Figure 2.

The interplay of local and systemic factors in abdominal inflammatory processes in the pathogenesis of endometriosis. The local inflammatory processes, metabolome, and estrobolome in the intestine can have systemic effects that contribute to the development of endometriosis. The pathophysiological concept underlying here is intricate and complex. Retrograde menstruation causes an increase in the number of endometrial cells and cellular debris in the pelvis, leading to a proinflammatory response that releases cytokines and growth factors. The body’s natural immune response is insufficient to break down these cells, resulting in the development of ectopic lesions. At the same time, the release of cytokines and growth factors can also disrupt gut function, causing dysbiosis. Dysbiosis may also affect intestinal epithelial cell function, stem cell activity, and the estrobolome, resulting in increased permeability that causes immunologic imbalance and low-grade systemic inflammation. This cycle can continue, with endometriosis lesions and dysbiosis exacerbating each other.