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The aetiologic origins of vulvodynia are poorly understood, yet recent evidence suggests a link to site\u2010specific inflammatory responses. Fibroblasts isolated from the vestibule of\n                      <jats:styled-content style=\"fixed-case\">LPV<\/jats:styled-content>\n                      patients are sensitive to proinflammatory stimuli and copiously produce pain\u2010associated proinflammatory mediators (\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u20106 and\n                      <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content>\n                      <jats:sub>2<\/jats:sub>\n                      ). Although\n                      <jats:styled-content style=\"fixed-case\">LPV<\/jats:styled-content>\n                      is a multifactorial disorder, understanding vulvar inflammation and targeting the inflammatory response should lead to treatment advances, especially for patients exhibiting signs of inflammation.\n                      <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\n                      \u03baB (already targeted clinically) or other inflammatory components may be suitable therapeutic targets.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Tweetable abstract<\/jats:title>\n                    <jats:p>Vulvodynia is a poorly understood, prevalent, and serious women's health issue requiring better understanding to improve therapy.<\/jats:p>\n                  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