What Is Scar Tissue in the Uterus? Causes and Effects

Scar tissue in the uterus forms when normal, hormonally responsive uterine tissue is replaced by tough, fibrous tissue after an injury or surgery. The condition most commonly associated with this process is Asherman’s syndrome, where bands of scar tissue called intrauterine adhesions develop inside the uterine cavity after damage to the deep layer of the uterine lining. But uterine scarring also takes other forms, including the defects left in the muscular wall after a cesarean delivery. The causes, the symptoms, and the stakes for future pregnancies vary depending on where and how badly the scarring develops.

How Uterine Scar Tissue Forms

The uterus has a remarkable ability to repair itself. Every menstrual cycle, the inner lining sheds and regrows from a deeper reserve layer called the basal layer. When that basal layer is damaged, though, the body’s repair system defaults to the same process it uses anywhere else: it fills the gap with fibrous connective tissue. In the uterine cavity, this fibrous tissue can form adhesions, which are bands of scar tissue that stick the walls of the uterus together or block parts of the cavity. The result is that normal, functional endometrium gets replaced by tissue that does not respond to hormones and has a poor blood supply.¹

A systematic review described the scarred endometrium as an “avascular and unresponsive” tissue with decreased thickness and receptivity, where damage to resident stem cells prevents the lining from regenerating properly.² That lack of blood supply and hormonal responsiveness is what drives most of the symptoms and fertility problems people experience.

The Most Common Causes

The overwhelming majority of intrauterine adhesion cases follow some kind of instrumentation of the uterus, especially when the uterus is pregnant or recently postpartum. The lining is particularly vulnerable during and just after pregnancy because the tissue is softer and the basal layer is more exposed. Surgery on a pregnant or recently pregnant uterus, such as a dilation and curettage (D&C) performed after a miscarriage or to remove retained placenta, is the single most common trigger. The classic triad of Asherman’s syndrome symptoms includes pain, menstrual abnormalities, and infertility.

But D&C is not the only surgical culprit. Myomectomy, the surgical removal of fibroids, also carries a meaningful risk of adhesion formation inside the uterine cavity. A study pooling data from multiple surgical approaches found the overall incidence of intrauterine adhesions after myomectomy was about 17%, though rates varied sharply by technique: roughly 36% after open abdominal surgery, about 10% after standard laparoscopic surgery, and around 12% after robotic surgery. The strongest predictor of adhesion formation was whether the surgeon entered the endometrial cavity during the procedure, which increased the odds nearly fivefold.³ The degree of tissue trauma during surgery, as well as the surgeon’s experience, also play a role in whether adhesions develop after laparoscopic myomectomy.⁴

Infection is another, less common pathway. Severe uterine infections, particularly those occurring after delivery (postpartum endometritis) or in the setting of tuberculosis in regions where it is endemic, can inflame the uterine lining enough to trigger the same scarring cascade. The infection does not need to be dramatic; chronic low-grade inflammation can gradually damage the basal layer and lead to adhesion formation over time.

Intrauterine Adhesions Versus Cesarean Scar Defects

When people hear “scar tissue in the uterus,” they tend to think of one thing. In practice, there are two fairly distinct patterns worth knowing about, because they affect different parts of the uterus and produce different problems.

Intrauterine adhesions (the Asherman’s pattern) form inside the uterine cavity itself, where the endometrial lining lives. These adhesions can range from thin, filmy strands to thick, dense bands that obliterate large portions of the cavity. Multiple classification systems exist to grade their severity based on how much of the cavity is involved, how dense the adhesions are, and how disrupted the menstrual pattern has become.⁵

Cesarean scar defects, often called an isthmocele or a “niche,” are a different beast. These form in the muscular wall (myometrium) of the lower uterus at the site where the incision was made during a cesarean delivery. Instead of healing as a uniform scar, the incision sometimes leaves a pouch-like indentation where the muscle did not fully close.⁶ Blood and fluid can pool in that pouch, and the thinned wall at the scar site can become a concern in future pregnancies. The proposed mechanism for the abnormal bleeding is that the pouch traps menstrual blood, which then drains slowly over days, causing prolonged spotting after a period ends.⁷

Effects on Menstruation

Changes to your period are often the first sign that something has gone wrong. The specific changes depend on how much of the uterine lining has been replaced by scar tissue and where the scarring sits.

When intrauterine adhesions block or replace a large area of the endometrium, periods become lighter or stop altogether, because there is simply less functional lining to shed. In severe cases, the uterine wall can contain dramatically more fibrous tissue than normal. One older but widely cited study using full-thickness biopsies found that affected uteri contained roughly 50% to 80% fibrous tissue, compared with 13% to 20% in healthy controls.⁸ Paradoxically, if adhesions block the cervix or lower uterus while the upper cavity still functions, menstrual blood can become trapped, causing cyclical pain without any visible bleeding.

Cesarean scar defects tend to cause the opposite pattern: instead of lighter periods, they often lead to prolonged spotting that lingers for days after the main period ends. Some people also develop intermenstrual spotting or brownish discharge between periods. The bleeding is not heavier per se; it is more drawn out, because blood collects in the niche and seeps out slowly.⁹

How Scar Tissue Affects Fertility

The fertility impact of uterine scar tissue operates through several pathways at once. Intrauterine adhesions can physically block the fallopian tubes where they open into the uterus, preventing sperm from reaching the egg. Even when the tubes are not blocked, the adhesions can disrupt the normal transport of sperm through the cervix and uterus. And perhaps most critically, the scarred endometrium is thinner, has fewer blood vessels, and does not respond to the hormonal signals that normally prepare it to accept an embryo. A systematic review described the process as endometrial fibrosis leading to “insufficient replacement of the endometrium” and an unresponsive lining that cannot support implantation.²

Cesarean scar defects can also impair fertility, though the mechanism is different. Fluid accumulating in the niche may create a hostile environment for sperm or early embryos. Some evidence also suggests that the chronic low-grade inflammation around a poorly healed scar may interfere with implantation. Both intrauterine adhesions and scar defects are associated with infertility, but their overlap with other causes of difficulty conceiving makes it hard to pin down exactly how much each contributes in any individual case.¹⁰

Risks During Pregnancy

Getting pregnant with uterine scar tissue is one challenge; staying pregnant safely is another. A scarred uterus raises the risk of several serious pregnancy complications, and the risks scale with the extent and location of the scarring.

Women with scarred uteri have higher rates of placenta previa (where the placenta covers the cervix), preterm delivery, postpartum hemorrhage, and uterine rupture compared with women whose uteri are unscarred. One study found rates of placenta previa around 6%, preterm delivery around 10%, and uterine rupture around 9% in the scarred group, all significantly higher than in controls.¹¹

Placenta accreta spectrum is one of the most feared complications. This occurs when the placenta grows too deeply into the uterine wall because the normal barrier between the placenta and the muscle has been disrupted by scarring. Research has clarified that accreta is essentially a consequence of uterine remodeling after surgery, most commonly after cesarean delivery. Large cesarean scar defects in the lower uterine segment are associated with failure of normal tissue formation in the scar area, allowing placental tissue to invade close to the outer surface of the uterus. The size of the scar defect and the remaining thickness of the muscle at the scar site determine how deeply the placenta can penetrate.¹²

Uterine rupture is rarer but carries immediate danger for both the mother and baby. About 90% of uterine ruptures occur in a scarred uterus, usually at the site of a prior cesarean or uterine surgery, with a rupture rate among women with a prior scar of roughly 0.5% to 0.7%. That rate increases with labor induction or augmentation.¹³ The risk profile is nuanced. One retrospective study found that factors associated with complete uterine rupture included abnormal fetal heart tracings, scar pain, and, counterintuitively, having had only one prior cesarean rather than two or more, possibly because surgeons and patients exercise more caution when the history includes multiple prior surgeries.¹⁴

When There Are No Symptoms at All

Not every person with uterine scar tissue knows about it. Mild intrauterine adhesions can exist without noticeably affecting periods or fertility. And cesarean scar defects are frequently discovered incidentally during imaging done for other reasons. Many women with an isthmocele have no symptoms and never require treatment.⁹ This matters because being told you have a “scar defect” on an ultrasound does not necessarily mean anything needs to be done about it. The clinical significance depends on whether the scar is causing symptoms or posing a risk to a future pregnancy.

Diagnosis

Hysteroscopy, where a small camera is inserted through the cervix to look directly inside the uterine cavity, is considered the gold standard for diagnosing intrauterine adhesions. It lets a surgeon see the adhesions, assess their severity, and often treat them in the same procedure. Other imaging methods play supporting roles: a hysterosalpingogram (an X-ray test where dye is injected into the uterus) can suggest the presence of adhesions and show how extensively the scar tissue has formed, while ultrasound, especially with saline infusion, can help identify cesarean scar defects.¹⁵ For cesarean scar niches specifically, transvaginal ultrasound is usually the first-line tool, with the defect appearing as a triangular fluid-filled pocket in the lower uterine segment at the scar site.⁷

Treatment and Preventing Recurrence

The primary treatment for intrauterine adhesions is hysteroscopic adhesiolysis: a surgeon uses a hysteroscope to cut or separate the scar bands and restore the shape of the uterine cavity. The procedure itself is conceptually straightforward, but the challenge is that adhesions tend to come back. The uterine walls, freshly traumatized by the very surgery meant to free them, can scar together again as they heal. Follow-up hysteroscopy a few months after the initial procedure is standard practice to check whether the cavity has stayed open.¹⁶

Preventing recurrence has been one of the more frustrating problems in the field. Several strategies are used, often in combination:

Intrauterine balloon: A small balloon catheter is placed inside the uterus after surgery and left for several days to physically keep the walls apart while the initial healing takes place.
Intrauterine device (IUD): A copper or hormonal IUD can serve as a spacer inside the cavity, though it covers less surface area than a balloon.
Barrier gels: Hyaluronic acid-based gels are applied to the uterine walls to coat the raw surfaces and reduce the chance of adhesion formation. A systematic review found that gel barriers had significant clinical effect on preventing adhesions, likely because they adhere to the injured surface for a prolonged time.¹⁷

A network meta-analysis comparing these strategies found that combining approaches tended to perform better than any single method alone. An IUD combined with hyaluronic acid gel appeared to produce the greatest improvement in adhesion severity scores, while hyaluronic acid gel alone was associated with the highest pregnancy rates.¹⁸ One cohort study comparing a balloon, an IUD, and hyaluronic acid gel head-to-head found no significant difference between the gel group and the control groups, a reminder that results from individual studies and pooled analyses do not always agree.¹⁹

The Estrogen Question

For years, estrogen therapy after adhesiolysis was considered standard practice. The logic made intuitive sense: estrogen stimulates endometrial growth, so giving it after surgery should help the lining regrow over the raw surfaces before adhesions can re-form. Many gynecologists still prescribe it. But a randomized trial put this assumption to the test and found that women who did not receive estrogen after surgery had essentially the same outcomes as those who did. At second-look hysteroscopy roughly two months after surgery, about 26% of women in both groups had recurring adhesions. Pregnancy rates within three years were also similar, with roughly 84% of women in the no-estrogen group becoming pregnant compared with about 90% in the usual care group, a difference that was not statistically meaningful. Live birth rates were likewise comparable.²⁰ This is one of those areas where clinical practice has not fully caught up with the evidence. If your doctor prescribes estrogen after adhesiolysis, it is worth discussing what the trial data actually showed.

Experimental Regenerative Approaches

Because severe Asherman’s syndrome can be resistant to conventional surgery, researchers have been exploring regenerative strategies aimed at helping the endometrium actually regrow rather than just cutting scar tissue away. One approach that has shown promise in animal studies is platelet-rich plasma (PRP), a concentrated solution derived from a patient’s own blood. In a mouse model of Asherman’s syndrome, PRP infused into the scarred uterine horn significantly reduced markers of fibrosis and more than doubled the number of embryo implantation sites compared with the untreated side. Most PRP-treated mice (about 83%) delivered healthy pups, while none of the untreated Asherman’s mice did.²¹ Other experimental approaches include stem cell therapies and bioengineered scaffolds designed to provide a structure for new endometrial tissue to grow on.¹ These remain in early research stages, and none have become standard treatments yet, but they represent a genuine shift in thinking from simply removing scar tissue to trying to restore the underlying tissue that was lost.

Myomectomy Scars on the Outer Wall

The discussion so far has focused on scarring inside the uterine cavity and at cesarean incision sites. But myomectomy also leaves scars in the muscular wall itself, particularly when fibroids are removed from deep within the myometrium. A study of nearly 700 patients who underwent follow-up examination after laparoscopic myomectomy found that about 9% had visible scarring on the uterine surface. The strongest factor associated with scar formation was complete penetration of the full thickness of the uterine muscle during the fibroid removal, which more than doubled the odds of a scar developing. Removal of a subserosal fibroid (one sitting on the outer surface, requiring less deep cutting) was actually protective.²² These myometrial scars matter primarily in the context of future pregnancy, where they carry a small but real risk of uterine rupture during labor, similar to a cesarean scar.

The Psychological Weight

The emotional toll of uterine scar tissue is easy to overlook in a discussion focused on anatomy and surgery, but it is real and well-documented. Asherman’s syndrome sits at an intersection of grief, uncertainty, and repeated medical procedures that can grind people down. A recent study found that psychological distress is highly prevalent among patients with Asherman’s syndrome, particularly those undergoing prolonged treatment or multiple hysteroscopies. The authors urged gynecologic surgeons to recognize the psychological burden, noting that it can affect treatment adherence, recovery, and satisfaction with care.²³ The condition often develops after a pregnancy loss, meaning patients may already be grieving when they learn the uterus has been damaged. Each follow-up hysteroscopy and each cycle spent waiting to see if the lining recovers adds another layer of emotional strain. Researchers have increasingly recognized psychological distress as a core feature of the condition, not just an afterthought.²⁴

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