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Nerve sprouting and neurogenic inflammation characterize the neurogenic detrusor overactive bladder of patients no longer responsive to drug therapies.

Authors
  • Traini, Chiara1
  • Del Popolo, Giulio2
  • Faussone-Pellegrini, Maria-Simonetta1
  • Guasti, Daniele1
  • Catarinicchia, Stefano1
  • Vannucchi, Maria Giuliana1
  • 1 Department of Experimental and Clinical Medicine, Histology and Embryology Research Unit, University of Florence, Florence, Italy. , (Italy)
  • 2 Department of Neuro-Urology, Careggi University Hospital, Florence, Italy. , (Italy)
Type
Published Article
Journal
Journal of Cellular and Molecular Medicine
Publisher
Wiley (Blackwell Publishing)
Publication Date
Jun 01, 2019
Volume
23
Issue
6
Pages
4076–4087
Identifiers
DOI: 10.1111/jcmm.14294
PMID: 30945429
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Urothelium and Lamina Propria (LP) are considered an integrate sensory system which is able to control the detrusor activity. Complete supra-sacral spinal cord lesions cause Neurogenic Detrusor Overactivity (NDO) whose main symptoms are urgency and incontinence. NDO therapy at first consists in anti-muscarinic drugs; secondly, in intra-vesical injection of botulinum toxin. However, with time, all the patients become insensitive to the drugs and decide for cystoplastic surgery. With the aim to get deeper in both NDO and drug's efficacy lack pathogenesis, we investigated the innervation, muscular and connective changes in NDO bladders after surgery by using morphological and quantitative methodologies. Bladder innervation showed a significant global loss associated with an increase in the nerve endings located in the upper LP where a neurogenic inflammation was also present. Smooth muscle cells (SMC) anomalies and fibrosis were found in the detrusor. The increased innervation in the ULP is suggestive for a sprouting and could condition NDO evolution and drug efficacy length. Denervation might cause the SMC anomalies responsible for the detrusor altered contractile activity and intra-cellular traffic and favour the appearance of fibrosis. Inflammation might accelerate these damages. From the clinical point of view, an early anti-inflammatory treatment could positively influence the disease fate. © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

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