IC/BPS Pathophysiology in Women
Interstitial Cystitis / Bladder Pain Syndrome is a multifactorial condition, disproportionately affecting women, involving urothelial dysfunction, neurogenic inflammation, mast cell activation, and central sensitization — a cascade that takes years to reverse without targeted intervention.
The IC/BPS disease cascade in the female bladder
Urothelial Barrier Disruption
Loss of GAG layer integrity allows urinary solutes (potassium, acid) to penetrate the urothelium, triggering subepithelial inflammation.
Mast Cell Activation
Tryptase and histamine released by activated mast cells increase vascular permeability and sensitize afferent C-fibers in the lamina propria.
Neurogenic Inflammation
Substance P and CGRP release from sensitized nerves perpetuate the inflammatory cascade through a neurogenic-immune feedback loop.
Detrusor Instability
Inflammatory mediators and urothelial ATP release activate purinergic receptors on smooth muscle, contributing to detrusor overactivity.
Central Sensitization
Chronic peripheral nociception leads to spinal cord wind-up and cortical reorganization, amplifying pain signals and broadening the pain field.
Symptom Complex
The culminating presentation: suprapubic pain, urinary urgency/frequency, dyspareunia, and pelvic floor hypertonicity — often misdiagnosed for years.