Objective: To investigate the pathogenesis of endometriotic pain.
Design: Retrospective nonrandomized immunohistochemical study.
Setting: A university hospital, Department of Gynecology.
Patient(s): Twenty human endometriotic specimens were selected from different lesions including ovarian endometrioma, peritoneal lesion, and deep infiltrating lesion. Premenopausal women with histologically diagnosed endometriosis were selected (mean age 39 years; range, 25-53 years). The chief complaint was dysmenorrhea, dyschezia, and dyspareunia. A rat endometriosis model was induced in 10 SLC-Sprague-Dawley rats (8 weeks old) by surgical autotransplantation of the uterus.
Intervention(s): Immunohistochemical staining of endometriotic specimens for alpha-smooth muscle actin (ASMA), neural cell adhesion molecule (NCAM), and nerve growth factor (NGF) expression.
Main outcome measure(s): Comparison of the immunoreactive staining of ASMA, NCAM, and NGF expression in human endometriosis and a rat endometriosis model.
Result(s): Morphological analysis revealed thick interstitium in both human and rat endometriotic lesions. The major components of fibrotic interstitium are smooth muscle cells, stained by anti-ASMA antibody, and nerve cells, stained by anti-NCAM antibody. Inflammatory cells are also present (e.g., macrophages and lymphocytes) as revealed by anti-NGF antibody staining.
Conclusion(s): These results suggest that the contraction of smooth muscle cells and the hyperalgia derived from innervation in the interstitial area is related to pain in endometriosis.