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Pain is one of the main clinical symptoms of endometriosis, but its underlying mechanism is still not clear. Recent studies have shown that the secretory mediators of mast cells activated by estrogen are involved in the pathogenesis of endometriosis-related pain, but how estrogen-induced mast cell mediators are involved in endometriosis-related pain remains unclear. Here, mast cells were found to be increased in the ovarian endometriotic lesions of patients. They were also closely located closely to the nerve fibers in the ovarian endometriotic lesions from of patients with pain symptoms. Moreover, fibroblast growth factor 2 (FGF2)-positive mast cells were upregulated in endometriotic lesions. The concentration of FGF2 in ascites and the protein level of fibroblast growth factor receptor 1 (FGFR1) were higher in patients with endometriosis than in those without endometriosis, and they were correlated with pain symptoms. In vitro , estrogen could promote the secretion of FGF2 through G-protein-coupled estrogen receptor 30 (GPR30) via the MEK/ERK pathway in rodent mast cells. Estrogen-stimulated mast cells enhanced the concentration of FGF2 in endometriotic lesions and aggravated endometriosis-related pain in vivo . Targeted inhibition of the FGF2 receptor significantly restrained the neurite outgrowth and calcium influx in dorsal root ganglion (DRG) cells. Administration of FGFR1 inhibitor remarkably elevated the mechanical pain threshold (MPT) and prolonged the heat source latency (HSL) in a rat model of endometriosis. These results suggested that the up-regulated production of FGF2 by mast cells through non-classic estrogen receptor GPR30 plays a vital role in the pathogenesis of endometriosis-related pain., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Xu, Wang, Guo, Chen, Ding, Zou, Zhu, Li and Zhang.)

Background: Many factors can affect the recurrence of endometriosis after surgery, however, whether endometriotic cyst fluid contributes to endometriosis recurrence after surgical excision of ovarian endometriomas remains unclear. The objective of this study was to determine the presence of endometrial cells in ovarian endometriosis cyst fluid and the potential differences between these cells and those in the cyst wall., Methods: Samples of cyst fluid (n = 39) and drainage fluid (n = 14) were collected from patients with ovarian endometriomas undergoing laparoscopic surgery. Drainage fluid from 14 patients without endometriosis was used as a control. The presence of endometrial cells in cyst fluid and drainage fluid was determined by cell culture in vitro and immunostaining. In addition, cyst fluid endometrial fragments and viscosity were analysed by transcriptome sequencing analysis and apparent diffusion coefficients, respectively. An animal model was used to confirm the ability of endometrial cells in cyst fluid to form new lesions., Results: We found endometrium-like tissues in 71.8% (28/39) of cyst fluid and 71.4% (10/14) of drainage fluid samples by histopathological examination, and the presence of endometrioid tissue in cyst fluid was related to the viscosity of the cyst fluid. The living endometrial cells in cyst fluid and drainage fluid were confirmed by cell culture in vitro and immunostaining. Moreover, the adhesion ability of endometrial fragments in cyst fluid was significantly higher than that of ectopic tissues in the cyst wall (P < 0.05). In addition, living endometrial cells in the cyst fluid were able to adhere and alive in the animal model., Conclusions: The existence of living endometrial cells with high adhesion ability in ovarian endometriotic cyst fluid may contribute to the recurrence of endometriosis after surgical excision of endometriomas due to cyst fluid outflow during the surgical procedure., (© 2022. The Author(s).)

Abstract: Triptorelin is one of the most commonly used gonadotropin-releasing hormone agonists and has been used in the treatment of deep infiltrating endometriosis (DIE). This study aimed to evaluate the efficacy and safety of up to 24 weeks of triptorelin treatment after conservative surgery for DIE.This prospective, non-interventional study was performed in 18 tertiary hospitals in China. Premenopausal women aged ≥18 years treated with triptorelin 3.75 mg once every 28 days for up to 24 weeks after conservative surgery for DIE were included. Endometriosis symptoms were assessed, using a visual analogue scale (0-10 cm) or numerical range (0-10), at baseline (pre-surgery) and routine visits 3, 6, 9, 12, 18, and 24 months after surgery. Changes in symptom intensity over time were primary outcome measures.A total of 384 women (mean [standard deviation] age, 33.4 [6.2] years) were analyzed. Scores for all symptoms (pelvic pain, dysmenorrhea, ovulation pain, dyspareunia, menorrhagia, metrorrhagia, and gastrointestinal and urinary symptoms) assessed decreased from baseline over 24 months. Cumulative improvement rates in pelvic pain, dysmenorrhoa, ovulation pain, and dyspareunia were 74.4%, 83.6%, 55.1%, and 66.9%, respectively. The 24-month cumulative recurrence rate (≥1 symptom) was 22.2%. The risk of symptom recurrence was higher in patients with ≥2 versus 1 lesion (odds ratio [OR] 2.539; 95% CI: 1.458-4.423; P = .001) and patients with moderate (OR 5.733; 95% CI: 1.623-20.248; P = .007) or severe (OR 8.259; 95% CI: 2.449-27.851; P = .001) pain versus none/mild pain. Triptorelin was well tolerated without serious adverse events.Triptorelin after conservative surgery for DIE improved symptoms over 24 months of follow up. The recurrence rate of symptoms was low and triptorelin was generally well tolerated.Trial registration number: ClinicalTrials.gov, NCT01942369., Competing Interests: The authors have no conflicts of interests to disclose., (Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.)