**2. Pathogenesis**

The etiology and pathogenesis of endometriosis are complex and still incompletely understood. So many theories have been developed:


Transplantation theory actually is divided from the first theory (implantation theory). During vaginal delivery, viable endometrial cells become implanted in the perineum, including the site of episiotomy and result in endometriotic lesions. Perineal lesion often occurs during vaginal delivery, but the incidence of PEM is rare. The reasons for rare incidence may include: (1) Bacteria existing in the perineal wound which can cause infection or even necrosis of the local tissues. The infection and necrosis is not appropriate for transplanted endometrial cells to live. (2) After delivery, the level of estrogen decreases, which also makes the growth of transplanted endometrial cells difficult.

We reported one case of PEM with no history of surgical manipulation or trauma of her perineal area. Perineal endometriosis without history of delivery can not be explained by transplantation theory. We tried lymphatic dissemination theory on this patient (Zhu et al., 2003). As there are rich lymphatic communications between uterus, cervix, vaginal and perineum, endometrial tissues can be transported by lymphatic routes and result in perineal endometriosis.

Nicola Cinardi et al., reported a special case of perineal scar endometriosis ten years after Miles' procedure for rectal cancer. The patient was a 35-year-old-female who was treated 10 years earlier at the same institution for a low rectal cancer. She presented with two discrete subcutaneous bulges within her perineal wound. Since the patient was asymptomatic and the complete work up for recurrent disease showed no evidence of malignancy, first line therapy was conservative. After two pregnancies and a caesarean section, the patient presented at our observation with enlarged and tender perineal nodules. The patient was treated with a wide excision of the perineal scar en-bloc with the nodules. Final pathology report was consistent with perineal scar endometriosis. In the report, the author suggests that direct implantation of endometrial tissue cannot explain all the cases. There are a variety of cases of primary cutaneous endometriosis without previous abdominal surgery at different sites such as umbilicus, vulva, perineum, groin, and extremities (Healy et al., 1995; Ideyi et al., 2003). From an etiologic perspective, the present case can be explained with postoperative menstrual implantation within the open perineal wound resulting from the procedure. Another mechanism of transplantation would see silent foci of unknown, asymptomatic pelvic endometriosis that could have been present at the time of surgery and have been disseminated within the wound edges. These foci developed into overt disease several years after surgery (Nicola et al., 2011).
