🩸 Dienogest & Progestin Therapy Simulator

Active Endometriotic Implants

Ectopic endometrial tissue responds to hormones outside the uterus.

• ~10%: Prevalence in reproductive age (women affected globally)
• 4-5: Common implant sites (peritoneum, ovaries, ligaments)
• ~7: Years to diagnosis (average diagnostic delay)
• ~70%: Chronic pelvic pain link (of endometriosis patients)

What ectopic implants are

Endometrial-like tissue grows outside the uterine cavity.

Implants carry estrogen and progesterone receptors, just like the uterine lining.

Why implants cause pain

Cyclic hormone shifts trigger local inflammation and bleeding.

Baseline tissue biology

Implants stay hormonally active without any suppressive therapy.

Dienogest Treatment Begins

A selective progestin starts blocking implant growth signals.

• Progestin: Drug class (19-nortestosterone derivative)
• 2 mg: Typical daily dose (oral, once daily)
• PR: Receptor target (progesterone receptor)
• Weeks: Onset of effect (not immediate)

Mechanism of action

Dienogest binds progesterone receptors on implant cells.

High receptor affinity gives strong local anti-proliferative activity.

Hormonal suppression

Ovulation and estrogen production are partly suppressed.

Anti-inflammatory action

Local cytokine and prostaglandin production is reduced.

Implant Regression & Decidualization

Ectopic tissue shrinks as decidualization drives atrophy.

• ~4 wk: Decidualization onset (after therapy start)
• Up to 50%: Implant volume reduction (by month 3-4)
• Progressive: Glandular atrophy (over weeks)
• Pseudopregnancy-like: Stromal decidual change (tissue state)

Decidual transformation

Stromal cells convert to a decidualized, non-proliferative state.

Decidualized tissue loses its capacity to bleed cyclically.

Glandular atrophy

Glandular epithelium thins and gradually becomes inactive.

Pain score decline

Reduced inflammation lowers reported pelvic pain scores.

Breakthrough Bleeding Phase

Irregular spotting is common during early months of therapy.

• ~50%: Patients reporting spotting (in first 3 months)
• Month 1-3: Typical peak timing (of treatment)
• Leading reason: Discontinuation cause (for stopping therapy)
• Most cases: Resolution by month 6 (settle with continued use)

Why bleeding occurs

Thinning endometrium becomes fragile during hormonal adjustment.

Bleeding is usually light and does not signal treatment failure.

Managing expectations

Counseling before therapy improves patient persistence.

Pattern over time

Spotting frequency typically declines after month three.

Sustained Suppression & Stability

Pain control improves and bleeding patterns stabilize long-term.

• ~70-80%: Pain reduction at 12 mo (from baseline VAS score)
• Rising: Amenorrhea rate (with continued use)
• Favorable: Long-term use profile (safety over years)
• Minimal: Implant activity at 12 mo (sustained suppression)

Durable pain relief

Continued dosing keeps implant activity consistently low.

Long-term dienogest use is associated with sustained symptom control.

Bleeding stabilization

Irregular spotting fades as endometrium adapts fully.

Adherence matters

Consistent daily dosing sustains long-term suppression.