The ovary is a paired organ, roughly the size and shape of an almond, that serves two jobs at once: it releases eggs capable of being fertilized, and it produces the steroid hormones that drive the menstrual cycle, shape secondary sex characteristics, and influence bone density, cardiovascular health, and mood. What makes the ovary structurally unusual is that it tears itself open and rebuilds on a monthly basis, cycling through tissue remodeling that would qualify as injury in most other organs. Understanding how the ovary is built helps explain why it can do this and why it eventually stops.
Where the Ovaries Sit and How They Are Anchored
Each ovary sits in a shallow depression on the lateral wall of the pelvis, tethered by a set of ligaments rather than rigidly fixed. The ovarian ligament connects the ovary to the uterus, while the suspensory ligament (also called the infundibulopelvic ligament) attaches it to the pelvic wall and carries the ovarian artery and vein. A fold of peritoneum called the mesovarium links the ovary to the broad ligament of the uterus. These attachments give the ovary some mobility, which matters during ovulation: the fimbriae at the end of the fallopian tube sweep over the ovarian surface to catch the released egg.
In a reproductive-age adult, each ovary measures roughly 3 to 5 centimeters long, 1.5 to 3 centimeters wide, and about 1 centimeter thick, though size fluctuates during the menstrual cycle as follicles grow and regress. The surface is covered by a single layer of cells historically called the “germinal epithelium,” a misnomer from the era when researchers believed eggs originated there. Below that lies a thin, dense capsule of connective tissue known as the tunica albuginea.
Internal Architecture
Traditionally, the ovary’s interior has been divided into three zones: cortex, medulla, and hilum. The cortex is the outer layer where follicles at various stages of development are embedded in a dense connective-tissue matrix. The medulla sits deeper and is looser, containing the bulk of the blood vessels, lymphatics, and nerves. The hilum is the point where the ovary meets the mesovarium and where its major vessels enter and exit. Researchers have recently argued that this three-part naming system is too simple, given the ovary’s complex micro-anatomy, and have proposed a more detailed, three-dimensional mapping approach to better describe regional differences in cell types and tissue composition.
The connective tissue surrounding the follicles, called the stroma, is far from passive scaffolding. It is a dynamic matrix of collagen, elastin, fibronectin, and laminin that actively influences how follicles grow and eventually rupture. Collagen is densest near the outer surface of the cortex and thins toward the medulla, while elastin concentrates near the border between cortex and medulla, especially around blood vessels.1PubMed Central. Spatio-temporal remodelling of the composition and architecture of the human ovarian cortical extracellular matrix during in vitro culture Changes in the organization and distribution of different collagen types influence the transition of dormant primordial follicles into active growth stages and play a role in the intense tissue remodeling that occurs during ovulation and reproductive aging.2PubMed. Characteristics of collagen in ovarian extracellular matrix and its relationship with the development of primordial follicles up to ovulation
How Follicles Develop
A person with ovaries is born with roughly one to two million primordial follicles, each containing an immature egg cell arrested in an early stage of cell division. By puberty, only about 300,000 to 400,000 remain, and of those, only around 400 will ever fully mature and ovulate over a reproductive lifetime. The rest gradually degenerate in a process called atresia.
Follicle development, or folliculogenesis, proceeds through a well-characterized sequence. The earliest primordial follicles consist of a small oocyte surrounded by a single flat layer of cells. Activation transforms them into primary follicles, where those surrounding cells become cuboidal. At the secondary stage, multiple layers of granulosa cells form, and a fluid-filled cavity called the antrum begins to appear. Antral follicles are classified by size: small, medium, large, and finally preovulatory, when the follicle is ready for the hormonal signal that triggers ovulation.3Fertility Science and Research. The Ovarian Folliculogenesis – A Mini Review The early stages of this process take months and are largely independent of the pituitary hormones that drive the later stages. By the time a follicle reaches the antral stage, it becomes responsive to follicle-stimulating hormone (FSH), and the monthly recruitment cycle kicks in.
Egg Maturation and the Trigger for Ovulation
The oocyte inside a growing follicle is stuck in the first phase of meiosis, the special type of cell division that halves the chromosome count. It stays paused because the surrounding granulosa cells actively maintain high levels of a signaling molecule called cyclic AMP inside the egg, which keeps the division machinery switched off. Signals from a molecule called natriuretic peptide C in granulosa cells also contribute to this brake by boosting another messenger, cyclic GMP, that diffuses into the oocyte.4PubMed. Molecular control of oocyte meiotic arrest and resumption
When a surge of luteinizing hormone (LH) arrives from the pituitary gland mid-cycle, it triggers a cascade of events in the follicle wall. Granulosa cells respond by producing growth factors that ultimately break the chemical brake on the oocyte, allowing it to resume dividing. At the same time, the follicle wall weakens. Enzymes called matrix metalloproteinases (MMPs) break down the collagen in the follicle’s basement membrane and outer layers, effectively digesting a hole through which the egg can escape.5PubMed Central. Gelatinase A and membrane-type matrix metalloproteinases 1 and 2 are responsible for follicle rupture during ovulation in the medaka Ovulation is, in a real sense, a controlled wound. Inflammatory signals flood the site, blood vessels break down, and a small amount of fluid and blood accompanies the released egg. Some people feel this as a brief, sharp pain on one side, known as mittelschmerz.
Hormone Production and the Two-Cell System
The ovary is one of the body’s major endocrine organs, producing estrogen, progesterone, and androgens. The follicle wall accomplishes estrogen synthesis through teamwork between two cell types. The outer theca cells, stimulated by LH, produce androgens because they exclusively express the enzyme needed for that conversion. Those androgens then pass to the inner granulosa cells, which are stimulated by FSH and express the enzyme aromatase, converting the androgens into estrogen.6PubMed. Follicular oestrogen synthesis: the ‘two-cell, two-gonadotrophin’ model revisited Neither cell type can produce estrogen alone. This division of labor means that hormone output is tightly coupled to follicle health: if the granulosa cells are damaged or the theca layer loses its blood supply, estrogen production falls.
Before ovulation, the dominant follicle is the major source of estradiol. After ovulation, the remnant of the follicle transforms into the corpus luteum, which shifts its output to progesterone, the hormone that prepares the uterine lining for possible implantation. If pregnancy occurs, the corpus luteum continues secreting progesterone for several weeks until the placenta takes over. If not, it degenerates.
The Life and Death of the Corpus Luteum
The corpus luteum is a temporary endocrine gland that forms at the ovulation site. After the egg is released, the remaining granulosa and theca cells undergo a dramatic transformation called luteinization: they enlarge, accumulate yellow lipid droplets (the Latin word “luteum” means yellow), and ramp up progesterone production. This transformation is accompanied by explosive blood vessel growth. New capillaries invade the formerly avascular granulosa layer, and vessel density climbs sharply in the first half of the luteal phase.7PubMed. Cyclic changes of vasculature and vascular phenotypes in normal human ovaries
If pregnancy does not occur, the corpus luteum begins to regress roughly 10 to 14 days after ovulation. This process, called luteolysis, involves programmed cell death in the luteal cells and the collapse of the blood vessel network that sustained them.8Endocrines. The Mechanisms of Angiogenesis and Apoptosis During the Functional Formation and Regression of the Corpus Luteum in the Ovarian Reproductive Endocrine System Vascular endothelial growth factor (VEGF), which fueled the initial blood vessel invasion, is downregulated during luteolysis, and the new vessels regress. Endothelial cells shorten, round up, and detach.9PubMed Central. Ovarian angiogenesis. Phenotypic characterization of endothelial cells in a physiological model of blood vessel growth and regression Over weeks, the corpus luteum shrinks into a small scar of connective tissue called a corpus albicans. Older ovaries accumulate these scars, giving the surface an increasingly rough, pitted appearance.
Blood Supply and Cyclical Vessel Growth
The ovary is one of the few adult organs where large-scale blood vessel formation and regression happen as a normal, recurring event. Outside of wound healing and pregnancy, most tissues in the body do not build new vascular networks after they finish developing. The ovary does this every cycle. Capillary networks form in the theca layer of growing follicles even at the preantral stage, and vessel density increases as follicles mature into dominant ones.7PubMed. Cyclic changes of vasculature and vascular phenotypes in normal human ovaries After ovulation, the vascular invasion of the corpus luteum is one of the fastest angiogenic events in the body, peaking around the mid-luteal phase before tapering off.10PubMed. Analysis of blood vessel maturation processes during cyclic ovarian angiogenesis This cyclical remodeling means the ovary is a useful natural model for studying how blood vessels grow and die under non-pathological conditions, which is why cancer researchers and vascular biologists have long been interested in it.
Nerve Supply and Rapid Regulation
The ovary receives input from the autonomic nervous system through two main routes: the superior ovarian nerve (SON), which travels along the suspensory ligament with the ovarian artery, and the ovarian nerve plexus (ONP), which follows the ovarian branch of the uterine artery. Both pathways can constrict ovarian blood vessels through alpha-1 adrenergic receptors, but the SON has an additional role: it can directly inhibit estradiol secretion via alpha-2 receptors.11PubMed Central. Autonomic nervous regulation of ovarian function by noxious somatic afferent stimulation In animal studies, cutting the SON on one side reduced the number of preovulatory follicles and changed the structural appearance of large follicles, including causing abnormal folding in their walls.12PubMed Central. Role of the superior ovarian nerve in the regulation of follicular development and steroidogenesis in the morning of diestrus 1 These findings suggest the nervous system does more than just regulate blood flow to the ovary; it may directly influence which follicles survive and how much hormone they produce, offering a mechanism by which stress or pain could rapidly alter ovarian function.
Immune Cells Inside the Ovary
The ovary is home to a resident population of immune cells, with macrophages being the most abundant white blood cells present. These macrophages are not there to fight infection. They participate in every major ovarian event: supporting follicle growth, facilitating the inflammatory-like process of ovulation, helping form the corpus luteum, and cleaning up cellular debris during luteolysis.13PubMed Central. New insight into the role of macrophages in ovarian function and ovarian aging As the ovary ages, changes in its macrophage populations are linked to declining function, making ovarian immunity a growing area of research in reproductive aging.
Tracking Ovarian Reserve
Because the vast majority of follicles are lost to atresia rather than ovulation, the pool of remaining follicles shrinks throughout life. Clinicians use the term “functional ovarian reserve” to describe the population of small, growing follicles that could potentially mature and ovulate. The most widely used blood marker for this is anti-Müllerian hormone (AMH), which is secreted by granulosa cells of small growing follicles. Serum AMH levels correlate strongly with the number of those follicles.14PubMed Central. Anti-Müllerian Hormone and Ovarian Reserve: Update on Assessing Ovarian Function
AMH is useful for predicting how the ovaries will respond to stimulation in fertility treatment, but it is often misunderstood as a direct measure of fertility. A low AMH value tells you the pool of recruitable follicles is small; it does not tell you whether the eggs in those follicles are healthy. Egg quality is more closely tied to age than to AMH level. Someone with a low AMH at 28 may still have eggs of good quality, while someone with a higher AMH at 42 faces the age-related decline in egg quality regardless of how many follicles remain.
What Happens to the Ovary After Menopause
Menopause marks the point when the ovary’s supply of responsive follicles is effectively exhausted. Structurally, the postmenopausal ovary looks quite different from its reproductive-age counterpart. The surface epithelium flattens and the surface itself becomes smoother, with fewer of the papillae and tiny crypts visible in younger ovaries. Primordial follicles are usually absent, though remnants of older, degenerated structures remain: corpora albicantia, scar tissue, and occasional simple cysts.15PubMed. Three-dimensional microanatomical dynamics of the ovary in postreproductive aged women Fibrosis becomes prominent, and the blood vessels show marked reduction in both number and caliber, with thickened walls and altered endothelial cells. Apoptotic and necrotic cells appear frequently in the surface epithelium. The organ shrinks substantially, sometimes to less than half its reproductive-age volume.
Polycystic Ovary Morphology
In polycystic ovary syndrome (PCOS), the ovary’s structure reflects a disruption in follicle selection. Instead of one follicle becoming dominant each cycle, multiple small antral follicles stall at an intermediate size, lining the periphery of the cortex in a pattern visible on ultrasound. The “cysts” in the name are actually follicles that have not progressed to ovulation. The ovaries often appear enlarged, and the stroma may be thickened and more echogenic on imaging. About 95% of people with the classic form of PCOS, characterized by excess androgens and irregular ovulation, also display this polycystic ovarian morphology on imaging.16PubMed Central. The Polycystic Ovary Morphology-Polycystic Ovary Syndrome Spectrum However, polycystic-appearing ovaries on ultrasound alone, without hormonal or ovulatory abnormalities, can be a normal variant, especially in younger people. Roughly half of those with this morphology but no clinical symptoms carry underlying steroidogenic changes suggestive of a mild or carrier form of the condition.
Primary Ovarian Insufficiency
Primary ovarian insufficiency (POI) refers to the loss of normal ovarian function before age 40. It affects roughly 1% of people with ovaries in that age group and can present as absent periods from puberty onward (primary amenorrhea) or as premature cessation of previously regular cycles (secondary amenorrhea).17PubMed Central. Premature ovarian failure The causes are varied: autoimmune destruction of ovarian tissue, exposure to certain chemotherapy drugs, environmental toxins, and genetic factors all play roles.18PubMed Central. Premature Ovarian Insufficiency: Past, Present, and Future X chromosome abnormalities, including Turner syndrome, are the most common genetic cause of primary amenorrhea with ovarian dysfunction. Mutations in over 60 genes have been linked to POI, underscoring a wide genetic heterogeneity.19Trends in Endocrinology & Metabolism. Ovary Anatomy: A Look at Structure and Function Ongoing genetic research is increasingly relevant because certain gene defects, particularly those affecting DNA repair pathways, may carry implications beyond fertility, including tumor predisposition.
Environmental Chemicals and Ovarian Disruption
A category of chemicals known as endocrine-disrupting compounds (EDCs) can interfere with ovarian structure and function. Bisphenol A (found in certain plastics), phthalates, dioxins, methoxychlor (a pesticide), and genistein (a plant estrogen in soy) have all been studied for their effects on the ovary. These substances can alter follicle development and disrupt the steroid hormone production pathways, potentially contributing to infertility, abnormal hormone levels, and accelerated follicle loss.20PubMed Central. Effects of Endocrine-Disrupting Chemicals on the Ovary The mechanisms vary by chemical: some mimic estrogen, some block androgen receptors, and others interfere with the signaling pathways that control which follicles are recruited into the growth pool. The practical difficulty is that exposure tends to be chronic and low-level, making it hard to pin down individual risk in everyday life.
How Ovaries Differ Across Species
The basic architecture of the ovary, with follicles embedded in a stromal matrix, is shared across vertebrates, but important differences exist. Most non-mammalian vertebrates grow and mature many follicles simultaneously, which makes sense given that fish, amphibians, and reptiles typically produce large numbers of offspring at once. Mammals are the exception, with most species selecting only one or a few dominant follicles per cycle.21PubMed Central. Comparative Histologic Evaluation of Vertebrate Ovaries Another striking difference involves how ovaries form in the first place. In mammals, ovarian development proceeds when the testis-determining gene SRY is absent, and pro-ovarian signaling pathways involving WNT4 and RSPO1 take over. In reptiles and birds, however, ovary formation is actively driven by estrogen rather than being a “default” pathway, suggesting that the mammalian mechanism evolved from an older, estrogen-dependent process.22PubMed Central. Organogenesis of the ovary: a comparative review on vertebrate ovary formation
Artificial Ovaries and Bioengineering
For people who lose ovarian function due to cancer treatment, POI, or other causes, researchers are working on bioengineered ovary systems designed to replicate the organ’s dual roles of egg maturation and hormone production. These artificial ovaries use scaffolds made from natural materials like collagen, fibrin, and alginate, or synthetic ones, seeded with granulosa and theca cells or stem cell-derived ovarian cells. Some experimental approaches use three-dimensional bioprinting or microfluidic “ovary-on-a-chip” platforms. Early results show promise in follicle survival and hormone secretion, though achieving complete egg maturation and functional blood vessel formation inside these constructs remains a significant challenge.23PubMed. Artificial ovary systems for fertility preservation: Current advances, bioengineering strategies, and translational perspectives If successful, such technology could offer not just fertility preservation but also a way to restore the hormonal environment that supports bone, heart, and brain health after ovarian loss, potentially as an alternative to conventional hormone replacement therapy.