Oral Virtual Presentation (Virtual only) ESA-SRB-ANZBMS 2021

Heterogeneity in the distribution of smooth muscle actin, collagen fibres and immune cells associated with superficial peritoneal endometriotic lesions (#188)

Eliza M Colgrave 1 , Janet R Keast 2 , Cameron J Nowell 3 , Peter AW Rogers 1 , Sarah J Holdsworth-Carson 1 , Jane Girling 1 4
  1. Gynaecology Research Centre, University of Melbourne Department of Obstetrics and Gynaecology, Royal Womens Hospital, Parkville, VIC, Australia
  2. Department of Anatomy and Physiology, The University of Melbourne, Melbourne, Victoria, Australia
  3. Imaging, FACS and Analysis Core, Monash Institute of Pharmaceutical Sciences, Monash University, Melbourne, Victoria, Australia
  4. Department of Anatomy, University of Otago, Dunedin, Aotearoa New Zealand

INTRODUCTION:  Endometriosis is characterised by lesions composed of “endometrial-like” tissue found in locations outside of the uterus.  Fibrosis is a key component of endometriosis, potentially contributing to disease progression, treatment responsiveness and variation in presentation.  However, fibrosis is not currently utilised in endometriosis diagnosis, unlike other pathologies including cancer.  The aim of this study was to analyse superficial peritoneal endometriotic lesions to determine if distinct lesion subtypes exist based on smooth muscle actin (SMA), collagen and leukocyte patterns, which could aid in improving disease classification.

METHODS:  This study employed tissues from 24 patients across the menstrual cycle with histologically confirmed endometriosis.  Immunofluorescence was used to demonstrate the CD10-positive stromal area of lesions (n = 271 lesions from 67 endometriotic biopsies), the SMA-positive tissue and the leukocyte population (CD45+ and CD68+) within and adjacent to lesions.  Second harmonic generation microscopy was employed to evaluate the morphology of type-1 collagen fibres within and surrounding lesions.

RESULTS:  The proportion of tissue occupied by leukocytes, SMA and collagen was low within endometriotic lesions but increased significantly in the adjacent non-lesion tissue.  We identified lesions where collagen fibres formed well aligned capsules around endometriotic lesions (defined by the CD10 border), versus lesions where collagen fibre distribution was random.  We also observed considerable inter- and intra-patient variability in the morphology of SMA and collagen within and surrounding lesions, which was dependent in-part on the biopsy location and morphology of endometriotic gland profiles.

CONCLUSIONS:  These data suggest there is considerable diversity in the presence of immune cells and morphology of SMA and collagen within and surrounding endometriotic lesions, even within individual patients and single biopsies. This heterogeneity presents a challenge to incorporating these cell and tissue types into any new endometriosis classification systems or prognostic approaches.