GS02: General Session II
Sunday, November 15, 2026
9:30 am - 10:45 am

Faculty: Linda Griffith, Cara R. King, Ted TM Lee, Hugh S. Taylor, Kelly Wright, Steven Young

9:30 AM  FAAGL - Signature Awards
9:45 AM  MedTalk II - #225 - Why Excision Surgery Hurts Women - Kelly Wright
10:00 AM Debate: #355 - What Drives Endometriosis? - Linda Griffith, Ted TM Lee, Cara R. King, Steven Young, Hugh S. Taylor
 

MedTalk II - #225 - Why Excision Surgery Hurts Women
Presenter: Kelly Wright

Description: I am an excision surgeon, and excision surgery hurts women. This tongue-in-cheek MEDTalk explores the concept that hinging on a particular treatment may lead to lack of scientific progress in understanding and treating a disease. The focus on excision surgery for the past three decades has been important in teaching patients how to advocate for themselves and find a capable physician who validates their disease and suffering. However, it has hindered scientific progress through focusing on endometriosis as a single end-organ disease rather than allowing a mindset shift into endometriosis as a systemic inflammatory disease. We have seen progress in other comparative fields such as inflammatory bowel disease, inflammatory skin diseases, and even ovarian cancer. Comparing ourselves to physicians who treat these diseases, we could not imagine a colorectal surgeon who cuts out small intestine every time there's a Crohn's flare. Similarly, the focus on excision surgery has led to overuse and potential abuse of this technique, seen in the proliferation of cash pay surgeons and marketing on social media. This MEDTalk challenges the paradigm of our current treatment standards and offers hope for the future with an introduction to the current targets and treatments being studied right now - monoclonal antibodies, targeted receptor inhibitors, and even simple medications already available on the market. Let's reframe the discussion to think about what a career treating endometriosis as a chronic systemic inflammatory disease would look like, as perhaps we'll find great satisfaction in treating patients well over treating them with repeated surgeries.

Learning Objectives: At the end of this course, the participant will be able to: 1) Describe the concept of hinging in medicine and how it may hinder scientific progress; 2) Describe current cutting-edge research in the pathophysiology of endometriosis; and 3) Evaluate the potential role of different medications in the treatment of endometriosis.

Debate: 355 - What Drives Endometriosis?
Chair: Ted TM Lee
Moderator: Cara R. King
Faculty: Linda Griffith, Steven Young, Hugh S. Taylor

Description: Endometriosis remains one of the most complex and incompletely understood diseases in gynecology. Surgeons see and excise lesions, but the biologic forces that initiate, sustain, and amplify the disease remain deeply intertwined. Endometriosis may be driven by altered endometrial function, impaired decidualization, metabolic dysfunction, inflammation, immune dysregulation, neuroangiogenesis, estrogen dependence, progesterone resistance, and pain-system remodeling.

This 45-minute Main Stage Debate will bring together three internationally recognized scientific leaders to address one central question:
What Truly Drives Endometriosis?
Rather than presenting three independent lectures, this session will be structured as a fast-paced debate among three complementary mechanistic models. Each speaker will make the strongest case for one biologic framework, followed by moderated crossfire, audience response polling, and clinical translation for the practicing endometriosis surgeon.

The goal is not to declare a single winning mechanism. The goal is to help the AAGL audience understand how disease biology should reshape surgical thinking, patient counseling, recurrence prevention, medical therapy, multidisciplinary care, and future research priorities.

Learning Objectives: After attending this session, the participant will be able to: 1) Compare leading mechanistic models of endometriosis pathogenesis, including metabolic/decidualization dysfunction, inflammatory and immune pathways, neuroangiogenesis, and endocrine/progesterone resistance mechanisms; 2) Explain how these mechanisms may contribute to pain, infertility, lesion persistence, recurrence, treatment response, and the mismatch between visual disease burden and patient symptoms; 3) Identify how mechanistic insights should influence surgical counseling, operative expectations, postoperative suppression, recurrence prevention, and multidisciplinary care; and 4) Recognize the limitations of a purely lesion-centered model of endometriosis and integrate biologic, inflammatory, hormonal, metabolic, neurologic, and patient-centered perspectives into comprehensive care.

Course Outline
10:00 AM Welcome, Introduction and Course Overview
T. Lee

10:05 AM Baseline Audience Poll
C. King

10:08 AM Endometriosis, Decidualization and Metabolism: An Emerging Model and Implications for Our Patients
S. Young

10:15 AM Endocrine Mechanisms: Estrogen/Progesterone Signaling and Progesterone Resistance
H. Taylor

10:22 AM Inflammation, Immunology, Pathogenesis, and Neuroangiogenesis
L. Griffith

10:29 AM Moderated Debate
T. Lee

10:39 AM Audience Re-Poll and Clinical Translation
C. King

10:42 AM Final Synthesis
T. Lee

10:45 AM Adjourn