An Update on the Various Theories of the Origin of Uterine Adenomyosis - A Systematic Review

Adenomyosis is a frequently diagnosed estrogen based gynaecological disorder, whose pathology as well as etiology is not clear. For the origination of Adenomyotic lesions as well as modes implicated in the evolution as well as propagation of the disease, till now two basic theories had been posited like implication of tissue injury as well as repair mechanisms and promote that adenomyosis occurs via invagination of endometrium basalis in the myometrium. Another theory which says that Adenomyotic lesions occurs secondary to metaplasia of displaced embryonic pluripotent mullerian remnants or differentiation of adult stem cells. But as far as Guo’s theory, both theories have apparent limitations, i.e., difficulty in falsification, explaining existing data, and making useful predictions. Based on the current understanding of wound healing, a new hypothesis, called endometrial-myometrial interface disruption (EMID), is proposed to account for adenomyosis resulting from iatrogenic trauma to EMI. The EMID hypothesis not only highlights the more salient feature, i.e., hypoxia, at the wounding site, but also incorporates epithelial mesenchymal transition, recruitment of bone-marrow-derived stem cells, and enhanced survival and dissemination of endometrial cells dispersed and displaced due to iatrogenic procedures. More importantly, the EMID hypothesis predicts that the risk of adenomyosis can be reduced if certain perioperative interventions are performed. Consequently, from a pathogenic standpoint, adenomyosis is not simply endometriosis of the uterus, and, as such, may call for interventional procedures that are somewhat different from those for endometriosis to achieve the best results.

Keywords: TIAR; Adenomyosis; mullerian remnants; adult stem cells; EMID; EMI trauma; collective cell migration.