How Does Surgery Cause Scar Tissue in Asherman Syndrome?

When your uterus heals by forming scar tissue (adhesions) instead of a healthy lining, it is usually because the deep, foundational layer of your endometrium has been injured. Normally, the uterus sheds and regenerates its lining every month. However, when deep surgical trauma—such as during a D&C (dilation and curettage)—damages this root layer, the body’s normal regeneration process can be disrupted ^[1]. Instead of fully rebuilding the soft, blood-rich tissue, the immune system triggers a repair response that can patch the damage with fibrotic scar tissue ^[1]. This can lead to the adhesions characteristic of Asherman syndrome, where opposing walls of the uterus may stick together ^[2]. Not every injury causes Asherman syndrome, and the extent of adhesions and functional loss varies widely from person to person ^[3].

The Role of the Basal Layer

The lining of your uterus (the endometrium) has two main layers: the functional layer that grows and sheds during your period, and the basal layer underneath it. The basal layer acts as the foundational root system. It contains the essential stem cells ^[4] and blood vessels ^[5] required to regrow the functional layer every month.

When a surgical procedure goes deep enough to damage this basal layer, it can impair the uterus’s ability to rebuild the soft, spongy lining it needs for menstruation and pregnancy ^[1][6]. If the normal lining cannot fully regenerate, the raw surfaces inside the uterine cavity may heal together, forming bands of scar tissue ^[1]. This structural change helps explain common symptoms of Asherman syndrome, such as significantly lighter or absent periods and difficulties supporting a pregnancy ^[1].

The Inflammatory Repair Response

When the basal layer is damaged, the immune system rushes in to protect the area, creating an inflammatory response ^[7]. In a healthy, superficial cut, inflammation settles down once the wound is closed. But in deep uterine trauma, research suggests this inflammation can sometimes become persistent ^[7].

During this process, specialized repair cells called macrophages release signals that prioritize rapid wound closure over careful tissue regeneration ^[8][9]. As a result, the body produces collagen-heavy scar tissue to seal the injury ^[2].

Cellular Changes: A Current Research Model

Researchers are still studying exactly how normal uterine cells turn into scar tissue. One leading theory involves complex biological mechanisms called epithelial-mesenchymal transition (EMT) and endothelial-to-mesenchymal transition (EndMT) ^[10].

In laboratory and animal studies, intense inflammatory signals can cause the normal cells lining the uterus and blood vessels to change their behavior ^[11][10]. Through EMT and EndMT, these cells are thought to transition into myofibroblasts—heavy-duty repair cells ^[10][12]. Instead of building delicate glands, myofibroblasts produce structural proteins like collagen, creating thick, stiff scar tissue designed to seal the wound ^[2][13]. While this is a proposed explanation based on ongoing research rather than settled human biology, it helps scientists understand why the uterus sometimes struggles to regenerate healthy tissue ^[14].

The Role of Infection

Surgical trauma alone can be sufficient to cause Asherman syndrome, but a concurrent infection can increase the risk of developing severe scar tissue ^[15]. An infection can amplify the inflammatory response, causing it to last longer and potentially recruit more scar-producing cells ^[15][16]. However, an infection is not required for adhesions to form, and many patients develop Asherman syndrome without any history of infection ^[16].

(Note: If you recently had a uterine procedure and are experiencing a fever, worsening pelvic pain, foul-smelling discharge, or heavy bleeding, contact your healthcare provider promptly, as these can be signs of an active infection.)