Lecture 7: Urogenital System
Slide 1: Title slide: Urogenital System
Main points: Covers Chapter 15
Slide 2: Cross section showing parts of the mesoderm
Main points:
1. There are three parts to the mesoderm: paraxial, intermediate, and lateral
plate.
2. Most of the urinary and genital systems develop from the intermediate
mesoderm.
Slide 3: Scanning electron micrograph of a cross section showing the parts of the
mesoderm
Slide 4: Illustration showing three kidney systems
Main points:
1. Three kidney systems form: the pronephros, mesonephros, and metanephros.
These three systems represent evolutionary development from lower to
higher vertebrate species—an example of ontogeny recapitulating phylogeny.
2. These systems form in the intermediate mesoderm that extends from cervical
to pelvic regions along the posterior wall.
3. Pronephros: segmented, forms in the cervical regions, rudimentary, barely
develops with little or no significance.
4. Mesonephros: unsegmented, forms in thoracic and upper lumbar regions,
may function briefly, consists of filtration units and a duct, degenerates
almost completely in females, but contributes to the duct work of the male
reproductive system.
5. Metanephros: definitive kidney system, forms in the pelvic region, begins
functioning in the 10th to 12th weeks.
6. All three systems are never present at the same time. Thus, as the pronephros
starts to degenerates (fourth week), the mesonephros is forming (fourth to
sixth weeks), and as it starts to disappear, the metanephros is forming (fifth
week).
Slide 5: Illustrations showing the urogenital ridge
Main points:
1. In the lumbar region, the gonads develop from a proliferation of mesoderm
and overlying epithelium. Together the gonads and mesonephros form the
urogenital ridge. Note that this ridge is retroperitoneal (covered by
peritoneum only on its anterior surface).
2. Excretory tubules form in the mesonephros and differentiate into Bowman’s
capsule around a tuft of capillaries called the glomerulus. This is the filtration
region for the kidney.
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3. The filtration units (Bowman’s capsule plus glomerulus) together with the
excretory tubules constitute a nephron, the functional unit of the kidney.
4. Two ducts form by pinching off of the epithelium: mesonephric (wolfian) and
paramesonephric (müllerian) ducts. Both ducts enter into the anterior portion
of the cloaca that will form the urogenital sinus.
5. The mesonephric duct is the collecting duct for the mesonephric kidney and
will contribute to the male reproductive ducts.
6. The paramesonephric duct parallels the mesonephric duct and contributes to
the female reproductive system.
Slide 6: Illustration showing formation of the metanephric kidney
Main points:
1. The ureteric bud grows off the caudal end of the mesonephric duct and into
intermediate mesoderm (the metanephric blastema) in the pelvic region.
2. The bud is responsible for inducing the mesoderm to form the kidney.
Slide 7:
Differentiation of the ureteric bud
Main points:
1. The ureteric bud forms the collecting system for the definitive kidney.
2. The ureteric bud lengthens and then starts to divide, eventually forming the
renal pelvis, major and minor calyces, and collecting tubules for the
definitive kidney.
Slide 8: Slide showing formation of nephrons
Main points:
1. As the ureteric bud branches in the metanephric blastema, it induces this
mesoderm to form filtration units (nephrons).
2. Thus, tubules form that eventually develop into Bowman’s capsules around
the glomeruli and proximal and distal convoluted tubules and Henle’s loops.
3. In turn, these filtration units hook up with the collecting ducts developing
from the ureteric bud via the distal convoluted tubules.
Slide 9: Illustration showing molecular regulation of kidney development
Main points:
1. Kidney induction represents another epithelial-mesenchymal interaction:
Epithelium of the ureteric bud interacting with intermediate mesoderm of the
metanephric blastema.
2. WT1 is expressed in the mesoderm, making it competent to respond to
induction by the ureteric bud.
3. WT1 regulates production of glial-derived neurotrophic factor (GDNF) and
hepatocyte growth factor (HGF), which cause the bud to branch. In turn, the
bud secretes fibroblast growth factor 2 (FGF2) and bone morphogenetic
protein 7 (BMP7), which stimulate growth of the mesoderm.
4. Tubule formation in the mesoderm is regulated by WNT9B and WNT6
secreted by the buds that cause expression of PAX2 and WNT4 in the
Sadler, T.W.: Langman’s Medical Embryology, 12e
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mesoderm. PAX2 causes the mesoderm to condense, and WNT4 causes the
condensations to differentiate into epithelial cells and form tubules.
5. The bottom line is that WT1 is the master gene for kidney development, and
mutations in this gene are responsible for Wilms’ tumor, a cancerous tumor
common in childhood.
6. If induction fails, the result is renal agenesis, and the fetus presents with
Potter sequence. There is oligohydramnios (too little amniotic fluid) because
the fetus drinks but cannot excrete, which results in compression of the
uterine cavity and, consequently, the fetus. This causes the baby to have a
flattened face, beak-like nose, and club feet. These fetuses are stillborn or die
shortly after birth due to the absence of the kidneys.
Slide 10: Illustration showing the early location of the kidneys in the pelvis
Main points:
1. Kidneys are initially formed in the pelvic region and are said to “ascend” into
their definitive location in the lumbar area.
Slide 11: Illustrations showing ascent of the kidneys from the pelvic region
Main points:
1. Kidneys ascend from the pelvis to the lumbar region.
2. This is mostly a passive process created by growth of the caudal region of the
embryo while the kidneys are held in their original positions.
Slide 12: Examples of pelvic and horseshoe kidneys
Main points:
1. Sometimes a kidney sticks in the pelvis during caudal growth of the embryo
and fails to ascend, resulting in a pelvic kidney.
2. During their early development in the pelvis, the kidneys are in close
proximity, and sometimes their tissues fuse. The result is a horseshoe kidney
that is blocked in its ascent by the inferior mesenteric artery.
Slide 13: Examples of congenital polycystic kidneys
Main points:
1. Autosomal recessive form: Cysts arise from collecting tubules, and renal
failure usually occurs in childhood.
2. Autosomal dominant form: More common than recessive form, with cysts
arising from all regions of the nephrons, but the disease is less severe than the
recessive form. Renal failure usually occurs in adulthood.
Slide 14: Examples of duplication defects in the ureters
Main points:
1. Complete and partial duplications may occur.
2. They are not usually symptomatic but may make it more difficult to pass
kidney stones.
Sadler, T.W.: Langman’s Medical Embryology, 12e
© Lippincott Williams & Wilkins, 2013
Slide 15: Illustrations showing formation of the hindgut and bladder
Main points:
1. Initially, both the urinary system and the gut enter into a common chamber
called the cloaca.
2. Proliferation of mesoderm from the floor of the pelvis causes formation of
the urorectal septum. This septum grows caudally until it completely
separates the rectal canal from the anterior portion of the cloaca called the
urogenital sinus. The tip of the urorectal septum forms the perineal body.
3. The upper portion of the urogenital sinus forms the bladder.
4. The allantois connects the bladder-forming region of the urogenital sinus to
the umbilicus. This is a vestigial structure that, in birds, serves as a
respiratory organ. It later forms a fibrous cord, the urachus, which ultimately
becomes the medial umbilical ligament.
5. The caudal part of the urogenital sinus forms the urethra.
Slide 16: Illustrations showing repositioning of the ureters and bladder formation
Main points:
1. As the region of the urogenital sinus that forms the bladder expands, it
incorporates portions of the mesonephric ducts into its posterior wall.
2. The incorporated portion of the ducts results in mesoderm contributing to the
posterior bladder wall, a region called the trigone. Later endoderm will grow
over this area.
3. Because the ureters are outgrowths from the mesonephric ducts, their position
is altered when the mesonephric ducts are incorporated into the bladder.
Thus, incorporation of the ducts causes the ureters to enter the bladder
directly.
4. If the embryo is a male, the mesonephric ducts remain to form the vas
deferens and ejaculatory ducts, which enter into the prostatic portion of the
urethra. Notice that the vas deferens crosses over the ureters.
5. If the embryo is female, the mesonephric ducts degenerate.
Slide 17: Illustration showing different locations for ectopic ureters
Main points:
1. Because of the nature of bladder formation, including repositioning of the
ureters, and because it develops from the urogenital sinus that contributes to
formation of the vagina, it is possible to develop an ectopically positioned
ureter.
2. The ureter may enter the urethra directly (a circumstance that can also occur
in males) or the vagina.
Slide 18: Illustration showing the final position of the ureters and vas deferens in a
male
Main points:
1. In the male, the mesonephric ducts differentiate into the vas deferens, and at
their caudal end, the seminal vesicle forms as an outpocketing. From the
Sadler, T.W.: Langman’s Medical Embryology, 12e
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point of formation of the seminal vesicle to where the duct enters the urethra,
the mesonephric duct forms the ejaculatory duct.
2. The prostate forms from endodermal buds (proliferations) from the urethra.
Slide 19: Illustrations showing urorectal septal defects and imperforate anus
Main points:
1. If the urorectal septum fails to descend completely, the gut tube will not be
separated from the urogenital portion of the cloaca, resulting in fistulas
between rectum and urethra (males) or vagina.
2. If the septum is misplaced slightly anteriorly, then separation of the gut tube
may occur, but it will be abnormally positioned. In this case, a fistula may
develop in the perineal region.
3. Normally, the lower portion of the rectum is derived from a proliferation of
ectoderm in the anal pit. If this fails, then imperforate anus results. This
defect may also occur if the anal membrane fails to degenerate. (See Lecture
6: Respiratory and Digestive System Development.)
Slide 20: Illustrations showing defects of the urachus
Main points:
1. Normally the allantois, which connects the bladder to the umbilicus,
constricts to form a fibrous cord called the urachus that then becomes the
medial umbilical ligament.
2. If the allantois fails to degenerate into a cord, then a fistula between the
bladder and umbilicus forms, and urine may leak from this region.
3. Cysts and sinuses represent variations on the theme.
Slide 21: Illustrations showing the relationship of the gonad to the mesonephros
Main points:
1. Gonadal tissue forms next to the mesonephric system and forms its own
ridge, the gonadal or genital ridge.
2. In combination, the region where the gonad and mesonephros are together
forms the urogenital ridge along the posterior body wall.
3. Note that the proximity of the mesonephros and gonad sets the stage for
tubules and ducts from the mesonephros to play a role in conduction of sperm
in the male.
Slide 22: The origin and migration of germ cells
Main points:
1. Germ cells are formed in yolk sac endoderm and have to migrate to the
genital ridge. They do so by going along the hindgut through the dorsal
mesentery and into the ridge. They start their migration in the fourth week
and reach the ridge by the sixth week.
2. Some teratoma-type tumors (see sacrococcygeal tumor, Lecture 2) are
thought to arise from germ cells that fail to make it to the genital ridge.
Sadler, T.W.: Langman’s Medical Embryology, 12e
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Slide 23: Illustration showing the relationship of germ cells to epithelium of the
genital ridge
Main points:
1. Once they arrive in the genital ridge, germ cells are surrounded by epithelial
cells derived from the surface of the gland.
2. Surface epithelial cells proliferate and extend into the gonad to form the
primitive sex cords.
Slide 24: Illustrations showing the origin of the seminiferous tubules
Main points:
1. In males, primitive sex cords lose their connection to the surface of the
gonad.
2. Epithelium remaining on the surface of the gland thickens to form a tough
outer covering, the tunica albuginea.
3. The cords become horseshoe shaped and, at puberty, will canalize to form the
seminiferous tubules.
4. Sertoli cells differentiate from some of the cells of the cords and secrete
antimüllerian hormone (also called müllerian-inhibiting substance), which
causes regression of the paramesonephric (müllerian) duct. Sertoli cells also
serve as nurse cells for sperm development.
5. Interstitial cells (of Leydig) differentiate from mesoderm between the sex
cords. These cells secrete testosterone, which causes maturation of the ducts
and tubules in the male. Testosterone is converted in some tissues to
dihydrotestosterone, which causes maturation of the external genitalia.
6. As the male duct system differentiates, tubules called the rete testis make
connections between the seminiferous tubules and some of the old
mesonephric tubules. Mesonephric tubules connected in this way form the
efferent ductules that conduct sperm into the old mesonephric duct, which
now forms the ductus deferens.
Slide 25: Illustration showing continued development of the male ducts
Main points:
1. Not all of the mesonephric tubules differentiate into efferent ductules, so the
remainder degenerate, although remnants exist called the paragenital
tubules.
2. Similarly, not all of the mesonephric duct is utilized to form the ductus
deferens, and its remnant forms the appendix epididymis.
3. By late fetal stages, the ductus deferens has become the vas deferens.
4. The seminal vesicle forms as a proliferating outpocketing of duct epithelium
near the prostate. From the point of the seminal vesicle to its opening into
the prostatic urethra, this portion of the ductus deferens forms the
ejaculatory duct.
5. At its proximal end, the ductus proliferates and becomes highly coiled,
thereby forming the epididymis.
Sadler, T.W.: Langman’s Medical Embryology, 12e
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Slide 26: Formation of oocytes and follicular cells
Main points:
1. In females, the original sex cords degenerate (the medullary cords), and a
second set of cords is formed near the surface of the ovary (cortical cords).
2. Follicular cells differentiate from these cortical cords and surround the germ
cells that have now differentiated into oogonia. Each oogonium, with its
surrounding follicular cells, forms a primary follicle.
3. By the time of birth, many of these oogonia will degenerate, and no more will
form, unlike males who, once they reach puberty, produce sperm for most of
the remainder of their life.
Slide 27: Illustrations showing differentiation of the ducts in females
Main points:
1. In females, there is no testosterone, so the mesonephric duct and tubules
degenerate. Remnants of the tubules form the epoophoron and paroophoron,
and a small remnant of the duct near the vagina forms Gartner’s cyst.
2. In the absence of Sertoli cells and their antimüllerian hormone, the
paramesonephric ducts remain and are stimulated by estrogens.
3. The proximal end of the paramesonephric duct forms the uterine (fallopian)
tube and grows finger-like projections (fimbriae) on its end near the ovary.
4. The caudal end of these ducts fuse to form the uterus and upper portion of the
vagina.
Interesting note: The uterine tube is open to the peritoneal cavity and ovulated eggs
must be caught by the fimbriae, which become sticky and start to beat at the time the egg
is ovulated. Also, eggs rupture through the ovarian epithelium directly into the peritoneal
cavity during the ovulatory process. Sometimes eggs make it into the tube, become
fertilized, and then fall back into the peritoneal cavity to become an ectopic pregnancy.
The most common site in the peritoneal cavity for this type of ectopic pregnancy to occur
is in the rectouterine (Douglas’) pouch, the lowest point in the cavity. The most common
site for all ectopic pregnancies is the uterine tube (a tubal pregnancy).
Slide 28: Illustrations showing formation of the broad ligament
Main points:
1. The urogenital ridge grows away from the posterior wall and rotates slightly,
moving the ovaries into a more transverse plane and closer toward the
midline.
2. This growth causes the paramesonephric ducts to come together caudally so
that they fuse and form the uterus.
3. Since the ridge is covered by peritoneum (retroperitoneal), it carries the
peritoneal layer with it. Eventually this layer drapes over the ovaries and
uterine tubes as the broad ligament.
4. At its cranial and caudal poles, mesoderm of the ridge thins to form the
ligaments of the ovary (see next slide).
Sadler, T.W.: Langman’s Medical Embryology, 12e
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Slide 29: Illustration showing the final relationship of the ovary, uterine tube, and
uterus
Main points:
1. Mesoderm of the urogenital ridge thins to form the suspensory ligament
(attached to the posterior wall) and proper ligament (attached to the uterus) of
the ovary.
Slide 30: Sagittal views showing induction of the vagina by the paramesonephric
ducts.
Main points:
1. Paramesonephric ducts enter into the posterior wall of the urogenital sinus.
Contact with the wall induces formation of the sinovaginal bulbs.
2. These bulbs grow out from the sinus as a solid group of cells that then
canalize to form the lower portion of the vagina.
3. The fused paramesonephric ducts form the upper portion of the vagina and
the cervix.
Slide 31: Frontal views of vaginal development
Main points:
1. Note that, at the site of fusion, the wall between the paramesonephric ducts
has to degenerate.
2. A small amount of tissue from the posterior wall of the urogenital sinus
remains as the hymen.
Slide 32: Examples of abnormalities of the uterus and vagina
Main points:
1. A variety of defects occur that are primarily due to problems with induction,
fusion of the paramesonephric ducts, or programmed cell death patterns
responsible for removal of cells.
2. In some cases, fusion may fail completely, resulting in a double vagina and
uteri.
3. Occasionally, one duct fails to contact the sinus, resulting in a rudimentary
horn. In this case, there is no outlet for blood once menstruation begins at
puberty.
Slide 33: Summary of differences between testes and ovarian development
Slide 34: Summary of genetic signals for testes and ovarian development
Main points:
1. In males, the sex-determining gene is called SRY (sex-determining region on
the Y chromosome). With the presence of this gene, testes develop, and the
fetus is male. It is the master gene for male development.
2. In females, WNT4 plays a primary role.
Sadler, T.W.: Langman’s Medical Embryology, 12e
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3. Note that the two signaling pathways interact to inhibit genes in one or the
other to assist with their specific patterns of development. Thus, SOX9 in
males inhibits WNT4 in their system so that this “female” gene is not active.
Likewise, DAX1 in females inhibits SOX9, which would normally activate
the male pathway.
Interesting note: Previously, females were thought to develop by default due to the
absence of the SRY gene. Not surprisingly, this is not true, and modern molecular
techniques have shown that there is an important signaling pathway in females just as
there is in males.
Slide 35: Views showing the early stages of external genitalia development
Main points:
1. These early stages of development are identical in both sexes.
2. In males, testosterone is converted to dihydrotestosterone to regulate
development of the external genitalia.
3. In females, absence of testosterone and the presence of estrogens regulate
development of this region.
4. At 4 weeks, proliferation of mesoderm creates swellings around the cloacal
membrane called the cloacal folds. Anteriorly, these folds unite to form the
genital tubercle.
5. Lateral to the cloacal folds, a second pair of swellings appears called the
genital swellings.
6. By the end of 6 weeks, the urorectal septum has separated the hindgut and
urogenital sinus portions of the cloaca, such that the cloacal folds are divided
into the urethral folds anteriorly and the anal folds posteriorly.
Slide 36: Illustrations showing differentiation of male genitalia
Main points:
1. In males, the genital tubercle lengthens to form the penis, and the urethral
folds come together and fuse, thus forming the penile urethra.
2. The genital swellings become the scrotal swellings as they enlarge and
eventually fuse to form the scrotum. The line of fusion creates the scrotal
raphe.
3. The very tip of the glans is canalized by a proliferation of ectoderm that
pushes inward to meet the urethra and then hollows to form an opening.
Slides 37 & 38: Examples of male fetuses and genitalia development
Slide 39: Examples of hypospadias
Main points:
1. Hypospadias is a defect resulting from a lack of closure in fusing regions of
the urethra or scrotum, creating openings that may leak urine.
Interesting note: These defects are increasing in frequency, and sperm counts are
declining (by 50% over the last 100 years), leading some investigators to hypothesize that
estrogen-like compounds accumulating in our environment are the cause. These factors
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are called endocrine disruptors and are derived from waste in the environment, primarily
plastics and chemicals. In some cases, plants convert these chemicals to phytoestrogens,
which are then ingested. On another note, it is interesting that closure of the neural tube
and the penile urethra and their closure defects are similar morphologically and may
involve some of the same cellular mechanisms.
Slide 40: Illustrations showing development of female external genitalia
Main points:
1. Females begin at 6 weeks with the same indifferent stage as males.
2. Development in females is characterized by less growth of the genital
tubercle, which becomes the clitoris, and absence of fusion between the
urethral folds, which form the labia minora, and the genital swellings, which
form the labia majora.
3. Once the paramesonephric ducts contact the urogenital sinus and induce
formation of the vagina, openings for the vagina and urethra become
separated.
Slide 41: View of female fetal genitalia
Main points:
1. At 11 weeks, the genital tubercle (clitoris) in female fetuses is as large as or
larger than in males. Consequently, it is difficult to determine sex with
ultrasounds until about the 13th week.
Slide 42: Example of female pseudohermaphrodism (adrenogenital syndrome)
Main points:
1. True hermaphrodites are rare and have both ovarian and testicular tissues
(ovotestes). Most are 46XX and have mostly female characteristics.
2. Pseudohermaphrodites are more common and are classified as male or female
based on their genotypic sex: XX female; XY male.
3. The most common form of female pseudohermaphrodism is the adrenogenital
syndrome. Biochemical defects in steroid biosynthesis (usually 21
hydroxylation) result in accumulations of ACTH and ultimately androgen
compounds. These androgens then stimulate the external genitalia to take on
a more male-like appearance—in this case, fusion of the labia majora and
enlargement of the clitoris.
Slide 43: Example of male pseudohermaphrodism
Main points:
1. A common cause for this type of abnormality is the androgen insensitivity
syndrome. Patients are XY and have testes. However, their external genitalia
lack receptors for testosterone, causing them to assume a female morphology.
2. Because testes are present, so is antimüllerian hormone; thus the
paramesonephric (müllerian) ducts are inhibited, and no uterus forms. The
vagina, if present at all, is short and blind ending.
Sadler, T.W.: Langman’s Medical Embryology, 12e
© Lippincott Williams & Wilkins, 2013
Slide 44: Summary of the signals for sexual differentiation
Slide 45: Illustrations showing testicular descent
Main points:
1. Testes develop in a retroperitoneal position in the lumbar region.
Consequently, they must migrate to the scrotum and, in so doing, pass
through the layers of the abdominal wall. As they pass through, each layer
contributes a layer surrounding the testes.
2. During the eighth week, the urogenital ridge thins caudally to form the caudal
genital ligament, which is supported by additional matrix material that
condenses into the gubernaculum.
3. The gubernaculum extends from the caudal pole of each testis and eventually
reaches the scrotum by passing through the inguinal canal. It assists in
pulling the testes into the scrotal sac.
4. Testicular descent is preceded by an outpocketing of peritoneum called the
processes vaginalis that migrates through the inguinal canal and into the
scrotal sac. Once the testis arrives in the scrotum, the processes wraps around
the gland, forming the visceral and parietal layers of the tunica vaginalis.
5. The testes should reach the inguinal canal by 7 months and be in the scrotum
at birth. In 3% of infants, the testes do not make it but will find their way by
3 months of age. In 1%, they will remain undescended, a condition called
cryptorchidism.
6. Factors regulating descent include testosterone and antimüllerian hormone
(müllerian-inhibiting substance), which act on the gubernaculum.
Interesting note: Testes require a lower temperature for sperm production. That is why
they migrate into the scrotum, where temperature can be maintained 2-3° lower than body
temperature.
Slide 46: Illustration showing coverings of the testes
Main points:
1. The inguinal canal is an oblique passageway through the layers of the
abdominal wall; as the processes vaginalis and testes migrate through the
wall, they are covered by these layers.
2. Note that the transversus abdominis muscle does not provide a covering.
This results because its insertion arches over the internal ring of the inguinal
canal, and so the testes do not migrate through this muscle layer.
Slide 47: Examples of defects related to the processes vaginalis
Main points:
1. Once the processes vaginalis reaches the scrotum, its connection to the
peritoneum pinches off and closes. If closure fails, then a tract remains
through which intestines may pass into the inguinal canal and sometimes all
the way into the scrotum. Herniation of intestines along this pathway is
called an indirect inguinal hernia.
Sadler, T.W.: Langman’s Medical Embryology, 12e
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2. If the pinching off occurs abnormally, cysts may form that can fill with fluid
to form hydroceles.
Slide 48: Illustration showing final positioning of the ovary
Main points:
1. Ovaries also descend, but not as far as testes. This descent is caused partly by
growth of the urogenital ridge toward the midline, but also because the
ovaries, like the testes, form a caudal genital ligament surrounded by the
gubernaculum that extends to the labia majora.
2. Due to growth of the uterus, this connection between the caudal pole and
labia majora is lost, and the caudal ligament attaches to the side of the uterus
to form the proper ovarian ligament.
3. The part of the caudal genital ligament extending from the side of the uterus
to the labia majora forms the round ligament of the uterus.
4. Sometimes the attachment of this ligament to the uterus fails to occur, and an
ovary may be located in the labia majora.
Interesting note: Since the ovaries do not descend, the inguinal canal in females is
rudimentary, and indirect hernias are rare.
Sadler, T.W.: Langman’s Medical Embryology, 12e
© Lippincott Williams & Wilkins, 2013