Endometriosis doesn’t grow at a single predictable rate. Unlike a tumor that doubles in size on a measurable schedule, endometriosis behaves differently from person to person, and even within the same person, lesions can grow, stay the same, or shrink on their own. A study of 135 premenopausal women who went without treatment found that over the follow-up period, half saw no change in their disease at all, about 37% experienced growth or new lesions, and 13% actually saw their disease partially regress.
Why There’s No Standard Growth Rate
Researchers have not established a “millimeters per year” figure for endometriosis because the disease simply doesn’t work that way. Some women are diagnosed with small, superficial spots that never progress. Others develop deep, aggressive nodules that infiltrate surrounding organs over a period of years. The growth depends on a complex interplay between your hormonal environment, your immune system’s response, and the type of lesion involved. This unpredictability is one of the reasons endometriosis is so difficult to manage and why two people diagnosed at the same stage can have very different experiences over the next decade.
What Drives Lesion Growth
Estrogen is the primary fuel for endometriosis. The most potent form, estradiol, binds to receptors on endometrial tissue and drives cell proliferation. What makes endometriosis particularly self-sustaining is that the lesions themselves can produce their own estrogen locally, independent of your ovaries. They ramp up the enzymes needed for estrogen production while dialing down the enzymes that would normally break estrogen down. This creates a feedback loop where lesions essentially feed their own growth.
At the same time, endometriotic tissue develops resistance to progesterone, the hormone that normally counterbalances estrogen and keeps endometrial tissue in check. The receptors that progesterone needs to bind to become suppressed through chemical changes to the DNA. The result is that estrogen’s growth signals go largely unopposed.
Inflammation plays an equally important role. Ectopic endometrial cells trigger a localized immune response, flooding the surrounding area with inflammatory molecules. Immune cells called macrophages produce excessive amounts of signaling chemicals that promote cell survival and adhesion. Meanwhile, natural killer cells, which would normally clear out misplaced tissue, show reduced activity in women with endometriosis. This allows the ectopic cells to evade immune clearance and continue establishing themselves. The inflammation also generates oxidative stress, which further amplifies the cycle of tissue damage and regrowth.
Superficial vs. Deep Lesions
The type of endometriosis matters enormously when thinking about growth behavior. Superficial peritoneal lesions sit on the surface of the pelvic lining and represent the most common form. These are the lesions most likely to remain stable or even regress, and they tend to be more responsive to hormonal fluctuations.
Deep infiltrating endometriosis is a different animal. These nodules penetrate more than 5 millimeters below the peritoneal surface and are composed mostly of hard, fibrous scar tissue. Only about 15 to 20% of the volume of a deep nodule is actually hormone-dependent endometrial tissue. The rest is dense fibrosis. Because of this composition, deep lesions behave more aggressively, infiltrating into surrounding organs like the bowels, bladder, or ureters. They also tend to persist even after menopause, since their fibrous bulk doesn’t depend on hormonal stimulation. Stopping periods through medication or menopause can stabilize these lesions, but it rarely makes them disappear.
The overall distribution follows a pyramid pattern: superficial lesions are by far the most common, affecting the vast majority of women with the disease, while severe deep lesions represent a smaller subset at the top.
How Hormonal Treatment Affects Growth
Hormonal therapies aim to suppress estrogen or create a progesterone-dominant environment, which should theoretically slow or stop lesion growth. In practice, the results are mixed. Several studies have found that progestin-based treatments don’t produce significant or predictable reductions in lesion volume, and some show no change in how actively the cells are dividing. One study found that a common progestin used for endometriosis produced no difference in tissue breakdown or gland shrinkage in ovarian endometriomas compared to no treatment at all.
Therapies that suppress estrogen more aggressively by shutting down the hormonal cycle at the brain level have shown more consistent effects on reducing blood vessel growth within lesions, which is one mechanism of slowing progression. But even here, deep endometriosis appears more resistant to regression with medical treatment than superficial disease. Some studies have reported substantial volume reduction with certain hormone combinations, but others have failed to replicate those findings. The takeaway is that hormonal treatment reliably manages symptoms like pain for many women, but its ability to physically shrink existing lesions is less certain.
How Quickly Endometriosis Returns After Surgery
Surgical removal of lesions is one of the most effective treatments, but endometriosis has a well-documented tendency to come back. A meta-analysis pooling data from 23 studies tracked recurrence of ovarian endometriomas after surgical excision. At 3 months post-surgery, the recurrence rate was about 4%. By 6 months it reached 14%, by 12 months 17%, and by 24 months it climbed to 27%. That means roughly one in four women who have endometriomas surgically removed will see them return within two years.
These numbers give an indirect window into growth speed. For a lesion to be detectable again on imaging within 3 to 6 months, the regrowth process begins almost immediately in some cases. For others, years may pass without recurrence. Whether post-surgical hormonal therapy slows this timeline remains an active question, though many clinicians prescribe it for that reason.
What Influences Your Individual Trajectory
Several factors shape whether your endometriosis is likely to progress, remain stable, or improve. Ongoing estrogen exposure is the biggest driver. Women who go through early puberty, have shorter menstrual cycles, or have never been pregnant accumulate more lifetime estrogen exposure, which provides more fuel for lesion growth. Conversely, pregnancy and breastfeeding temporarily suppress the hormonal environment that feeds endometriosis.
The stage at diagnosis also matters, but not always in the way you might expect. Mild-looking disease doesn’t always stay mild, and advanced disease doesn’t always keep advancing. The study of expectant management found that disease stability was actually the most common outcome, even in women with deep pelvic endometriosis who chose not to treat. This suggests that for a meaningful proportion of women, the disease reaches a plateau and stays there for extended periods.
Inflammation levels, genetic predisposition, and the degree of progesterone resistance in your tissue all contribute to how aggressively the disease behaves. None of these are things you can measure at home, which is part of why monitoring through imaging and symptom tracking over time remains the most practical way to understand your own disease trajectory.