Effects of hormonal treatment on the expression of collagen type I, matrix metalloproteinase-1, and tissue inhibitor of metalloproteinases-1 in endometriosis.
Matsuzaki. Sachiko S; Canis. Michel M
Key Findings
- Continuous combined oral contraceptives, progestins, and GnRH agonists all lowered collagen type I levels in deep infiltrating endometriosis (DIE) lesions.
- These same hormonal treatments did not significantly affect collagen levels in ovarian endometrioma (OV) lesions.
- TIMP‑1, a protein that blocks tissue breakdown, was naturally lower in DIE than OV and was further reduced by hormonal therapy only in DIE.
Practical Outcomes
- For people with DIE, using hormonal regimens—including GnRH agonists—may help reduce fibrotic tissue and potentially improve symptoms. The same approach does not appear to help ovarian endometriomas, so expectations should be limited to DIE. This finding is mainly relevant to endometriosis management rather than general longevity or performance goals.
Summary
Hormone therapies like combined oral contraceptives, progestins, and GnRH agonists (the same class as gonadorelin) can shrink the scar‑like tissue (fibrosis) in deep infiltrating endometriosis, but they don’t change the fibrous tissue in ovarian endometrioma.
Abstract
Endometriosis is an estrogen-dependent disease, and hormonal treatment is the most common treatment. Both deep infiltrating endometriosis (DIE) and ovarian endometrioma (OV) are characterized by dense surrounding fibrotic tissue. However, no studies have examined the effect of hormonal treatment on fibrosis in endometriotic lesions. In the present study, we evaluated the effects of hormonal treatment on collagen type I, matrix metalloproteinase-1 (MMP-1), and tissue inhibitor of metalloproteinases 1 (TIMP-1) protein expression in DIE and OV lesions. Immunohistochemical analyses in a total of 228 patients were performed on paraffin-embedded endometriosis tissue samples collected prospectively. Among them, a total of 164 patients who underwent laparoscopic surgery for DIE and/or OV received preoperative hormone treatment (continuous combined oral contraceptive [CO], progestin, or gonadotropin-releasing hormone agonist [GnRHa]) for at least three months prior to surgery. For comparison, paired endometrial and endometriotic samples were used from 40 age-matched patients with DIE and/or OV, as well as endometrial samples from a total of 24 women undergoing tubal ligation or reversal. Continuous CO, progestins, and GnRHa decreased collagen type I protein expression in DIE but had no significant effect on OV. Furthermore, TIMP-1 protein expression in DIE was significantly lower than in OV, and hormonal treatment further decreased TIMP-1 expression in DIE but not in OV. The decreased fibrosis observed in DIE may be due, in part, to decreased levels of TIMP-1 resulting from hormonal treatment. Hormonal treatment reduces fibrosis in DIE. However, it has no significant effect on OV.
Study Information
pubmed
2025
2025-10-24T00:00:00.000Z
10.1016/j.ejogrb.2025.114788
25