Endometriosis is a chronic, estrogen-dependent condition characterized by the presence of endometrial tissue outside the uterus, leading to pelvic pain and infertility. It affects 6-10% of women of reproductive age and is often under-diagnosed, with a mean latency of 6.7 years from symptom onset to diagnosis. The disease is associated with significant quality of life issues and high healthcare costs, estimated at $69.4 billion annually in the U.S. The pathogenesis of endometriosis remains unclear, with several theories proposed, including retrograde menstruation, coelomic metaplasia, and embryonic Mullerian rests. Retrograde menstruation is the most widely accepted theory, involving the migration of endometrial cells into the peritoneal cavity through the fallopian tubes. Other theories suggest that endometrial cells may originate from non-uterine tissues or stem/progenitor cells. Endometriosis is influenced by genetic factors, hormonal changes, and immune system dysfunction. Endometrial cells may survive and implant due to genetic predisposition, estrogen dependence, and progesterone resistance. These cells can evade immune clearance, attach to the peritoneal lining, and invade surrounding tissues. Inflammation plays a key role in the disease process, with increased levels of cytokines and growth factors contributing to the progression of endometriosis. Endometriotic lesions can progress through different stages, including red vesicular, black powder-burn, and fibrotic, with implications for treatment and management. The disease is associated with significant pain and infertility, and research is ongoing to develop novel diagnostic and therapeutic approaches. Understanding the molecular mechanisms of endometriosis is crucial for improving diagnosis, treatment, and prevention strategies.Endometriosis is a chronic, estrogen-dependent condition characterized by the presence of endometrial tissue outside the uterus, leading to pelvic pain and infertility. It affects 6-10% of women of reproductive age and is often under-diagnosed, with a mean latency of 6.7 years from symptom onset to diagnosis. The disease is associated with significant quality of life issues and high healthcare costs, estimated at $69.4 billion annually in the U.S. The pathogenesis of endometriosis remains unclear, with several theories proposed, including retrograde menstruation, coelomic metaplasia, and embryonic Mullerian rests. Retrograde menstruation is the most widely accepted theory, involving the migration of endometrial cells into the peritoneal cavity through the fallopian tubes. Other theories suggest that endometrial cells may originate from non-uterine tissues or stem/progenitor cells. Endometriosis is influenced by genetic factors, hormonal changes, and immune system dysfunction. Endometrial cells may survive and implant due to genetic predisposition, estrogen dependence, and progesterone resistance. These cells can evade immune clearance, attach to the peritoneal lining, and invade surrounding tissues. Inflammation plays a key role in the disease process, with increased levels of cytokines and growth factors contributing to the progression of endometriosis. Endometriotic lesions can progress through different stages, including red vesicular, black powder-burn, and fibrotic, with implications for treatment and management. The disease is associated with significant pain and infertility, and research is ongoing to develop novel diagnostic and therapeutic approaches. Understanding the molecular mechanisms of endometriosis is crucial for improving diagnosis, treatment, and prevention strategies.