterus is important because septate
uteri are treated using transvaginal hysteroscopic
resection of the septum, while if surgery is
possible and/or indicated for the bicornuate
uterus, an abdominal approach is required to
perform metroplasty
)Class VI )arcuate uterus
 Arcuate uterus has a single
uterine cavity with the outer
contour of the uterus
convex or flat.
 This form is often
considered a normal
variant since it is not
significantly associated
with the increased risks of
pregnancy loss and the
other complications found
in other subtypes.
 The uterine anomaly is seen in
the female offspring of as many
as 15% of women exposed to
DES during pregnancy.
 Female fetuses who are affected
have a variety of abnormal
findings that include uterine
hypoplasia and a T‑shaped
uterine cavity.
 Patients also may have abnormal
transverse ridges, hoods, stenosis
of the cervix, and adenosis of the
vagina with increased risk of
vaginal clear cell carcinoma.
Imaging findings are
pathognomonic for this anomaly.
Fallopian tube anomalies
 Include:
 aplasia,
 atresia,
 hypoplasia (very long & thin),
 accessory horn or ostia and tubal
 It may cause infertility or ectopic
Vaginal anomalies
Vaginal septa:
 Longitudinal septa:
 Partial or complete septa extending
antroposteriorly in the vagina results from
failure of disappearance of the fused Mullerian
structure, this may be associated with normal
uterus or duplicate uterus
 Occasionally the septum may not be in the
midline and may not communicate externally
leading to lateral pouch containing menstrual
Transverse vaginal septum
 Complete or perforated
 Rare occurs at the junction of upper and middle 1/3 of

 When there is no perforation in the septum retention of

mucoid material may occur before puberty leading to
 After puberty menstrual flow becomes hidden and
accumulate in the vagina, uterus and tubes giving a
picture like imperforate hymen
 If the septum is perforated patient may complain
of dyspareunia and it may cause dystocia in labor
 Double or separate vagina.
 Vaginal agenesis (absent(
 This could be partial or complete
 Complete vaginal agenesis may be a part of Mullerian
agenesis, here the vagina is represented by a small
pouch (part derived from U.G.S.)
 Patient usually have normal external genitals and lower
vagina derived from the urogenital S.
 Ovaries are normally developed
 Present usually with primary amenorrhea
 In 50% urinary anomalies present e.g. absent or pelvic
:)Treatment of vaginal agenesis )absent

 Construction of new vagina (McIndoe’s

operation): involves the development of a
space between the bladder and rectum by
blunt dissection and inserting a skin-graft-
covered mold (from thigh) into the cavity
allowing epithelialization. This undergoes
metaplasia and loss its keratinization.
 Gradual dilatation (Frank’s method) Frank’s
non-operative procedure used progressive
larger dilators inserted by the patient to
gradually deepen and widen the canal
External genital anomalies
 Aplasia: obliteration of
perineum (absence of anal,
urethral or genital orifices). This
may be combined with limb
 Fusion: agglutination of labia
(postnatal inflammation(
Imperforate hymen
 Cryptomenorrhea (haematocolpos ‑ haematometra ‑
 The vaginal plate develops near the junction of the
lower part of the vagina and the vestibule.
Canalization of this plate is generally completed by
the 6th. Month of fetal life. Failure of the final process
of canalization occurs and results in imperforate
hymen which obstruct the menstrual outflow
 Presentation: Usually present with primary
amenorrhea with monthly pain
 Sometimes present with retention of urine due to
collection of blood in vagina (hematocolpos), uterus
(hematometra) and tubes (hematosalpinx)
 Treated by cruciate incision or excision of hymen
Ovarian anomalies
 Accessory or supernumerary ovaries
 Failure of descent
 Gonadal dysgenesis (Turner' s syndrome( streak gonads,
chromosomal pattern is XO, sex chromatin negative, in. 3/
100.000 full term births, vagina and uterus develop. The patient
complaining of primary amenorrhea. Examination revealed no
secondary sex characters, short stature, webbing of the neck,
cubitus vulgus and coarctation of aorta
 Androgen insensitivity (testicular feminization syndrome):
male but Mullarian inhibitory factor (MIF) is present.
Testosterone receptors absent. Phenotypically female: no pubic
or axillary hair ‑ no vagina or tubes or uterus, small vaginal
pouch, external genitalia female type ‑ well develop breast.
X‑linked recessive.
Ovarian anomalies )cont.)
 Super female(XXX): may be normal female & give birth
to children. Others, may be amenorrheic with mental
 True Hermaphrodites: presence of both ovarian &
testicular tissues in the gonads
 Female pseudohermaphrodites: Partially masculinized
female – XX, presented by ambiguous genitalia
 Causes: ‑
 Maternal intake of androgens.

 Androgenic tumors

 Congenital adrenal hyperplasia.

 Male pseudo hermaphrodites:

 Incompletely masculinized male XY
 Partial androgen insensitivity
 Inadequate androgen.
 No MIF.
Clinical presentation of congenital
malformation of the female genital tract
 Nothing (asymptomatic
 Menstrual problems:
 Primary amenorrhea
 Menorrhagia
 Hypomenorrhea
 Dysmenorrhea
 Premature ovarian failure
 Dyspareunia
 Infertility
 Pelvic endometriosis
 Pelvic / abdominal mass
 Urinary complication & malformation (pelvic kidney)
 Pregnancy complication (abortion, premature labour,
malpresentation and obstructed labour)
 IUCD cannot be inserted in abnormal shaped uterus
 Malformation of the external genitalia