2007
DOI: 10.1016/j.ajog.2006.12.038
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Enhanced synthesis of proinflammatory cytokines by vulvar vestibular fibroblasts: implications for vulvar vestibulitis

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Cited by 63 publications
(79 citation statements)
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“…On the one hand, primary dyspareunia could mainly be the result of inherent pathophysiological abnormalities (e.g., congenital defect of urogenital sinus-derived epithelium, genetic variants reducing the ability to fight pathogens/increasing the proinflammatory response, impairment in pain-regulatory mechanisms) combined with psychosocial characteristics like trait anxiety (Babula, Linhares, Bongiovanni, Ledger, & Witkin, 2008;Burrows, Klingman, Pukall, & Goldstein, 2008;Granot et al, 2004). Conversely, biomedical and behavioral factors (e.g., OC, infections, nonindicated self-treatment) may mostly explain secondary dyspareunia by creating prolonged inflammation of the vulvar mucosa and peripheral sensitization (Bohm-Starke, Hilliges, Falconer, & Rylander, 1998;Foster et al, 2007).…”
Section: Discussionmentioning
confidence: 96%
“…On the one hand, primary dyspareunia could mainly be the result of inherent pathophysiological abnormalities (e.g., congenital defect of urogenital sinus-derived epithelium, genetic variants reducing the ability to fight pathogens/increasing the proinflammatory response, impairment in pain-regulatory mechanisms) combined with psychosocial characteristics like trait anxiety (Babula, Linhares, Bongiovanni, Ledger, & Witkin, 2008;Burrows, Klingman, Pukall, & Goldstein, 2008;Granot et al, 2004). Conversely, biomedical and behavioral factors (e.g., OC, infections, nonindicated self-treatment) may mostly explain secondary dyspareunia by creating prolonged inflammation of the vulvar mucosa and peripheral sensitization (Bohm-Starke, Hilliges, Falconer, & Rylander, 1998;Foster et al, 2007).…”
Section: Discussionmentioning
confidence: 96%
“…Production of inflammatory cytokines such as Interleukin (IL)-1, IL-6, tumor necrosis factor ␣ and IL-8 follow infection with this organism [20,21] , similar to the cytokines found in the vestibular tissue of localized vulvodynia after incubation with ␣ -melanophore-stimulating hormone plus yeast [22] . A possible similarity in genetic disposition to infection may be involved in the etiologic role of H. pylori and localized vulvodynia.…”
Section: Discussionmentioning
confidence: 90%
“…The former point is supported by an experimental mouse model of LPV that confirmed that repeated vulvovaginal infections with C. albicans are sufficient to cause chronic vulvar pain behavior and increased vulvar peptidergic innervation, a finding that parallels observations in the clinical literature [2,4]. Furthermore, some women with chronic vulvar pain may be exceptionally vulnerable to C. albicans exposure, as indicated by enhanced contact sensitivity to intradermal C. albicans injections and increased fibroblast-mediated cytokine production [7,11]. The question remains, how does the vestibule uniquely mediate these symptoms, and how can we differentiate normal vulvar nociceptive processes from pathological ones?…”
mentioning
confidence: 76%