Bladder neck contracture: incidence, mechanisms, and therapeutic advances

Abstract

Bladder neck contracture (BNC) is a progressive narrowing of the bladder neck and adjacent posterior urethra, primarily caused by fibrotic tissue proliferation and scar formation. It commonly occurs following prostate surgery or radiotherapy. Its pathogenesis involves acute and chronic inflammatory responses triggered by surgical or radiation-induced injury, transdifferentiation of fibroblasts into myofibroblasts, and excessive extracellular matrix (ECM) deposition, mediated by the interplay of transforming growth factor beta (TGF-β)/Smad signaling and mechanotransduction feedback. Clinically, patients present with voiding difficulty, a weakened urinary stream, increased post-void residual volume, and urinary retention, which may be complicated by urinary tract infections, bladder stones, and renal impairment. Diagnosis is based on medical history, urodynamic studies, ultrasound, voiding cystourethrography(VCUG), and cystoscopic evaluation. Treatment follows a stepwise approach ranging from conservative management to endoscopic and then surgical interventions. First-line therapies include transurethral dilation or incision, often combined with local anti-scar agents and intermittent self-catheterization. Refractory or recurrent cases may require open or robot-assisted reconstructive surgery. Robot-assisted surgery, with its high-definition 3D visualization, multi-degree-of-freedom instrumentation, and precise suturing, significantly reduces the incidence of BNC and provides a minimally invasive option for complex reconstructions. Future research directions focus on regenerative medicine, tissue-engineered scaffolds, and anti-fibrotic pharmacotherapy, aiming to fundamentally interrupt the fibrotic cascade. Personalized risk stratification and early intervention are expected to enhance long-term outcomes and quality of life.