Endometriosis, Mechanically

What Endometriosis Is — and Why It’s Bigger Than Reproduction

How It Works, Step by Step

1. Seeding — Cells travel from the uterus into the pelvis through retrograde flow, lymphatic or blood spread, or arise through local tissue transformation.
2. Implantation — They attach, develop their own small blood supply, and survive outside the uterus.
3. Hormonal cycling — Each wave of estrogen and progesterone drives growth and shedding.
4. No outlet — Blood has nowhere to go; it irritates surrounding tissues.
5. Inflammation — Immune cells flood the area, releasing cytokines and oxidants.
6. Repair and fibrosis — The body “patches” the irritation with collagen and fibrin, forming adhesions.
7. Feedback loop — Every cycle repeats the damage, thickening the scars and deepening pain⁠^{(2, 3)}.

Why It’s a Whole-Body Condition

Although the disease begins in reproductive tissue, its reach extends far beyond it⁠⁽⁴⁾:

• Digestive system — Adhesions can bind or distort bowel segments.
• Urinary system — Lesions on the bladder or ureters alter function.
• Nervous system — Inflammation reshapes pain signaling; pain persists even when hormones are stable.
• Immune system — Macrophages and inflammatory mediators remain active, maintaining fatigue and systemic inflammation.
• Endocrine & metabolic feedback — Local estrogen production can perpetuate the cycle.
• Cardiovascular and general health — Chronic inflammation contributes to oxidative stress that affects multiple organs.

Endometriosis is therefore not a “uterus problem.”

It’s a multisystem disorder of inflammation, tissue repair, and neural adaptation.

The Six-Phase System Cycle

Each phase of the menstrual cycle can be viewed mechanically — as a flow system that alternates between pressure, release, and repair.

Every step offers an engineering parallel, a potential design concept, and an existing medical tool that already performs part of that job elsewhere.

Phase One: Baseline — Corrosion Points Form

• Biology: Small dormant implants secrete low-level inflammatory signals, making pelvic surfaces less smooth.
• Analog: Early rust or biofilm formation on pipes.
• Imagined biological fix: A renewably applied “anti-stick” coating that prevents attachment and keeps organs gliding.
• Existing partial tools: Absorbable anti-adhesion barriers used after surgery (hyaluronic-acid or cellulose films)⁠⁽⁵⁾; hydrogel coatings on implants that prevent cell buildup.

Phase Two: Follicular Phase — Pressure & Proliferation

• Biology: Estrogen surges, prompting implants to grow new vessels and swell.
• Analog: Pressure building inside a sealed chamber.
• Imagined fix: A local hormone buffer that absorbs estrogen peaks without suppressing the whole endocrine system.
• Existing tools: Localized hormone-releasing IUDs (such as LNG-IUS)⁠⁽⁶⁾; programmable hormone-delivery pumps used in other endocrine conditions.

Phase Three: Ovulation — Inflammatory Spike

• Biology: The ovulatory burst increases prostaglandins and cytokines, briefly heightening inflammation.
• Analog: An electrical surge in a circuit.
• Imagined fix: An “immune capacitor” — a biocompatible medium that temporarily binds inflammatory molecules and releases neutral by-products slowly.
• Existing tools: Cytokine-filtering cartridges used in sepsis and autoimmune therapy⁠⁽⁷⁾; nanoparticle carriers that sequester and release specific molecules.

Phase Four: Luteal Phase — Congestion & Stagnation

• Biology: Progesterone dominates; fluid movement slows and fibrin begins to deposit — the early stage of scarring.
• Analog: Sediment collecting in low-flow plumbing.
• Imagined fix: Gentle, periodic peritoneal “rinses” with enzyme solutions that break fibrin before it hardens.
• Existing tools: Peritoneal-dialysis systems — proven technology for safe, cyclical lavage⁠⁽⁸⁾; low-intensity ultrasound to maintain circulation.

Phase Five: Menstrual Phase — Internal Bleed & Pooling

• Biology: Ectopic implants bleed into the pelvic cavity; free fluid pools and then clots⁠⁽⁹⁾.
• Analog: A localized leak in a hydraulic system.
• Imagined fix: A temporary micro-drain that opens only during bleeding, removes fluid, neutralizes iron, and self-seals.
• Existing tools: Closed suction drains used post-surgery; resorbable hemostatic matrices that absorb and deactivate blood components⁠⁽¹⁰⁾.

Phase Six: Chronic Phase — Fibrosis & Adhesion

• Biology: Repeated cycles of injury and repair produce fibrotic plaques; nerves grow into scars, locking in pain⁠⁽¹¹⁾.
• Analog: Scale accumulating inside pipes.
• Imagined fix: Periodic “descaling” — enzymes or targeted energy that soften early scar tissue, followed by re-lubrication of organ surfaces.
• Existing tools: Laparoscopic adhesiolysis (manual scar release); post-surgical adhesion barriers; experimental enzyme or ultrasound scar-modifiers⁠⁽¹²⁾.

Current Medical Solutions — and Where They Fall Short

Standard treatments focus on suppressing hormones, relieving pain, or excising visible lesions⁠⁽¹³⁾:

• Non-steroidal anti-inflammatory drugs (NSAIDs) for pain management.
• Hormonal suppression — combined contraceptives, progestins, or GnRH modulators — to slow implant growth⁠⁽¹⁴⁾.
• Conservative laparoscopic surgery to remove implants and scar tissue⁠⁽¹⁵⁾.
• Hysterectomy (with or without ovaries) for severe or recurrent disease⁠⁽¹⁶⁾.
• Multidisciplinary pain programs including physiotherapy and psychological support⁠⁽¹⁷⁾.

Why these don’t fully work:

1. They target symptoms, not the underlying mechanical loop — bleeding → fluid → inflammation → scar → adhesion.
2. Hormonal drugs act systemically, often bringing side effects and fertility trade-offs⁠⁽¹⁴⁾.
3. Surgery treats the visible damage but can’t prevent new micro-bleeds or adhesions; recurrence remains common⁠⁽¹⁵⁾.
4. Care is episodic rather than cyclical; it doesn’t synchronize with the body’s monthly rhythm.
5. The model is reactive, not preventative.

A systems approach asks different questions:

How can we preserve flow? Reduce stagnation? Protect surfaces? Interrupt scarring before it begins?

A Systems Approach — Designing Personalized, Dynamic Interventions

Each person’s pattern of inflammation, fluid buildup, and scarring is unique.

A systems plan begins by identifying the dominant phase causing the most disruption, then pairing it with a maintenance companion to keep the background stable.

Example frameworks:

• Fluid-dominant → Primary: timed lavage or drainage (Phase 5) + Secondary: enzyme or iron-binding maintenance (Phase 4).
• Fibrosis-dominant → Primary: periodic scar-softening or barrier placement (Phase 6) + Secondary: anti-adhesion coatings (Phase 1).
• Inflammation-dominant → Primary: local hormone or cytokine buffering (Phase 2 & 3) + Secondary: gentle, ongoing immune modulation.

This method shifts care from damage control to system stewardship — maintaining flow, limiting chronic inflammation, and reducing recurrence.

How This Approach Improves Life

• Fewer flares: Intervening before blood or fibrin accumulate lessens pain spikes.
• Lower cumulative damage: Early scar prevention maintains organ mobility.
• Reduced drug burden: Localized modulation can replace broad hormone suppression.
• Preserved fertility: Less scarring supports reproductive function.
• Greater quality of life: Less fatigue, fewer surgeries, more predictable comfort.
• Sustainable self-care mindset: From “treat when it breaks” to “keep it flowing.”

Endometriosis, seen through this lens, is a fluid-dynamics problem entwined with immune repair.

Solving it means restoring flow rather than merely stopping growth.

Collaboration and Next Steps

I’m open to collaborating with clinicians, biomedical engineers, and researchers interested in translating these system concepts into safe, ethical pilot studies or prototypes.

My goal is to bridge patient experience with mechanical and biological innovation — to build pathways that make living with endometriosis gentler, more predictable, and ultimately more preventable.

References

1. The Lancet. “Endometriosis as a systemic inflammatory disease.” 2021.
2. Frontiers in Immunology. “Immune microenvironment and Th17/IL-17 pathways in endometriosis.” 2023.
3. Reproductive Sciences. “Iron overload and fibrosis in endometriosis.” 2024.
4. CMAJ. “Diagnosis and management of endometriosis.” 2023.
5. Surgical Innovation Journal. “Adhesion barriers and peritoneal surface engineering.” 2022.
6. Journal of Obstetrics and Gynaecology Research. “Localized hormone delivery devices in reproductive health.” 2023.
7. Critical Care Medicine. “Cytokine adsorption and immune filtration technologies.” 2022.
8. Peritoneal Dialysis International. “Clinical safety of cyclic peritoneal lavage.” 2022.
9. Mayo Clinic. “Endometriosis: Diagnosis and Treatment.” 2024.
10. Annals of Surgery. “Resorbable hemostatic agents and iron binding biomaterials.” 2023.
11. Nature Reviews Endocrinology. “Fibrosis and nerve ingrowth in endometriosis pain.” 2023.
12. Frontiers in Surgery. “Energy-based scar modulation techniques.” 2024.
13. BMC Women’s Health. “Comparative review of eight international guidelines for endometriosis treatment.” 2022.
14. MDPI Pharmaceuticals. “Hormonal treatment of endometriosis: a narrative review.” 2023.
15. Reproductive Medicine Review. “Recurrence after surgical management of endometriosis.” 2022.
16. Verywell Health. “Using Hysterectomy to Treat Endometriosis.” 2024.
17. PMC. “Comprehensive multimodal care for endometriosis-related pain.” 2024.