Implantation theory |
Retrograde menstruation allowing implantation of endometrial glands in pelvic peritoneum |
Coelomic metaplasia |
Transformation of peritoneal mesothelium or other cell types into endometrial tissue |
Hormonal induction |
Oestrogen-driven proliferation of endometrial lesions or metaplasia by hormonal stimulation |
Inflammation and oxidative stress |
Recruitment of immune cells and their production of cytokines which promotes endometrial growth |
Immune dysfunction or deficiency |
Prevention of eliminating menstrual debris and promotion of implantation and growth of endometrial lesions |
Apoptosis suppression |
Survival of endometrial cells by suppression of apoptotic pathways |
Genetic |
Alteration of cell types to endometriosis lesions |
Stem cells |
Transformation of haematopoietic, bone marrow or mesenchymal stem cells to endometriosis |
Lymphatic, haematogenous metastasis |
Spread of endometrial cells by lymphatic or haematogenous vessels |
Embryonic cell remnants |
Mullerian duct rests, Wolffian duct rests |
Multiple factors |
Combination of in situ development and endometrial transplantation and implantation |
New theory of endometriosis aetiology from primordial germ cells |
The eutopic and ectopic endometrium originating from primordial germ cells |