Acknowledgement:
I would like to thank my fellow Lauren Hammock, M.D. for her work on this lecture. She did all of the literature search and organized the material. She will be the first author on a review article on this topic to be published in an upcoming issue of the Journal of Cutaneous Pathology.

Spongiotic Dermatitis
Patients with spongiotic dermatitis usually present with itching, but may also experience pain with dyspareunia and fissuring around the introitus if the mucosa is involved. [6] Patients present clinically with ill-defined erythematous papules and plaques with or without lichenification. Spongiotic dermatitis may often go unrecognized by gynecologists who fail to take a dermatologic history. It is characterized histologically by intercellular edema (spongiosis) and perivascular inflammatory infiltrates, accompanied by irregular acanthosis and hyperkeratosis in the subacute and chronic states. Irritant and allergic contact dermatitis may be very difficult to distinguish, and often coexist. [8] Vulvovaginal fungal infections often present with similar histologic features, and for this reason are discussed along with the spongiotic dermatitides.

Irritant contact dermatitis, in which there is direct toxicity of a substance without an allergic component, appears to have a particular predilection for the vulva. [9, 10, 11] Irritating substances include medications such as podophyllin, antiseptics, douches, antifungals, lubricants, contraceptives, and sanitary pads. Additionally, the vulva is prone to excess friction and overheating due to occlusive clothing and physical activity. [6] Histologically, lesions show epidermal spongiosis, keratinocyte ballooning with necrosis, occasional apoptotic keratinocytes, and increased dermal edema. Increased numbers of Langerhans cells may also be diffusely scattered in the upper dermis. [12, 13, 14]

Allergic contact dermatitis is defined as a disorder incited by contact with an allergen to which there has been previous sensitization. Lesions typically develop within 12 to 48 hours post-exposure, and may extend outside the area of contact. [15] In studies of patients with anogenital allergic contact dermatitis for which patch testing has been performed, clinically relevant allergies have been found in up to 58% of patients. The main offenders in these studies are scented products, medications, corticosteroids, and local anesthetics. [16, 17] A more recent study reported that one of the most common allergens is benzocaine, which is found in many over-the-counter anesthetic preparations. [18] Histologically, allergic contact dermatitis may show spongiotic vesicles within the epidermis. The lax tissues of the vulva, however, often favor marked dermal edema over vesiculation, leading to a common misdiagnosis of angioedema. [7] An infiltrate of lymphocytes, Langerhans cells and eosinophils in a perivascular distribution is also commonly seen.

Seborrheic dermatitis may involve the vulva as well as other flexural areas. Scaly, ill-defined orange-pink lesions may be seen in the genitocrural folds, as this area has a high concentration of sebaceous glands. Lesions are often somewhat oily in appearance. Histologically, they may have a more psoriasiform appearance, making distinction from psoriasis difficult. Pityrosporum ovale may have a pathogenetic role, as well as increased lipids, moisture, and maceration of the skin frequently seen in this area. [8, 19, 20]

Patients with atopic dermatitis rarely complain specifically of vulvar involvement if there is widespread eczema elsewhere. However, one study showed up to 78% of patients with vulvar dermatitis to have atopic dermatitis by history. [2] Patients present with erythema between the labia, in the perianal region, and in the natal cleft. Gynecologists, to whom the patients are often referred, may fail to take a dermatologic history, and the condition frequently goes unrecognized. Histologically, the skin shows of spongiosis with or without vesiculation, focal exocytosis of lymphocytes, and degranulated mast cells. Poorly formed areas of parakeratosis are often present.

Chronic scratching and rubbing of pruritic lesions alters the epidermis and papillary dermis, and results in the clinical appearance of thickened skin seen with lichen simplex chronicus. Clinically, vulvar lichen simplex chronicus presents as an ill-defined hyperkeratotic lesion with lichenification and frequent hyperpigmentation. Mucosal surfaces may be gray-white and better localized than lesions on the external labia. [21] Tissues may frequently appear edematous and fissured. [8] Histology shows hyperparakeratosis with irregular psoriasiform epidermal hyperplasia, a prominent granular layer, and variable perivascular chronic inflammation. Thickened collagen bundles occupy the papillary dermis and lie in vertical streaks in parallel with elongated rete ridges. Because numerous disorders may be pruritic, the histologic features of lichen simplex chronicus are often superimposed on many pathologic disorders. Consequently, a patient with lichen simplex chronicus who does not respond to topical steroid therapy should be biopsied to exclude a coexisting dermatosis or neoplasia. Pathologists should also be aware of the possibility of a more worrisome underlying process such as lichen sclerosus or squamous cell carcinoma. [1] Carlson, et al saw lichen simplex chronicus either overlying or adjacent to lesions of lichen sclerosus in 82% of the cases studied. [22]

Candida albicans, the most common fungal infection of the vulva, is carried in the genital tract of approximately 20% of healthy women, but only about 5% of women suffer repeated episodes of candidiasis. [23] Vulvovaginal candidiasis is likely an overdiagnosed condition, however, and was found to be the true cause of vulvar symptoms in only 10% of patients in one study following diagnosis with positive culture and/or presence of hyphae on biopsy. [6] The majority of women with chronic vulvovaginal candidiasis are immunocompetent, although there are a number of well-known associated factors. A florid dermatitis often accompanies the candidiasis, and a hypersensitivity reaction likely plays a role in some patients. These patients suffer longstanding classic symptoms of itchy, moist and erythematous lesions with negative cultures and biopsy results likely secondary to low numbers of the organism. The dramatic response of such patients to antifungal therapy further lends support for an immune mechanism. Vulvar samples are best taken by a scraping. [6] Histology shows spongiosis with infiltration of the epidermis and stratum corneum with neutrophils that often coalesce into micropustules. The underlying dermis is markedly edematous with a perivascular and interstitial neutrophilic infiltrate. Spores and pseudohyphae may be seen with PAS stains, but culture is needed for speciation.

Although vulvar psoriasis is further discussed below, brief mention is warranted here due to the marked clinical and histologic overlap with candidiasis. Patients with widespread psoriasis elsewhere rarely complain specifically of vulvar involvement, however a fungal stain is essential in biopsies from this region prior to making a diagnosis of vulvar psoriasis.

Vesiculobullous Dermatoses
Patients with autoimmune or infectious vesiculobullous diseases present with cutaneous and mucosal blisters and ulcerations. Localized vulvar involvement in the immunobullous dermatoses, though uncommon, may be misdiagnosed or go unrecognized, particularly in children, where it may be mistaken for sexual abuse. [24]

Bullous pemphigoid is the most common of the immunobullous diseases. It affects primarily elderly patients and presents on the trunk, extremities, and intertriginous areas as large, tense blisters on an erythematous base. Bullous pemphigoid has a negative Nikolsky sign. Vulvar involvement in patients with bullous pemphigoid has been reported in 9% of adult patients. However, 40% of children with bullous pemphigoid have vulvar involvement. [25, 26, 27, 28, 29] Additionally, several cases of bullous pemphigoid in children have shown localized vulvar involvement. [24, 30, 31, 32] Histology may show either the cell-rich or the cell-poor variant. In both variants, the blister arises at the dermal-epidermal junction. Blisters arise on erythematous skin in the cell-rich variant, and numerous eosinophils are present in a perivascular and interstitial distribution. In the cell-poor variant, the blisters develop on clinically normal skin. There are scant perivascular lymphocytes and a few eosinophils scattered throughout the dermis and in the blister lumen. Immunofluorescence studies show IgG and C3 in a linear distribution at the dermal-epidermal junction. IgG antibodies are directed at both a 230kD protein (BPAg1) and a second 180kD protein (BPAg2). [33, 34] The principal BPAg1 protein is localized to basal keratinocytes and is associated with the cytoplasmic attachment site of hemidesmosomes. The second smaller BPAg2 protein is a hemidesmosomal antigen that extends to the lamina lucida. The distribution of these two antigens in skin accounts for the propensity of the disease to affect certain sites. The BPAg1 protein has been shown to be highly expressed in the groin region, as well as the back and axillae. [35]

Vulvar lesions of pemphigus vulgaris resemble those on mucosal or cutaneous surfaces elsewhere. Lesions consist of painful nonhealing erosions on mucosal surfaces, or flaccid bullae that rupture to leave a denuded base. Pemphigus vulgaris clinically has a positive Nikolsky sign, in contrast with bullous pemphigoid. Involvement of the vulva commonly occurs in association with widespread disease elsewhere, but may rarely occur as a primary manifestation. [36] Histologic features show spongiosis followed by acantholysis and blisters in a predominantly suprabasalar location. Acantholysis may extend into adnexal structures, and downward growth of epidermal strands may give rise to a 'villous' appearance. Care should be taken to biopsy earlier blisters. Immunofluorescence studies demonstrate IgG in the squamous intercellular cell surface areas in approximately 95% of cases, and titers correlate well with disease activity. IgG autoantibodies to desmoglein 1 and desmoglein 3 play a primary role in blister formation. [37] These antigens are expressed at lower levels in the groin region than in the head and neck region, buccal mucosa, and axillae, accounting for the appearance of vulvar lesions only in the presence of widespread disease elsewhere. [35]

Although cicatricial pemphigoid is much less common than bullous pemphigoid or pemphigus vulgaris, the mucosa is frequently affected, and is often the only feature. The genitalia are commonly involved by blisters and erosions that heal with extensive scarring, often leading to vaginal stenosis and labial fusion. [38] In one study of 26 adult patients with cicatricial pemphigoid, over half had vulval involvement which tended to be extensive, deforming, and refractory to therapy. [39] Histology shows a subepidermal blister with a variable inflammatory infiltrate at the base. There may be an underlying dermal scar due to the tendency of lesions to recur at sites of previous lesions. Immunofluorescence studies are similar to those of bullous pemphigoid, partially because the two entities share a common target antigen in the 180 kD minor bullous pemphigoid antigen. Another less common target antigen involved in the pathogenesis of cicatricial pemphigoid is epilegrin, which is associated with anchoring filaments at the junction of the lamina lucida and the lamina densa. [40]

Epidermolysis bullosa acquisita is the rarest of the subepidermal vesiculobullous diseases, but vulvar involvement is frequent, occurring in one of two adults and two of three children in one series. [39] Patients present with blisters that heal with scarring and milia formation on both mucosal and cutaneous sites. Epidermolysis bullosa acquisita is similar clinically and histologically to bullous pemphigoid. There is a subepidermal blister with only fibrin and a few inflammatory cells in the lumen, and a variable superficial dermal inflammatory infiltrate. This disease is distinguished from bullous pemphigoid by indirect immunofluorescence studies of the patient's serum antibodies on salt-split normal skin. The antigen and antibody localize to the floor of the blister, [41] where the target antigen has been identified as collagen type VII in the anchoringfibril. [42] Epidermolysis bullosa acquisita is associated with the HLA class II antigen DR-2 in both children and adults. [43, 44, 45]

Herpes genitalis, or herpesvirus type 2 (HSV), is transmitted by close physical or sexual contact, and may be transmitted by asymptomatic individuals due to viral shedding that frequently occurs in the absence of a clinical lesion. Primary infection occurs in patients without evidence of prior disease who have no HSV antibodies. The virus establishes latency in the sensory sacral ganglia, and 50-80% of patients suffer recurrences within one year with menstruation as a common trigger. [46, 47] Paresthesia and burning may precede the appearance of visible lesions. Patients may have hip or leg pain as well as pain and tenderness at the lesional site. Systemic symptoms are common in primary HSV infections, and candidal superinfection occurs in 14% of these patients. [48] Clinically, lesions present as erythematous papules that progress to vesicles and ulcerations. The presence of HSV ulcers is also a risk factor for acquisition of HIV. [49, 50] Crusting occurs on epithelial surfaces, followed by re-epithelialization. Labial adhesions may rarely occur in vulvar lesions, but do not usually require surgical intervention. Histology shows marked epithelial degeneration and acanthosis of basal keratinocytes. Keratinocytes show nuclear swelling with focal multinucleation, nuclear molding, and chromatin margination. Eosinophilic inclusion bodies may be prominent, and neutrophils are frequent. Late lesions show marked epidermal necrosis involving the hair follicle and pilosebaceous units. Biopsies should be taken from an early lesion. The virus may be identified by culture, direct immunofluorescence, and molecular testing.

Papulosquamous Dermatoses
The papulosquamous dermatoses present as cutaneous papules or thick scaly plaques, and tend to have a similar clinical appearance on the vulva. Lesions on the labia majora are dry and scaly, whereas intertriginous lesions are smooth, moist, and erythematous. Psoriasis and lichen planus are the most common papulosquamous dermatoses and those most likely to involve the vulva.

Psoriasis vulgaris is a chronic relapsing papulosquamous dermatitis affecting approximately 2% of the population. A precise pattern of inheritance has not been identified, but a genetic proclivity does exist. Friction and occlusion caused by tight clothing may precipitate vulvar involvement by psoriasis in individuals who are already genetically predisposed. The clinical appearance varies from gray, scaly plaques on the mons pubis and labia majora to erythematous, glossy plaques without scale in intertriginous folds. [51] Although psoriasis does not typically involve mucosal surfaces, some patients with definite psoriasis elsewhere may complain of itching in the labia minora without a definite clinical lesion, which is possibly attributable to psoriasis. [8] The diagnosis of psoriasis is usually clinically evident by the appearance of lesions elsewhere, although vulvar findings may rarely represent the only manifestation. [52] The histology shows acanthosis with parakeratosis, regular elongation of rete ridges, and a minimal to absent granular layer. Collections of neutrophils in the epidermis (Munro's abscesses) and dermal perivascular inflammation are often present.

Lichen planus is a common entity of unknown etiology whereby patients develop pruritic, flat-topped papules and plaques with a network of fine, white striae. Lesions occur preferentially on the surfaces of the wrists, trunk, thighs, and genitalia. Lesions on the vulva are usually part of a generalized eruption, and are found on keratinized skin with or without Wickham's striae on the inner aspect of the vulva. Post-inflammatory hyperpigmentation may follow healing. Vulvar lesions were observed in 19 of 37 women with lichen planus in one series. [53] Histology shows wedge-shaped hypergranulosis with irregular, "saw-toothed" acanthosis. A band-like lymphocytic infiltrate in the superficial dermis abuts the epidermis, and numerous colloid bodies may be seen at the dermal-epidermal junction. A cell-mediated immune mechanism likely plays a role in the pathogenesis, and there is an association with HLA-DR1 in the more common non-familial cases. [54]

Sclerosing Dermatoses
Although connective tissue diseases may involve the vulva, the most common vulvar sclerosing dermatosis is lichen sclerosus. The female anogenital region is the most commonly affected area, and about 11% of women with lichen sclerosus anogenital lesions also have extragenital lesions. [55] Lichen sclerosus may also occur in children as young as one year. [56] Patients usually present clinically with itching, burning, or dyspareunia, however asymptomatic lesions may be incidentally discovered as a small white patch. The extent of lesions does not seem to correlate with symptoms. While some patients may have architectural preservation with only pallor and ecchymosis, [57] there is often loss of distinction between the labia majora and labia minora, with sclerosis of the introitus in a "figure-of-eight" pattern that also involves the perianal region. Lesions may progress to leave only a pinhole-shaped opening posteriorly. [8] Vaginal involvement does not occur. The histology of lichen sclerosus lesions may vary according to the age of the lesions and secondary changes that may be present due to persistent rubbing. Subepidermal sclerosis and vacuolar interface changes are nearly always present. Established lesions show a dermal zone of pink, hyalinized fibrosis beneath which lies an inflammatory infiltrate. Epidermal changes may include irregular epithelial hyperplasia or effacement of the rete ridge pattern, and follicular keratin plugging. [1] Although the etiology of lichen sclerosus is unknown, both a familial predisposition and an autoimmune link have been established. Efforts to find an infectious causal agent have shown conflicting results. The changes of lichen sclerosus are frequently found in association with squamous cell carcinoma of the vulva. A study of 39 cases of vulvar squamous cell carcinoma showed lichen sclerosus in surrounding skin in 65% of cases. However, that study also showed that lichen sclerosus was an infrequent finding in earlier lesions of VIN (4%), and concluded that squamous cell carcinoma was more likely to develop in older women with longstanding and established lichen sclerosus. These findings lend further support to the idea that there are two subsets of women who develop squamous cell carcinoma: one younger HPV-associated subset and one older group who develop squamous cell carcinoma in a setting of chronic inflammation and lichen sclerosus. In this same study, loss of p53 was seen in keratinocytes from lichen sclerosus lesions in patients from this latter group, and likely plays an important role in carcinogenesis. [22]

Summary
Inflammatory, non-neoplastic epidermal alterations of the vulva can be correctly diagnosed using classification schemes applied to skin elsewhere on the body. A wide range of inflammatory disorders may occur on the vulva, and they may have a similar clinical presentation to HPV lesions. However, HPV is incurable and often is treated surgically. Accordingly, as inflammatory dermatoses commonly occur on the vulva and are often curable with topical therapy, an awareness of these entities and an ability to distinguish them from HPV are imperative.

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