Uterine fibroids are made primarily of smooth muscle cells and collagen, bound together by a dense scaffolding of connective tissue called extracellular matrix. Think of them as a firm, rubbery ball of abnormal muscle tissue wrapped in a thick web of structural protein. They aren’t cancerous, but their composition explains why they feel hard, grow slowly, and can become surprisingly large.
The Two Main Cell Types
At the cellular level, a fibroid contains two key players: mutated smooth muscle cells and supporting cells called fibroblasts. The smooth muscle cells are the ones that started the problem. A single cell in the wall of the uterus picks up a genetic mutation and begins dividing in a disorganized way, eventually forming a distinct mass. These cells look similar to normal uterine muscle under a microscope, but they’re arranged in chaotic, swirling bundles rather than the orderly layers of healthy tissue. Pathologists describe the pattern as spindle-shaped cells woven into “intersecting fascicles,” which essentially means interlocking whorls, almost like a fingerprint.
The second cell type, fibroblasts, can make up a surprisingly large portion of the tumor. Up to 40% of a fibroid may consist of fibroblast populations that carry no mutations at all. These cells aren’t the ones driving the growth. Instead, they appear to be recruited by the mutated muscle cells, and their main job is producing the collagen and connective tissue that gives fibroids their characteristic firmness.
The Collagen That Makes Them Hard
If you’ve ever seen a fibroid during surgery or in a medical image, you know they’re dense and solid. That’s largely because of extracellular matrix, the structural material packed between and around the cells. The Mayo Clinic compares it to mortar between bricks. Fibroids contain significantly more of this material than normal uterine tissue, and that’s what makes them fibrous (and gives them their name).
The dominant protein in this matrix is collagen, particularly type I collagen, which is the same tough protein found in tendons and bone. Fibroids contain higher concentrations of type I, type III, and type V collagen compared to the surrounding normal uterine wall. This collagen overload is a defining feature of fibroids and is part of what makes them so physically stiff. Over time, a small cluster of dividing cells transforms into what the Mayo Clinic describes as “a firm, rubbery mass distinct from nearby tissue.”
Why Stiffness Fuels More Growth
Here’s where the composition of a fibroid creates a self-reinforcing cycle. Research from Fertility and Sterility has shown that fibroid cells are sensitive to the stiffness of their surroundings. When fibroid cells were grown on stiff surfaces in the lab, they produced nearly eight times more fibronectin (a key structural protein) than cells on softer surfaces. They also showed roughly double the levels of proteins that drive cell division.
In practical terms, this means the stiffer a fibroid gets, the more its cells are stimulated to produce additional collagen and connective tissue, which makes it stiffer still, which stimulates more growth. This mechanical feedback loop helps explain why fibroids tend to grow steadily over years and why larger fibroids often grow faster than small ones.
The Genetic Spark Behind It All
The muscle cells in a fibroid aren’t just randomly abnormal. Most carry a specific, identifiable genetic mutation. The single most common one affects a gene called MED12, found in roughly 56% of fibroids worldwide, though individual studies have reported rates anywhere from 31% to 80%. This mutation occurs in a tiny, specific spot on the gene (codon 44 of exon 2), and it’s not inherited from your parents. It’s a somatic mutation, meaning it happens spontaneously in one uterine muscle cell during your lifetime.
Each fibroid is its own independent growth, arising from its own single mutated cell. That’s why a person can have multiple fibroids of different sizes, in different locations, each with a different mutation driving it.
How Fibroids Differ From Normal Uterine Tissue
The wall of the uterus (the myometrium) is made of smooth muscle too, so fibroids and the tissue they grow in share a basic building block. But the differences are significant. Normal uterine muscle is organized in smooth, coordinated layers designed to contract during menstruation and childbirth. Fibroid tissue is disorganized, with thick bundles of muscle cells growing in random directions, surrounded by far more collagen than you’d find in healthy tissue.
The blood supply also differs. Normal uterine muscle has a denser network of blood vessels than fibroids do. Research published in Human Reproduction found that the surrounding myometrium consistently had greater blood vessel density than fibroids of any size. Fibroids don’t build their own vascular system. Instead, they piggyback on the existing uterine blood supply, with vessels running along the direction of the muscle bundles. Small fibroids tend to have especially narrow blood vessels, which is one reason large fibroids sometimes outgrow their blood supply and develop areas of degeneration in their centers.
The Pseudocapsule: A Natural Border
Fibroids don’t blend into the uterine wall. They’re surrounded by a thin layer called a pseudocapsule, which acts as a boundary between the fibroid and normal tissue. Under an electron microscope, this layer looks like compressed normal uterine muscle, not fibroid tissue. It contains its own network of blood vessels and nerve fibers, functioning almost like a neurovascular shell around the tumor.
This distinction matters for treatment. Because the pseudocapsule is structurally part of the healthy uterine wall rather than part of the fibroid itself, surgeons who remove fibroids (myomectomy) aim to shell out the fibroid while preserving this layer. Keeping the pseudocapsule intact helps maintain the structural integrity of the uterus, which is particularly important for people who want to become pregnant afterward.
How Common Fibroids Are
Fibroids are extremely common. Global estimates from 2021 put the number of people living with fibroids at nearly 120 million, up from about 66 million in 1990. That year alone, roughly 10 million new cases were diagnosed worldwide. The highest prevalence rates are found in Eastern Europe, where nearly 7,000 per 100,000 women are affected. The lowest rates are in Australasia, at about 980 per 100,000. These numbers are expected to continue rising modestly through at least 2036, driven largely by improved detection and aging populations.