V pain & Excess Nerve proliferation (MORE)

[Guest guest]

More on the subject, Dee~

Vulvar vestibulitis syndrome (VVS) is a subset of vulvodynia that is characterized by severe pain during attempted vaginal penetration to pressure localized to the vulvar vestibule, and redness (erythema) of the vulvar vestibule.

A subset of vulvar vestibulitis is called vestibulodynia, which combines the three symptoms with constant pain at the vestibule. Increased awareness of VVS has led to exciting new research. This review will examine current concepts regarding the diagnosis, etiology, and treatment of VVS.

Until recently, neither the cause of VVS nor what causes the underlying pain was known. However, in the last few years, increased awareness of vulvar vestibulitis syndrome (VVS) has led to exciting new research. This research focuses on many different aspects of VVS including possible genetic, infectious or allergic causes, and on multiple treatment regimens. Even basic assumptions of early researchers have been questioned, leading to a greater understanding of VVS.

We now know that women with VVS feel pain at the vestibule because they have an increased number of nerve endings in the vestibule. A woman with VVS can have up 30 times the number of nerve endings (3000%) as compared to women who do not have sexual pain. The nerve endings are called nociceptors. Nociceptors are the nerve endings that are responsible for sensing pain and stretch.

So what caused this increase in the number of nerve endings?

Women with Primary VVS are women who have pain ever since their first attempt at intercourse. In fact, most women with primary VVS have had pain when they first started to use tampons. Approximately 20-25% of women with VVS have primary VVS. Women with primary VVS almost never have had completely pain free intercourse.

The current hypothesis is that the neuronal proliferation in primary VVS is a congenital problem (birth defect). Current evidence supporting this hypothesis is that the tissue of the vestibule is completely different tissue than the tissue of the vaginal above the hymen (embryologically, morphologically, and histologically).

Therefore, it is plausible that a woman could have a congenital problem in the vestibule without having any problem in the vagina. This hypothesis is further supported by the fact that there is a very high concordance of women with VVS and interstitial cystitis (a similar pain syndrome of the bladder and urethra). The bladder and urethra are derived from the same tissue as the vestibule.

Women with secondary VVS have pain beginning after some period of pain free intercourse. Women with secondary VVS also have a proliferation of nerve endings, but unlike women with primary VVS, they are not born with it.

Instead, women with secondary VVS have 'acquired' these nerve endings. To explain this unfortunate acquisition is slightly more complicated than in primary VVS.

Over the last 5 years scientist have been pasting together several different pieces of information to get a congruent explanation of secondary VVS.

The pieces of information are as follows 1) women with VVS have much more sensitive skin throughout their whole body as compared to women without VVS. 2)

In addition to a proliferation of nerve endings in the vestibule, there is a proliferation of mast cells in the vestibule.

Mast cells are the white blood cells that are responsible for allergic and inflammatory reactions. 3) Up to 50% of women with VVS have a defect in one of 2 genes (IL1-RA, IL-1 beta) that are responsible for limiting inflammatory conditions in the body. If we put these (and other) pieces of information together, a new hypothesis is emerging. (Actually, we must give credit to Dr. Stanley Marinoff who first published this hypothesis in 1986- long before there was data to support it.)

VVS may be initiated by an allergic reaction to a chemical irritant in the vulvar vestibule. This irritation – possibly to topical antifungals, other medications, or chemicals- causes mast cells to migrate to the vestibule.

If the irritation persists, activation of mast cells leads to an uncontrolled proliferation of nociceptors in the mucosa.

This hypothesis explains why up to 80% of women with VVS complain of an acute onset of symptoms that includes burning and itching, which then progress to severe pain on touch. The pain on touch often then persists even after the initial symptoms of itching and burning disappear. Of course, further studies are ongoing to assess the validity of this hypothesis.............

Source: