The hormonal influences remain the same; however, scar tissue inside the uterus will generally prevent the full scope of uterine changes as described above. One theory suggests that the lack of endometrial growth is due to a complex biochemical feedback loop in which the uterus restricts the proliferation of endometrium. Others include significant damage to the basal layer of the endometrium (critical for the growth of the functional layer) or reduced blood flow to the endometrium either from fibrosis of the muscular layer of the uterus or because the scars which seal the uterus closed (partially or completely) reduce blood flow to the endometrium.

Hysteroscopy with lysis of the scar tissue can in many cases help restore normal uterine function in terms of endometrial response to hormonal stimulation. Unfortunately sometimes even after the scar tissue is resected the prior damage to the endometrium will lead to a chronically thin endometrium (i.e., it will undergo the correct proliferative and secretory changes, however full endometrial growth potential will not be recognized). This may be due to a complex chemical feedback mechanism not yet fully understood by medical science.

Thin endometrium is counteracted by a short course of sequential exogenous estrogen to encourage endometrial re-epithilialization (regrowth) and progesterone. In many cases once the uterus is mostly free of scar tissue this course of action can help restore more normal uterine function, and decrease the chance of rescarring.

In a few cases however the endometrial basal layer has been so badly denuded (scarred) that estrogen therapy will not help. This result is more common after fibroid removal surgery.