Design: Preclinical
Setting: Translational, pre-clinical mouse model
Patients or Participants: Intact 8 ± 8-week old female immunocompetent mice, with B6(Cg)-Tyrc-2JTg(UBC-mCherry)1Phbs/J (stock #017614) used as donor mice and B6(Cg)-Tyrc-2J/J (stock # 000058) used as recipient mice.
Interventions: Five methods of endometriosis induction were used: (1) laparoscopic placement of decidualized endometrial implants, (2) placement of decidualized endometrial implants via laparotomy, (3) laparoscopic tissue slurry injection, (4) tissue slurry injection via laparotomy, and (5) discrete implantation into menstruating mice via laparoscopy (N=10/paradigm).
Measurements and Main Results: After induction of endometriosis, all mice demonstrated normal estrus cyclicity. Endometriosis occurred in 100% of mice in group 1, 80% of group 2, 20% of group 3, 10% of group 4, and 100% of group 5. There was a statistically significant difference between group 1 and 2 of 1.6 (p = .009, 95% CI (.39, 2.80)), indicating that laparoscopic placement of endometrial implants was superior to laparotomy in induction of endometriosis. The methods used in group 1 and group 5 were equally effective, with a difference of 0.10 in the estimated average number of lesions (p =.89, 95% CI (-1.33, 1.53)).
Conclusion: nduction of endometriosis was most successful via laparoscopic placement of endometrial implants using menstruating donor and recipient mice. Normal estrus cyclicity was achieved afterwards, and lesions were identified >30 days post-induction. This indicates a new mouse model that can be used in preclinical endometriosis research.
Dykstal, KO*1, Coté, J1, Howe, C2, Gelineau-van Waes, J3. 1Obstetrics & Gynecology, Creighton University, Omaha, NE; 2Creighton University, Omaha, NE; 3Pharmacology & Neuroscience, Creighton University, Omaha, NE