**1. Introduction**


vulvar symptoms [3]. During the examination, the clinician should carefully examine the vulva and pay attention to skin or mucosal color (erythema and intense red); texture can provide clues to correct diagnosis (e.g., slight hyperkeratosis and thickened skin) existence of any lesions, which seems unusual for such macules, papules, or ulcers [4, 5]. Ulcers of vulva are diagnostically challenging due to variation in clinical morphology [4, 5]. The primary morphology is clinically relevant for identifying because it can significantly narrow the differential diagnosis. Diagnosis of vulvar ulcers based solely on clinical findings is often inaccurate, in most cases depending on sexually transmitted infections, but the differential diagnosis can include also dermatoses, trauma, neoplasms, hormonal-induced ulcers, drug reactions, or ulcer of unknown etiology [6, 7].

Subsequent to the completion of detailed observation, the clinician can decide for the diagnosis, if additional tools are necessary like speculum examination, vulvoscopy, or dermoscopy. The benefit of vulvoscopy remains controversial [8]. The contribution of dermoscope is mainly for the evaluation of both pigmented and nonpigmented lesions, presence of scarring, and loss of architecture but required training to identified benign structures and suspicious, worrisome features. It is crucial to document the number, type, size, border characteristics, and depth of lesions, discharge if present, tenderness, and presence or absence of local lymphadenopathy, which could influence mode of treatment [9, 10]. Cultures should be taken if there is suspicion for an infection, and final genital biopsies were recommended without to be prerequisite for the completion of the definitive diagnosis. It is an all common finding for a clinician to be frustrated by pathology report because it is sometimes difficult for the gynecologist due to inherent challenges to approach the obtaining tissue from the genitalia.

In 1976, Freidich classified skin disorders of the vulva into three categories: (a) hyperplastic dystrophy, (b) lichen sclerosus, and (c) dystrophy with or without atypia. For example, the term of hyperplastic dystrophy was used to include completely different clinical features, such as psoriasis, chronic lichen planus, and Bowen's disease [11].

Due to diagnostic problems resulting from this classification, in 1989, the International Society for the Study of Vulvar Diseases established a new terminology, which has been maintained to date [12]. Nonneoplastic epithelial lesions were delineated as follows: (a) lichen sclerosus and atrophicus, (b) squamous cell hyperplasia (former hyperplastic dystrophy without atypia), and (c) other diseases of vulva, a category in which various injuries occur, such as psoriasis, lichen planus, fungal infections, and condyloma acuminata. Since cytological atypia is found in this category, the damage is "changing" category and now belongs to the VIN classification [12].

#### **2. Disorders of the vulva**

#### **2.1 Dermatopathies**

"Dystrophy" of the vulva is an abnormality of the vulva epithelium. Epithelial growth may be hypoplastic, hyperplastic, or abnormal in some other way [13, 14].

#### *2.1.1 Atrophic and hypertrophic disorders*

Atrophic and hypertrophic disorders of the vulva come under the general term of dystrophies (formerly characterized as "precancerous" conditions). The skin,

**35**

*Depigmentation's Disorders of the Vulva, Clinical Management*

cases, the disease can relapse despite the surgical procedure [15].

the narrower "gynecological" or histological sense [16–21].

These alterations include:

• Scuamous cell hyperplasia

• Mixed lichen sclerosus and atrophicus

• Condyloma acuminata

• Lichen sclerosus

• Psoriasis

[16, 20, 21].

• Lichen planus

*2.1.1.1 Lichen sclerosus*

accompanied by itching and pain.

depending on the damage, may be appeared as white, dry, and thin or thickened, while hyperkeratosis and decreased vasculature are histologically present [15]. These alterations are mainly attributed to estrogen deficiency and, to this end, are often observed after menopause. The disorders may extend to the vaginal entrance, the perineum, etc. Usually there is intense pruritus, and the scratching it entails may result in an interception to the continuity of the skin. In addition to pruritus, there may be a burning sensation and dyspareunia, especially if the damage (usually atrophy) extends to the vaginal entrance [15]. For the treatment of pruritus, anti-inflammatory creams and topical corticosteroids are used (about two times a day). Antibiotic treatment is also administered in a transfection. In the absence of symptomatic treatment with conservative treatment and very intense annoyances of the patient, a simple vulvectomy can be chosen as "final" solution provided that the patient has been informed about the fact that in the half of the

Because of the fact that these disorders may coexist with malignancy, careful monitoring of the patient is required, and in doubt, multiple biopsies are required to exclude intraepithelial neoplasia (vulvar intraepithelial neoplasia/VIN) or cancer. Biopsies are often subjected to vulvovaginal screening after a 1–2% acetic acid solution is applied. However, the likelihood of developing invasive cancer in the soil of previous lesions is low. Given that these situations are well known, their descriptive "encyclopedic" terminology (in brackets, in italics) is not mentioned in

The term dystrophic lesions of the vulva according to literature like writhing, leukoplakia, lichen sclerosus and atrophicus, it is preferable to not be used anymore

"Lichen sclerosus" (LS) is a term used for a benign, chronic, progressive dermatological condition characterized by (intense) inflammation [22–25]. The epithelium is getting thinner, and some characteristic dermatological changes appeared

In general, lichen sclerosus appears in the skin of the genitalia. It was first described by Hallopeau and Darier at the end of the nineteenth century as a variety of lichen planus, which is not acceptable today. The term lichen sclerosus (and/ or atrophicus) should no longer be used, as forms of lichen sclerosus are not all atrophic. When there is coexistence of squamous cell hyperplasia, it is characterized

as "mixed squamous cell hyperplasia and lichen sclerosus" [26–32].

*DOI: http://dx.doi.org/10.5772/intechopen.83595*

#### *Depigmentation's Disorders of the Vulva, Clinical Management DOI: http://dx.doi.org/10.5772/intechopen.83595*

depending on the damage, may be appeared as white, dry, and thin or thickened, while hyperkeratosis and decreased vasculature are histologically present [15]. These alterations are mainly attributed to estrogen deficiency and, to this end, are often observed after menopause. The disorders may extend to the vaginal entrance, the perineum, etc. Usually there is intense pruritus, and the scratching it entails may result in an interception to the continuity of the skin. In addition to pruritus, there may be a burning sensation and dyspareunia, especially if the damage (usually atrophy) extends to the vaginal entrance [15]. For the treatment of pruritus, anti-inflammatory creams and topical corticosteroids are used (about two times a day). Antibiotic treatment is also administered in a transfection. In the absence of symptomatic treatment with conservative treatment and very intense annoyances of the patient, a simple vulvectomy can be chosen as "final" solution provided that the patient has been informed about the fact that in the half of the cases, the disease can relapse despite the surgical procedure [15].

Because of the fact that these disorders may coexist with malignancy, careful monitoring of the patient is required, and in doubt, multiple biopsies are required to exclude intraepithelial neoplasia (vulvar intraepithelial neoplasia/VIN) or cancer. Biopsies are often subjected to vulvovaginal screening after a 1–2% acetic acid solution is applied. However, the likelihood of developing invasive cancer in the soil of previous lesions is low. Given that these situations are well known, their descriptive "encyclopedic" terminology (in brackets, in italics) is not mentioned in the narrower "gynecological" or histological sense [16–21].

These alterations include:


*Depigmentation*

the obtaining tissue from the genitalia.

Bowen's disease [11].

VIN classification [12].

**2.1 Dermatopathies**

**2. Disorders of the vulva**

*2.1.1 Atrophic and hypertrophic disorders*

vulvar symptoms [3]. During the examination, the clinician should carefully examine the vulva and pay attention to skin or mucosal color (erythema and intense red); texture can provide clues to correct diagnosis (e.g., slight hyperkeratosis and thickened skin) existence of any lesions, which seems unusual for such macules, papules, or ulcers [4, 5]. Ulcers of vulva are diagnostically challenging due to variation in clinical morphology [4, 5]. The primary morphology is clinically relevant for identifying because it can significantly narrow the differential diagnosis. Diagnosis of vulvar ulcers based solely on clinical findings is often inaccurate, in most cases depending on sexually transmitted infections, but the differential diagnosis can include also dermatoses, trauma, neoplasms, hormonal-induced ulcers, drug reactions, or ulcer of unknown etiology [6, 7].

Subsequent to the completion of detailed observation, the clinician can decide for the diagnosis, if additional tools are necessary like speculum examination, vulvoscopy, or dermoscopy. The benefit of vulvoscopy remains controversial [8]. The contribution of dermoscope is mainly for the evaluation of both pigmented and nonpigmented lesions, presence of scarring, and loss of architecture but required training to identified benign structures and suspicious, worrisome features. It is crucial to document the number, type, size, border characteristics, and depth of lesions, discharge if present, tenderness, and presence or absence of local lymphadenopathy, which could influence mode of treatment [9, 10]. Cultures should be taken if there is suspicion for an infection, and final genital biopsies were recommended without to be prerequisite for the completion of the definitive diagnosis. It is an all common finding for a clinician to be frustrated by pathology report because it is sometimes difficult for the gynecologist due to inherent challenges to approach

In 1976, Freidich classified skin disorders of the vulva into three categories: (a) hyperplastic dystrophy, (b) lichen sclerosus, and (c) dystrophy with or without atypia. For example, the term of hyperplastic dystrophy was used to include completely different clinical features, such as psoriasis, chronic lichen planus, and

Due to diagnostic problems resulting from this classification, in 1989, the International Society for the Study of Vulvar Diseases established a new terminology, which has been maintained to date [12]. Nonneoplastic epithelial lesions were delineated as follows: (a) lichen sclerosus and atrophicus, (b) squamous cell hyperplasia (former hyperplastic dystrophy without atypia), and (c) other diseases of vulva, a category in which various injuries occur, such as psoriasis, lichen planus, fungal infections, and condyloma acuminata. Since cytological atypia is found in this category, the damage is "changing" category and now belongs to the

"Dystrophy" of the vulva is an abnormality of the vulva epithelium. Epithelial growth may be hypoplastic, hyperplastic, or abnormal in some other way [13, 14].

Atrophic and hypertrophic disorders of the vulva come under the general term of dystrophies (formerly characterized as "precancerous" conditions). The skin,

**34**


The term dystrophic lesions of the vulva according to literature like writhing, leukoplakia, lichen sclerosus and atrophicus, it is preferable to not be used anymore [16, 20, 21].

#### *2.1.1.1 Lichen sclerosus*

"Lichen sclerosus" (LS) is a term used for a benign, chronic, progressive dermatological condition characterized by (intense) inflammation [22–25]. The epithelium is getting thinner, and some characteristic dermatological changes appeared accompanied by itching and pain.

In general, lichen sclerosus appears in the skin of the genitalia. It was first described by Hallopeau and Darier at the end of the nineteenth century as a variety of lichen planus, which is not acceptable today. The term lichen sclerosus (and/ or atrophicus) should no longer be used, as forms of lichen sclerosus are not all atrophic. When there is coexistence of squamous cell hyperplasia, it is characterized as "mixed squamous cell hyperplasia and lichen sclerosus" [26–32].

#### *Depigmentation*

Lichen sclerosus is considered as the most common chronic lesion in vulva, referred to a chronic atrophy that usually observed after menopause. Clinically, vulva is glossy and dry, with no folds. The lesions are often symmetrical. Although the condition is observed over a wide range of ages, it has an increased incidence in women aged 50–59 years. Postmenopausal women and young girls are usually afflicted before menstruation. There is no clear justification. There is sufficient evidence of involvement of autoimmune mechanisms in the pathogenesis of lichen sclerosus. It is known that 21% of patients with lichen sclerosus also suffer from autoimmune disease more often than with thyroid disease. It is reported that 22% of patients with lichen sclerosus have an inherited history, and that 44% have one or more autoantibodies. Also, there is a correlation with HLA II antigens. There are studies associating inflammatory factors, e.g., Borrelia infection, with the development of lichen sclerosus. It is also reported that there is overexpression of wild-type P53 protein in lichen sclerosus, which occupies areas adjacent to squamous cell carcinoma (SCC) in which HPV is not detected.

Typically, the rash of lichen sclerosus begins as white polygonal papules, which flock to plaques. Typically, candlesticks and/or clearly cracked plugs appear on the surface of the plate, and they are similar to attached nozzles. Over time, plugs and craters may disappear by dropping a smooth, often porcelain plaque, and they rarely show up. Thus, the skin appears white and thin, although it may be present in SCH [26–32]. Originally, lichen sclerosus may have a bubbling consistency and is characterized by edema of the prepuce clitoris and telangiectasia of labia and purpura. Stretch marks appear mainly in the middle perineal line. Bullous lichen sclerosus is often accompanied by bleeding within the lesion, and the fillet can disappear. Later, labia minora and structures around clitoris disappeared too. The epithelium of the vagina and the cervix is not affected. However, there may be lesions in the forehead of the skin, which will lead to its constriction. Perianal lesions are described in 30% of cases [26–32].

Lichen sclerosus is a benign vulva condition associated to chronic and often progressive character with dermatologic location. Among the clinical findings are included marked inflammation, epithelial thinning, distinct dermal alterations like pruritus, and pain by varying degrees. The described lesions appear most frequently in the labia minora, but the early disease course affects not the vulvar architecture. During the disease progresses, the following pathological signs may be possible to occur: sexual dysfunction, fissuring in perineal region and around the clitoris, distinction between labia majora and minora, edema from inflammation, purpural lesions, and excoriations ecchymoses given fragility of the affected skin region [5, 33]. The main symptom is pruritus. Pain occurs if there are corrosions and stretch marks. Itching is intense during the night and may be so intense that it stops sleeping. Discomfort occurs when there is erosion, stretch marks, or narrowing of vaginal orifice [26–32]. Some women are asymptomatic, and LS is a random finding. Most of them had active childhood disease, which resulted in skin atrophy without symptomatology. Occasionally, hyperkeratosis and ecchymosis occur, which should be treated [26–32]. In childhood, the lesions are similar to adult lesions. But the ecchymosis may protrude and can be so intense that it leads us wrongly to the suspicion of sexual abuse. The diagnosis in most patients is indicated by the clinical picture, but its confirmation by histopathological examination is considered necessary. LS should be differentiated from lichen planus, vaginal pemphigoid, psoriasis, VIN, and SCC, and this is done by biopsy under colposcopic control. Ulcers, nodules, and granulomas should be controlled to exclude malignancy. The formation of hyperkeratotic plaques and erosions, which do not exist despite the applied treatment, suspects malignant transformation [26–32, 34].

**37**

echymoses [44–47].

*2.1.1.2 Squamous cell hyperplasia*

observed (**Figures 1** and **2**).

*Depigmentation's Disorders of the Vulva, Clinical Management*

infiltration under the homogenate area [33, 38–39].

lichen sclerosis, which may also be asymptomatic [33, 38].

Generally, the management should perform in twofold.

The first step aims to resolve LS symptoms, vulvar, and vaginal pain.

The second step's goal is to reduce the disease signs like hyperkeratosis fissuring

The oldest term leukoplakia ("chronic inflammatory disease of the mucosa which results in keratinization of the epithelium and in the formation of white spots") is still reported today. The disorder is characterized by white, tough, and overwhelmed, hyperkeratotic "plaques" of the vulvar epidermis, and a disorder of "hormonal homeostasis" in its etiology. Histologically, squamous cell hyperplasia is

Histologically, there is a decrease in subcutaneous fat, atrophy of all skin layers, and destruction of elastic tissue. The dermis is of some degree vitreous degeneration and round cell collections [35–37]. Typical histological findings are also including a thinned epidermis with areas hyperkeratosis, acanthosis, a broad band of homogenized collagen under the dermo-epidermal ligament, and lymphocyte

Few patients have thickening of the epidermis, and these are those who have not been responding to LS and who are at increased risk of developing SCC. Due to the frequent association of LS with autoimmune diseases, the appropriate control should be performed. In particular, the possibility of autoimmune thyroid disease

Squamous cell carcinoma (SCC) in women with LS is a common malignancy described. There are also reports of basal cell carcinoma and melanoma. The risk of developing SCC is about 5%. However, histopathologic examination in woman with lichen sclerosus during follow-up revealed squamous cell carcinoma. The role of HPV as a causative agent in malignant transformation is not entirely clear. There are studies suggesting the existence of two types of SCC: one type occurs in older patients with chronic LS disease and the other type is in younger women without LS but with proven infection by oncogenic HPV types. Although there is no evidence of the role of HPV as a causative agent in the development of SCC on LS, there is the theoretical risk of developing SCC from the topical use of corticosteroids, which may promote the development of HPV oncogenic strains, since it was found that in 20% of cases LS, there may be HPV infection [40–43]. More recent reports support the strong relationship of vulvar invasive squamous cell carcinoma and LS, so that lichen sclerosus is considered as precancerous damage [33]. It is not uncommon for women with carcinoma of vulva from squamous cells to also have undiagnosed

The role of midwives, especially those who have increased initiatives due to their position (e.g., the one who works in the Center of Health), is very important to properly direct these postmenopausal women. It is well known that empirical use of ointments in precancerous or cancerous lesions of the vulva delays proper treatment and requires a high degree of suspicion of the doctor and midwife for malignant malignancy [33, 38]. There is no universally accepted treatment for women with lichen sclerosus. The treatment includes education and support, change of behavior to ensure good pudding hygiene, medication, and, in a small proportion of cases, surgery or photochemotherapy. The medical treatment of the condition includes the topical use of corticosteroids, such as clobetasol [44–47]. The major importance of LS treatment is proved by the fact that about 80% of invasive squamous cell carcinoma (SCC) of the vulva in elderly patients was associated with untreated, long-term conditions of lichen sclerosus (the final stage of the vicious cycle of itching-scratching-itching).

*DOI: http://dx.doi.org/10.5772/intechopen.83595*

should be investigated [26–32, 34].

#### *Depigmentation's Disorders of the Vulva, Clinical Management DOI: http://dx.doi.org/10.5772/intechopen.83595*

*Depigmentation*

Lichen sclerosus is considered as the most common chronic lesion in vulva, referred to a chronic atrophy that usually observed after menopause. Clinically, vulva is glossy and dry, with no folds. The lesions are often symmetrical. Although the condition is observed over a wide range of ages, it has an increased incidence in women aged 50–59 years. Postmenopausal women and young girls are usually afflicted before menstruation. There is no clear justification. There is sufficient evidence of involvement of autoimmune mechanisms in the pathogenesis of lichen sclerosus. It is known that 21% of patients with lichen sclerosus also suffer from autoimmune disease more often than with thyroid disease. It is reported that 22% of patients with lichen sclerosus have an inherited history, and that 44% have one or more autoantibodies. Also, there is a correlation with HLA II antigens. There are studies associating inflammatory factors, e.g., Borrelia infection, with the development of lichen sclerosus. It is also reported that there is overexpression of wild-type P53 protein in lichen sclerosus, which occupies areas adjacent to squamous cell

Typically, the rash of lichen sclerosus begins as white polygonal papules, which flock to plaques. Typically, candlesticks and/or clearly cracked plugs appear on the surface of the plate, and they are similar to attached nozzles. Over time, plugs and craters may disappear by dropping a smooth, often porcelain plaque, and they rarely show up. Thus, the skin appears white and thin, although it may be present in SCH [26–32]. Originally, lichen sclerosus may have a bubbling consistency and is characterized by edema of the prepuce clitoris and telangiectasia of labia and purpura. Stretch marks appear mainly in the middle perineal line. Bullous lichen sclerosus is often accompanied by bleeding within the lesion, and the fillet can disappear. Later, labia minora and structures around clitoris disappeared too. The epithelium of the vagina and the cervix is not affected. However, there may be lesions in the forehead of the skin, which will lead to its constriction. Perianal

Lichen sclerosus is a benign vulva condition associated to chronic and often progressive character with dermatologic location. Among the clinical findings are included marked inflammation, epithelial thinning, distinct dermal alterations like pruritus, and pain by varying degrees. The described lesions appear most frequently in the labia minora, but the early disease course affects not the vulvar architecture. During the disease progresses, the following pathological signs may be possible to occur: sexual dysfunction, fissuring in perineal region and around the clitoris, distinction between labia majora and minora, edema from inflammation, purpural lesions, and excoriations ecchymoses given fragility of the affected skin region [5, 33]. The main symptom is pruritus. Pain occurs if there are corrosions and stretch marks. Itching is intense during the night and may be so intense that it stops sleeping. Discomfort occurs when there is erosion, stretch marks, or narrowing of vaginal orifice [26–32]. Some women are asymptomatic, and LS is a random finding. Most of them had active childhood disease, which resulted in skin atrophy without symptomatology. Occasionally, hyperkeratosis and ecchymosis occur, which should be treated [26–32]. In childhood, the lesions are similar to adult lesions. But the ecchymosis may protrude and can be so intense that it leads us wrongly to the suspicion of sexual abuse. The diagnosis in most patients is indicated by the clinical picture, but its confirmation by histopathological examination is considered necessary. LS should be differentiated from lichen planus, vaginal pemphigoid, psoriasis, VIN, and SCC, and this is done by biopsy under colposcopic control. Ulcers, nodules, and granulomas should be controlled to exclude malignancy. The formation of hyperkeratotic plaques and erosions, which do not exist despite the applied treatment, suspects

carcinoma (SCC) in which HPV is not detected.

lesions are described in 30% of cases [26–32].

malignant transformation [26–32, 34].

**36**

Histologically, there is a decrease in subcutaneous fat, atrophy of all skin layers, and destruction of elastic tissue. The dermis is of some degree vitreous degeneration and round cell collections [35–37]. Typical histological findings are also including a thinned epidermis with areas hyperkeratosis, acanthosis, a broad band of homogenized collagen under the dermo-epidermal ligament, and lymphocyte infiltration under the homogenate area [33, 38–39].

Few patients have thickening of the epidermis, and these are those who have not been responding to LS and who are at increased risk of developing SCC. Due to the frequent association of LS with autoimmune diseases, the appropriate control should be performed. In particular, the possibility of autoimmune thyroid disease should be investigated [26–32, 34].

Squamous cell carcinoma (SCC) in women with LS is a common malignancy described. There are also reports of basal cell carcinoma and melanoma. The risk of developing SCC is about 5%. However, histopathologic examination in woman with lichen sclerosus during follow-up revealed squamous cell carcinoma. The role of HPV as a causative agent in malignant transformation is not entirely clear. There are studies suggesting the existence of two types of SCC: one type occurs in older patients with chronic LS disease and the other type is in younger women without LS but with proven infection by oncogenic HPV types. Although there is no evidence of the role of HPV as a causative agent in the development of SCC on LS, there is the theoretical risk of developing SCC from the topical use of corticosteroids, which may promote the development of HPV oncogenic strains, since it was found that in 20% of cases LS, there may be HPV infection [40–43]. More recent reports support the strong relationship of vulvar invasive squamous cell carcinoma and LS, so that lichen sclerosus is considered as precancerous damage [33]. It is not uncommon for women with carcinoma of vulva from squamous cells to also have undiagnosed lichen sclerosis, which may also be asymptomatic [33, 38].

The role of midwives, especially those who have increased initiatives due to their position (e.g., the one who works in the Center of Health), is very important to properly direct these postmenopausal women. It is well known that empirical use of ointments in precancerous or cancerous lesions of the vulva delays proper treatment and requires a high degree of suspicion of the doctor and midwife for malignant malignancy [33, 38].

There is no universally accepted treatment for women with lichen sclerosus. The treatment includes education and support, change of behavior to ensure good pudding hygiene, medication, and, in a small proportion of cases, surgery or photochemotherapy. The medical treatment of the condition includes the topical use of corticosteroids, such as clobetasol [44–47]. The major importance of LS treatment is proved by the fact that about 80% of invasive squamous cell carcinoma (SCC) of the vulva in elderly patients was associated with untreated, long-term conditions of lichen sclerosus (the final stage of the vicious cycle of itching-scratching-itching). Generally, the management should perform in twofold.

The first step aims to resolve LS symptoms, vulvar, and vaginal pain.

The second step's goal is to reduce the disease signs like hyperkeratosis fissuring echymoses [44–47].

#### *2.1.1.2 Squamous cell hyperplasia*

The oldest term leukoplakia ("chronic inflammatory disease of the mucosa which results in keratinization of the epithelium and in the formation of white spots") is still reported today. The disorder is characterized by white, tough, and overwhelmed, hyperkeratotic "plaques" of the vulvar epidermis, and a disorder of "hormonal homeostasis" in its etiology. Histologically, squamous cell hyperplasia is observed (**Figures 1** and **2**).

#### **Figure 1.**

*VIN lesions are usually characterized by a change in color on the skin of the vulva. They are usually white and/ or gray.*

#### **Figure 2.**

*VIN lesions: The rarities are lesions in red and brown. Their surface may be flat or abnormal.*

This chronic and recurrent condition may occur at any age but is more common in older patients and usually manifests with pruritus. Less often, it occurs with dyspareunia or pain. It is an autoimmune condition and is associated with other autoimmune diseases such as malignant anemia, thyroid disease, diabetes mellitus, systemic lupus erythematosus, primary biliary cirrhosis, and bullous pemphigoid. Histologically, the skin appears thin with loss of the crevices found between the nipples. Surface skin is vitrified, and a set of chronic inflammatory cells is observed beneath it [48–53].

Clinically, the skin appears white, thin, and corrugated but may be overlapped and keratinized, if there is coexistence of squamous cell hyperplasia. There may also be symphysis of the clitoris or the vulva. The diagnosis is made by biopsy. Lichen sclerosus is a nonneoplastic condition but can coexist with vulvar intraepithelial neoplasia, while there is correlation with invasive squamous cell carcinoma of the vulva in 2–5% of cases. This is describing the reason why possible long-term monitoring is required every 6–12 months [26–32].

Treatment is required, especially if the condition is symptomatic, and a strong local topical steroid cream (e.g., Dermovate per 12-hour period) is usually used, which is gradually replaced by a milder formulation (e.g., hydrocortisone per hour, 24 h or less) as the symptoms require. Fluorinated corticosteroids or testosterone

**39**

*Depigmentation's Disorders of the Vulva, Clinical Management*

ointment may also be helpful. Vulvectomy has no position in this case, as the recur-

Psoriasis is manifested as dry, red, and papular rash, which is usually clearly circumscribed and extends to the thighs. Diagnosis occurs easily when bleeding is observed during the removal of classic silver-like scars. It may be difficult to differentiate psoriasis from candida infection or dermatitis because the vulva is very often fluid. Candida infection should be ruled out. The lesions can be treated locally with coal tar preparations, ultraviolet maize, steroid creams, or other suitable drugs [54–56].

It is a chronic papular rash with a bluish hue, which is located in the vulva and the bendable surfaces. It may be appeared in other areas like the mucous membrane of the oral cavity, and the diagnosis is enhanced by finding other lesions. Oral lesions precede genital lesions in one-third and simultaneously appear in half of women affected from the disease. After the vulva should be a vaginal examination, the walls of the vaginal may have following pathological abnormalities: erythema erosions and bleeding friable tissue. It is usually idiopathic but can also be related to medications. The treatment includes use of strong steroids locally or ultraviolet light, and the disease tends to subside within the next 2 years. Surgery removal

The lesions of this disease can appear anywhere on the body with a predilection in the genital area. It can be confused with LS, associated to lack the classical signs of inflammation, possible coexistence with LS based on autoimmunogenity. In contrast to LS, which has predilection for hypoostrogenic states, vitiligo can be appeared at any age. No skin biopsies are necessary. Autoimmune thyroid disease is associated to vitiligo. Treatment includes administration of topical steroids and vitamins D, E, C, and B12. Surgery remains a viable option in unresponsive local-

They are vulva disorder associated to pain. Shallow ulcers most commonly occur on the oral mucosa and less commonly on the genital mucosa. The reasons are uncertain, and risk factors include stress, infections, hormonal factors, vitamin deficiency, and family history. The diagnosis result from exclusion of various genital ulcers causing in most cases in assumption of sexually transmitted infection. Aphthosis appears in simple and rare complex form, and the recurrence rate is about 20% of the general population. For the treatment, it is important to educate the patients to conform in skin and wound care and administration of topical corticosteroid propionate ointment in cases of complex aphthosis [63–71]. Apthae should differentiate from Behcet syndrome, a disorder that causes inflammation of the blood vessels throughout the body, and could affect the vuvla causing open sores in the vulva. Furthermore, vulva aphthous ulcers could appear in patients

*DOI: http://dx.doi.org/10.5772/intechopen.83595*

*2.1.1.3 Psoriasis*

*2.1.1.4 Lichen planus*

should be avoided [57–62].

*2.1.2.1 Vitiligo*

*2.1.2.2 Apthtae*

*2.1.2 Others: vitiligo, intertrigo, aphthae*

ized disease to conventional therapies [63–71].

with HIV infection, Chrohn disease, and ulcerative colitis.

rence rate after surgery is about 50% [26–32].

ointment may also be helpful. Vulvectomy has no position in this case, as the recurrence rate after surgery is about 50% [26–32].
