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Vulvodynia: A Common and Under-Recognized Pain Disorder in Women and Female Adolescents -- Integrating Current Knowledge into Clinical Practice

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The pathophysiology of Vulvodynia remains inconclusive. (See Vulvodynia Pathophysiology References 1-50.) However, research to date supports the theory that multiple mechanisms predispose, trigger and perpetuate symptoms.

  • Co-morbidities:  painful bladder syndrome, fibromyalgia, irritable bowel syndrome, temporomandibular disorder are significantly associated with Vulvodynia.

  • Genetics: Some women with Vulvodynia have a genetic predisposition that (i) increases the risk of candidiasis or other infections, (ii) prolongs inflammatory responses or (iii) affects their response to oral contraceptive pills. 

  • Hormonal factors: In some women the use of combined hormonal contraceptives has been associated with an increased risk of Vulvodynia. 

  • Inflammation: Based on either histological, immunological or biochemical studies, inflammation has been associated with Vulvodynia. There is an increase in the number of mast cells and degranulated mast cells.

  • Musculoskeletal: Pelvic floor overactivity is frequent.

  • Neurologic mechanisms: Higher sensitivity to stimulation in non-genital areas is seen. Brain imaging studies depict function changes. 

  • Neuroproliferation: Increase in the density of nerve endings in the vestibule, i.e., nociceptors with increased density of the vanilloid receptor VR1. This leads to increased sensitivity. 

  • Psychosocial factors: Anxiety, depression, childhood victimization, posttraumatic stress, mood or anxiety disorder

  • Structural defects: There are reports that repair of pelvic floor prolapse is associated with the resolution of vulvodynia. 

 

 

Our understanding of the pathophysiological mechanisms of vulvodynia is in its infancy. This diagram compares the mechanisms of normal pain transmission to the proposed pathophysiologic transmission of pain in women with vulvodynia. It is likely that different mechanisms, influenced by several predisposing, triggering and maintaining factors, as well as genetic and environmental factors, will be identified. 

 

 

One possible pathophysiological mechanism of Vestibulodynia is neuroproliferation. A special nerve fiber staining, PGP 9.5, was used to depict small nerve fibers in patients with Vestibulodynia and women without Vestibulodynia undergoing vestibular biopsy for other conditions. Subepithelial and intraepithelial nerve fibers were detected only in patients with Vestibulodynia. The fibers penetrated the basal membrane and continued vertically for more than half the distance to the epithelial surface. Branching of the nerve fibers within the epithelium was rarely seen (Bornstein 1997, Bornstein 2008).

 

 

In Vestibulodynia there is frequently an increase in mast cell number and activity. Here, mast cells, stained by Giemsa, show degranulation as evidenced by the extracellular red granules, in a X600 microscopic field. The discharged granules contain Tryptase, Histamine, Serotonin, Histamine, Bradykinin, Heparanase, Nerve Growth Factor, etc. Some of these enzymes may participate in the pathogenesis of Vestibulodynia (Bornstein 2004).

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