The placenta is a temporary fetomaternal organ that develops during pregnancy and forms the principal interface between the maternal and fetal circulations. It enables exchange of gases, nutrients and waste products, produces hormones, and contributes to immunological and metabolic functions required for fetal development.
The placenta is a temporary fetomaternal organ that develops during pregnancy and establishes the principal interface between the developing fetus and the mother. It supports fetal growth by permitting exchange of oxygen, carbon dioxide, nutrients, water, electrolytes, metabolic waste products, and numerous other substances between the maternal and fetal circulations.
The placenta is also an important endocrine and immunological organ. It produces hormones required for maintenance and progression of pregnancy, modifies maternal physiology, and participates in regulation of the maternal-fetal interface. Although maternal and fetal blood come into close anatomical relationship within the placenta, they normally remain within separate circulatory systems.
The placenta develops at the site of implantation within the uterus.
In a typical pregnancy it is attached to the endometrium of the uterine body, commonly along the anterior or posterior wall and often toward the upper uterus.
At term, the human placenta is typically a discoid organ.
Its broad surface is attached to the uterine wall, while the umbilical cord connects its fetal surface to the fetus.
The dimensions of the placenta vary among pregnancies. At term, it is commonly approximately 15 to 20 cm in diameter and around 2 to 3 cm thick near its central region.
Its weight is commonly approximately 500 to 600 g, although substantial normal variation occurs.
The placenta develops from both fetal and maternal tissues.
The principal components are:
The chorion frondosum forms the principal fetal component of the placenta.
It contains extensively branched chorionic villi supplied by fetal blood vessels.
The decidua basalis forms the maternal component of the placenta.
It is the region of pregnancy-modified endometrium located between the implanted conceptus and the underlying myometrium.
| Component | Origin | Major Role |
|---|---|---|
| Chorion frondosum | Fetal | Forms villous fetal portion |
| Decidua basalis | Maternal | Forms maternal placental portion |
| Chorionic villi | Fetal | Contain fetal vessels and provide exchange surface |
| Intervillous space | Contains maternal blood | Bathes chorionic villi |
| Chorionic plate | Fetal | Forms fetal surface region of placenta |
| Basal plate | Fetomaternal interface | Forms maternal-facing placental boundary |
Placental development begins during implantation as the trophoblast differentiates into cytotrophoblast and syncytiotrophoblast.
The invasive syncytiotrophoblast penetrates maternal endometrial tissue and develops lacunae that eventually communicate with maternal blood vessels.
The trophoblast is the outer cellular component of the blastocyst and makes a major contribution to the fetal side of the developing placenta.
During implantation it differentiates into cytotrophoblast and syncytiotrophoblast.
The cytotrophoblast consists of distinct mononuclear trophoblastic cells with mitotic activity.
These cells contribute to growth of the trophoblast and formation of developing chorionic villi.
The syncytiotrophoblast is the multinucleated outer trophoblastic layer.
It invades maternal tissues, contributes to formation of the placental exchange interface, and produces important pregnancy-related hormones.
During implantation, spaces develop within the syncytiotrophoblast and merge to form trophoblastic lacunae.
Maternal blood subsequently enters these spaces as maternal vessels are opened by the invading trophoblast.
Chorionic villi are branching projections of fetal chorionic tissue that extend into maternal blood within the intervillous space.
They dramatically increase the surface area available for exchange between the maternal and fetal circulations.
Primary chorionic villi develop when columns of cytotrophoblastic cells extend into the surrounding syncytiotrophoblast.
They represent the earliest structural stage of villous development.
Secondary chorionic villi form when extraembryonic mesoderm grows into the cores of primary villi.
The villi therefore acquire a mesodermal core surrounded by trophoblastic layers.
Tertiary chorionic villi develop when fetal capillaries form within the mesodermal cores of secondary villi.
These vessels establish connections with the developing fetal circulation and permit effective placental exchange.
| Stage | Structure |
|---|---|
| Primary villus | Cytotrophoblastic core covered by syncytiotrophoblast |
| Secondary villus | Extraembryonic mesoderm enters the villous core |
| Tertiary villus | Fetal blood vessels develop within the mesodermal core |
Larger stem villi provide structural support for branching villous trees and connect them to the chorionic plate.
Progressive branching from larger villi produces increasingly smaller villous structures specialized for exchange.
Terminal villi are small peripheral branches of the villous tree that provide extensive surface area for maternal-fetal exchange.
Fetal capillaries within these villi lie close to the trophoblastic surface, reducing the diffusion distance for exchanged substances.
Some chorionic villi function as anchoring villi, attaching the chorionic structures to the maternal decidua.
These attachments help stabilize the developing placenta within the implantation site.
Many villous branches project freely into the maternal blood-filled intervillous space.
These floating villi are extensively involved in exchange between maternal blood and fetal capillaries.
Chorionic villi associated with the decidua basalis continue to grow and branch extensively, producing the chorion frondosum.
This densely villous region forms the fetal component of the definitive placenta.
Villi on the side of the chorionic sac away from the implantation site progressively regress.
This region becomes the relatively smooth chorion laeve.
| Feature | Chorion Frondosum | Chorion Laeve |
|---|---|---|
| Villi | Persist and branch extensively | Regress |
| Appearance | Bushy or villous | Smooth |
| Relationship | Associated with decidua basalis | Associated with nonplacental membranes |
| Fate | Forms fetal placenta | Forms smooth chorion |
The decidua basalis lies beneath the implanted conceptus and develops into the maternal component of the placenta.
It contains maternal vessels and specialized decidual tissue involved in supporting and regulating placental development.
During implantation, endometrial stromal cells enlarge and accumulate glycogen and lipids in a process called the decidual reaction.
The resulting decidual tissue contributes to the maternal environment surrounding the developing placenta.
The chorionic plate forms the fetal surface of the placenta.
It is associated with the chorion and contains branches of the umbilical vessels that radiate across the fetal surface before entering the villous trees.
The basal plate forms the maternal-facing boundary of the placenta.
It includes decidual tissue and trophoblastic components at the interface between the placenta and uterine wall.
The intervillous space is the maternal blood-filled space surrounding the chorionic villi.
Maternal blood entering this space directly bathes the external surfaces of the villi but normally does not directly mix with fetal blood inside the villous capillaries.
The maternal surface of the delivered placenta is relatively rough and is divided into irregular regions called cotyledons.
It corresponds to the side that was attached to the uterine wall.
The fetal surface is smooth and shiny because it is covered by amnion.
Branches of the umbilical vessels can be seen radiating across this surface from the umbilical cord insertion.
| Feature | Maternal Surface | Fetal Surface |
|---|---|---|
| Appearance | Rough and lobulated | Smooth and shiny |
| Major feature | Cotyledons | Umbilical vessels |
| Covering | Associated with decidual tissue | Covered by amnion |
| Orientation | Faces uterine wall | Faces fetus and amniotic cavity |
The maternal surface is subdivided into approximately 15 to 20 cotyledons.
Each cotyledon contains one or more major villous trees and associated branches.
Placental septa extend from the maternal side toward the chorionic plate and partially subdivide the intervillous space.
They do not normally divide the intervillous space into completely isolated compartments.
Maternal blood reaches the placenta through uterine spiral arteries.
These vessels discharge blood into the intervillous space, where it circulates around the chorionic villi before returning through maternal endometrial veins.
Spiral arteries are maternal uterine vessels that undergo substantial remodeling during normal placental development.
This remodeling helps establish a low-resistance maternal blood supply to the intervillous space.
The basic maternal placental pathway can be represented as:
Fetal blood reaches the placenta through the two umbilical arteries.
These arteries carry relatively deoxygenated blood from the fetus toward the placenta.
The two umbilical arteries enter the placenta through the umbilical cord and branch across the chorionic plate.
Their branches ultimately supply capillary networks within the chorionic villi.
Within the chorionic villi, fetal blood passes through extensive capillary networks positioned close to maternal blood in the intervillous space.
This close relationship permits efficient exchange while maintaining separation of the two circulations.
After exchange within the placental villi, oxygenated and nutrient-rich fetal blood is collected into veins that ultimately form the single umbilical vein.
The umbilical vein carries this blood from the placenta toward the fetus.
Maternal and fetal blood normally do not directly mix within the placenta.
Maternal blood occupies the intervillous spaces, while fetal blood remains within vessels and capillaries of the chorionic villi.
The tissues separating maternal blood from fetal blood are collectively described as the placental barrier or placental membrane.
The composition and thickness of this barrier change as pregnancy progresses.
Early in pregnancy, the placental barrier includes:
As pregnancy progresses, the exchange barrier becomes thinner in many regions.
The cytotrophoblastic layer becomes discontinuous, fetal capillaries approach the trophoblastic surface, and diffusion distance is reduced.
The placenta permits transfer of many substances between maternal and fetal circulations through mechanisms including:
Oxygen passes from maternal blood to fetal blood across the placental interface, while carbon dioxide moves primarily in the opposite direction.
The placenta therefore performs the gas-exchange function that the fetal lungs cannot perform before birth.
Nutrients transferred through the placenta include glucose, amino acids, fatty acids, vitamins, minerals, electrolytes, and water.
Different substances use different transport mechanisms depending on their chemical and physiological properties.
Fetal metabolic waste products are transferred to maternal blood for elimination by maternal organs.
These include carbon dioxide and nitrogenous waste products such as urea.
Glucose is a major fetal energy substrate and crosses the placenta primarily through facilitated transport.
Maternal glucose availability therefore has an important influence on fetal metabolism and growth.
Many amino acids are transported actively across the placenta.
This enables the fetus to obtain substrates required for protein synthesis and growth.
Minerals such as calcium and iron are transferred across the placenta through regulated mechanisms.
These substances are important for fetal skeletal development, hematopoiesis, and numerous metabolic processes.
Maternal IgG antibodies can cross the placenta through receptor-mediated mechanisms.
This provides the fetus and newborn with passive immunity against selected pathogens encountered previously by the mother.
The placenta produces numerous hormones and signaling molecules that influence maternal physiology, fetal development, and maintenance of pregnancy.
Important placental hormones include:
Human chorionic gonadotropin (hCG) is produced primarily by syncytiotrophoblast.
During early pregnancy, it maintains the corpus luteum and thereby supports continued ovarian progesterone production.
The placenta becomes an important source of progesterone as pregnancy progresses.
Progesterone supports the uterine environment, contributes to maintenance of the endometrium, and influences uterine smooth muscle activity.
The placenta participates in production of estrogens during pregnancy.
Placental estrogen synthesis depends partly on precursors supplied through interactions with maternal and fetal tissues.
Human placental lactogen, also called human chorionic somatomammotropin, is produced by syncytiotrophoblast.
It contributes to metabolic adaptations of pregnancy and supports preparation of the mammary glands for lactation.
The placenta is metabolically active and synthesizes, modifies, stores, and transports numerous substances.
It is therefore much more than a passive diffusion membrane.
The placenta participates in regulation of the maternal immune response to pregnancy.
The maternal-fetal interface must permit close contact between maternal tissues and genetically distinct fetal tissues while limiting destructive immune responses.
The umbilical cord connects the fetus to the fetal surface of the placenta.
It contains the major vessels carrying fetal blood to and from the placenta.
A normal umbilical cord usually contains:
These vessels are embedded within Wharton jelly and covered externally by amnion.
The umbilical cord commonly inserts near the central region of the fetal placental surface, although normal variation occurs.
Insertion may also be eccentric or marginal.
A marginal cord insertion occurs when the umbilical cord attaches near the placental edge.
This differs from the more common central or eccentric insertion.
In velamentous insertion, umbilical vessels traverse the fetal membranes before reaching the placental disc rather than remaining protected within the cord until placental insertion.
These exposed membranous vessels are more vulnerable to compression and injury.
The placenta changes continuously throughout gestation.
Villous branching increases, exchange surfaces expand, fetal capillary relationships become more efficient, and endocrine activity changes according to the needs of the pregnancy.
As gestation advances, terminal villi become increasingly specialized for exchange.
The distance between maternal blood and fetal capillaries decreases in many regions, improving diffusion efficiency.
The fetal surface of the placenta is covered by amnion.
The amnion is continuous with the membrane covering the umbilical cord and with the amniotic sac surrounding the fetus.
The chorionic plate forms an important structural component of the fetal placental surface.
Chorionic villi arise from this fetal tissue and project toward the maternal side into the intervillous space.
The placenta is attached to the decidualized endometrium rather than directly to normal myometrium.
Abnormally deep trophoblastic attachment or invasion into the uterine wall forms the anatomical basis of placenta accreta spectrum disorders.
Placenta previa occurs when placental tissue is located abnormally low in the uterus and overlies or lies near the internal cervical os.
Its anatomical relationship to the cervix can interfere with the normal route of delivery and can be associated with significant bleeding.
Placenta accreta spectrum describes abnormal placental attachment associated with deficient normal decidual separation and varying degrees of invasion into the uterine wall.
The spectrum includes placenta accreta, increta, and percreta.
In placenta accreta, placental villi are abnormally attached to the uterine wall because the normal decidual interface is deficient.
This can prevent normal placental separation after delivery.
In placenta increta, chorionic villi invade into the myometrium.
This represents deeper involvement than placenta accreta.
In placenta percreta, placental tissue penetrates through the myometrium and may extend through the uterine serosa into adjacent structures.
The urinary bladder is an important neighboring organ that may be involved in severe cases.
Placental abruption is premature separation of a normally implanted placenta from the uterine wall before delivery of the fetus.
Separation can disrupt maternal vessels and compromise placental exchange.
Placental insufficiency broadly refers to inadequate placental function that limits the ability of the placenta to meet fetal physiological requirements.
Impaired uteroplacental blood flow or abnormalities of placental structure can contribute to restricted fetal growth and other complications.
Normal pregnancy involves trophoblast-associated remodeling of maternal spiral arteries.
The vessels become adapted to provide relatively high-volume, low-resistance blood flow to the placenta.
Abnormalities of placentation and incomplete physiological remodeling of spiral arteries are strongly associated with the pathophysiology of preeclampsia.
The disorder involves complex interactions among placental, vascular, immunological, and maternal factors.
A placental infarct is an area of ischemic necrosis resulting from interruption of maternal blood supply to placental tissue.
Small infarcts may occur without major consequences, while extensive involvement can reduce functional placental tissue.
After delivery, the placenta can be examined for completeness, size, shape, cord insertion, membrane abnormalities, vascular lesions, and other structural findings.
Examination of the maternal surface is particularly important for identifying missing placental tissue that may remain within the uterus.
Placental tissue remaining within the uterus after delivery can interfere with normal uterine contraction and contribute to postpartum bleeding and other complications.
Inspection of the delivered placenta can help identify suspected incomplete placental separation.
Following delivery of the fetus, uterine contractions contribute to separation of the placenta from the uterine wall.
The placenta, fetal membranes, and attached umbilical cord are subsequently expelled during the third stage of labor.
The number and arrangement of placentas in multiple pregnancy depend on zygosity and, for monozygotic twins, the timing of embryonic division.
Placental masses in dichorionic pregnancies may remain separate or become externally fused as pregnancy progresses.
Monochorionic twins share a chorion and therefore share a placental structure.
Vascular connections between the fetal circulations can occur within a shared monochorionic placenta.
Twin-to-twin transfusion syndrome can occur in monochorionic twin pregnancies when placental vascular connections produce an imbalanced distribution of blood between the twins.
Its occurrence is directly related to the shared placental circulation.
The placental barrier selectively regulates transfer but does not completely isolate the fetus from maternal substances.
Some medications, infectious agents, toxic substances, antibodies, and other molecules can cross or affect the placenta.
The placenta is essential for maintaining pregnancy and supporting fetal growth. It functions simultaneously as an exchange organ, endocrine gland, metabolic tissue, vascular interface, and immunological boundary. Its highly branched chorionic villi provide a large surface through which maternal and fetal physiological systems can interact while normally maintaining separate blood circulations.
Placental location, attachment, vascular development, and function have major clinical importance. Abnormal placental position can produce placenta previa, abnormal attachment or invasion can produce placenta accreta spectrum, and premature separation can result in placental abruption. Abnormal placental vascular development and impaired spiral artery remodeling are also important in disorders involving placental insufficiency and preeclampsia.
Understanding placental anatomy provides a central connection between implantation, trophoblast development, chorionic villi, fetal membranes, uterine circulation, umbilical circulation, fetal growth, pregnancy endocrinology, maternal-fetal exchange, and obstetric complications.