Format

Send to

Choose Destination
BJOG. 2017 Jan;124(2):210-218. doi: 10.1111/1471-0528.14157. Epub 2016 Jun 17.

A review of the available clinical therapies for vulvodynia management and new data implicating proinflammatory mediators in pain elicitation.

Author information

1
Department of Environmental Medicine, University of Rochester, Rochester, NY, USA.
2
Department of Obstetrics and Gynecology, University of Rochester, Rochester, NY, USA.
3
Department of Microbiology and Immunology, University of Rochester, Rochester, NY, USA.

Abstract

Localised provoked vulvodynia (LPV) is a common, chronic, and disabling condition: patients experience profound pain and a diminished quality of life. The aetiologic origins of vulvodynia are poorly understood, yet recent evidence suggests a link to site-specific inflammatory responses. Fibroblasts isolated from the vestibule of LPV patients are sensitive to proinflammatory stimuli and copiously produce pain-associated proinflammatory mediators (IL-6 and PGE2 ). Although LPV is a multifactorial disorder, understanding vulvar inflammation and targeting the inflammatory response should lead to treatment advances, especially for patients exhibiting signs of inflammation. NFκB (already targeted clinically) or other inflammatory components may be suitable therapeutic targets.

TWEETABLE ABSTRACT:

Vulvodynia is a poorly understood, prevalent, and serious women's health issue requiring better understanding to improve therapy.

KEYWORDS:

PGE 2 ; Dectin-1; IL-6; NFκB; fibroblast; inflammation; vestibulitis; vulvar pain; vulvodynia

PMID:
27312009
PMCID:
PMC5164873
DOI:
10.1111/1471-0528.14157
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center