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450 Non-neoplastic Lesions of the Vulva
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Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 39 Histologically, a plasma cell infil-
trate is the hallmark of this disease
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 40 The squamous epithelium in
these patients frequently shows mild spongiosis and may
be partially detached or absent
Microscopy
Aplasmacellinfiltrate is the hallmark of this
disease (Fig. 39). The histologic examination classically shows a squamous epithelium with mild
spongiosis that may be partially detached or absent
(Fig. 40). Flattening of the squamous cells with
“lozenge-shape” or “diamond-shape” (horizontal
axes longer than vertical axes) can be seen in
suprabasal epithelia layers. The underlying mucosa
displays a band-like infiltrate rich in plasma cells
with occasional mast cells, eosinophils, lymphocytes, and neutrophils(Fig. 41). As plasma cells are
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 41 The mucosa displays a band-like
infiltrate rich in plasma cells with occasional mast cells,
eosinophils, lymphocytes, and neutrophils. Red cell
extravasation is also noted
part of the usual repertoire in inflammatory diseases affecting mucosal surface, plasma cells
should make up >50% of infiltrate to consider
plasma cell vulvitis (Virgili et al. 2005). Less than
25% of plasma cells in the infiltrate is considered
nonspecific. Vascular proliferation and dilated cap-
illaries are seen in this disease associated with red
cell extravasation. Later on, hemosiderin deposition can be detected using iron stain (Fig. 42a, b).
Plasma cell vulvitis can show mucinous metaplasia
that should not be confused with extramammary
Paget disease (Thomson et al. 2007).
Immunophenotype
Analysis of the plasma cell population with kappa
and lambda CISH shows a polyclonal infiltrate
with kappa: lambda ratio of 2:1. If the clinical
presentation is not characteristics, the patient has
high risk sexual activities and/or is
immunosuppressed, and immunostaining with
antibodies against Treponema pallidum to evalu-
ate for syphilis may be considered.
Differential Diagnosis
Many diseases can be considered in the differential diagnosis of plasma cell vulvitis. Especially
important are the distinction from vulvar erosive
lichen planus, squamous cell carcinoma in situ,
syphilis, and extramammary Pagets disease.
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Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 42 With time, the red cell
Although plasma cell vulvitis and erosive lichen
planus share the presence of a band-like infiltrate
rich in plasma cells, lichen planus displays
involvement of the basal layer in the form of
vacuolar changes and dyskeratotic keratinocytes
not seen in plasma cell vulvitis. Loss of
keratinocytic maturation, full thickness cytologic atypia, and brisk mitotic activity point to
squamous cell carcinoma over plasma cell
vulvitis. Plasma cells are also an important component of the inflammatory infiltrate seen in
syphilis; however, immunohistochemical stain
against Treponema pallidum can be used to sep-
arate these diseases. Furthermore, primary chancres tend to ulcerate, and in primary and
secondary syphilitic lesions, granulomatous
infiltrate, vasculitis and lichenoid, or
psoriasiform changes can be seen. Rare cases of
plasma cell vulvitis may undergo mucinous
metaplasia raising the differential diagnosis of
extramammary Pagets disease. The nuclear
atypia, glandular formation, positive GATA3,
and CEA antibodies as well as mixed infiltrate
favor extramammary Pagets disease.
Psoriasis
Definition
Chronic relapsing papulosquamous dermatosis
characterized by increased proliferative activity
of the squamous epithelium.
extravasation leads to hemosiderin deposition (a) that can
be highlighted with iron stain (b)
Clinical Features
Psoriasis is a chronic skin condition that affects
between 1% and 2% of the US population
(Gudjonsson and Elder 2007). Vulvar psoriasis
represents approximately 5% of patients suffering
from chronic vulvar itching or burning (Kapila
et al. 2012). The incidence of vulvar psoriasis in
patient with psoriasis is estimated as 2–7%. The
perianal region is frequently affected in these
women. Although most of the patients are adults,
prepubertal girls can be affected (Morris et al.
2001). Vulva psoriasis should be considered as a
possible diagnosis in patients presenting with erythematous vulvitis without vaginitis (Kapila et al.
2012). There is no unifying explanation of the
etiopathology of psoriasis. The most recent data
supports a complex interplay of polygenetic, environmental, and autoimmune factors. Recently,
epigenetic involvements, such as the DNA methylation, chromatin modi fications, and noncoding
RNA regulation, are proposed to play seminal
roles in the pathogenesis of this disease (Shao
and Gudjonsson 2020; Billi et al. 2019). Psoriasis
has a polygenic inheritance with HLA-C
(PSORS1) major gene mapped to 6p21.3.
PSORS1 gene is seen especially in adolescent
patients with acute onset of disease (Nestle et al.
2009). Proposed immunity factors involved in this
disease include multiple cytokines (especially
interferons) and in flammatory cells (e.g., T-cell
lymphocytes). Irrespective of the pathogenic
mechanism, the final event is the acceleration of
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452 Non-neoplastic Lesions of the Vulva
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the cell cycle of the keratinocytes leading to
hyperproliferation and inflammation. Musculoskeletal and cardiovascular manifestations can be
concomitant with cutaneous psoriasis.
• Incidence
2–4% of Caucasians.
• Age
Commonly affects patients younger than
40 years (approximately 75%). In children, it
is the third cause of vulvar dermatitis after
contact dermatitis and lichen sclerosus
(Morris et al. 2001).
• Sex
Both sexes are equally affected.
• Site
Vulvar psoriasis frequently affects the mons,
labia majora, and inguinal folds.
• Treatment
Extent and severity of the disease define the
type of treatment. Topical medications include
retinoids, corticosteroids, and calcineurin
inhibitors while systemic medications include
methotrexate, cyclosporine, and retinoids. Bio-
logics have also been used in these patients
such as in the case of etanercept, infliximab,
adalimumab, efalizumab, and ustekinumab
(Foulkes et al. 2018). Close follow-up is
required in these patients due to the potentially
severe impact of genital psoriasis on patient’s
psychological and social well-being.
• Outcome
Typically, chronic course with relapses and
remissions.
areas of the vulva lead to fissure formation, maceration of the lesion, and loss of white silver scale.
This is the case of inverse psoriasis seen in the
intertriginous that presents as shiny lesions without scale (Fig. 43). Frequently, superinfection by
yeasts, fungi, and bacteria is noted. The presence
of pustules in erythematous plaques is defined as
pustular psoriasis. Reiter disease combined conjunctivitis, urethritis, and arthritis with
psoriasiform cutaneous lesions like annular circinate vulvitis, keratoderma blenorrhagicum, and
nail dystrophy. Pruritus is the main complaint in
these women. In addition, pain and rawness with
severe decreased quality of like in severe cases are
encountered. Approximately a quarter of patients
experience lesions induced by trauma on
uninvolved skin, also known as “koebnerization”
(Weiss et al. 2002). Involvement of the gluteal
cleft is often present and can be a clinical clue
for diagnosis. Frequently, extragenital lesions in
areas prone to trauma (e.g., elbows, knees, scalp,
trunk, and nails) can be seen in these women
(Fig. 44).
Microscopy
In a review of 188 vulvar biopsies in a tertiary
academic center, psoriasis was the diagnosis in
1.1% of cases (Chan and Zimar owski 2015).
Macroscopy
Psoriasis displays a wide range of clinical presentations depending on the area of the vulva
affected. Classic psoriatic lesion can be seen as
well as its variants like inverse psoriasis,
sebopsoriasis, and pustular psoriasis. The classic
psoriatic lesion is usually observed in hear-bearing skin in the form of unilateral or bilateral
sharply circumscr ibed erythematous plaque
(s) with silvery white scale. Removal of the scale
leads to pinpoi nt bleeding also called Auspitz
sign. The warmth, moisture, and friction of certain
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 43 Red, clinically nonscaling but
well-demarcated plaques of inverse psoriasis, with maceration of skin folds mimicking candidiasis. (Courtesy of
Dr. Libby Edwards)
Non-neoplastic Lesions of the Vulva 453
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neutrophils or Munro microabscesses and
intraspinous collections of neutrophils or
spongiform pustules of Kogoj are also part of
the spectrum of histologic features (Fig. 45c).
The papillary dermis shows dilated and tortuous
vessels an d perivascular lymphocytes admixed
with neutrophils. Isolated eosinophils may be
present, especially in eruptive p soriasis and
cases affecting the pe diatric age group. In
advanced lesions, epidermal changes as seen in
lichen simplex chronicus are superimposed to
the classic changes previously described.
Differential Diagnosis
Psoriasis shares with superficial fungal infection
the presence of neutrophils in the stratum corneum;
special stains like PAS orGMS can help to identify
the fungal forms (e.g., Candida sp. and dermatophytes) in the surface. Lichen simplex chronicus
unlike psoriasis shows irregular acanthosis, hypergranulosis, nonconfluent parakeratosis, and dermal
fibrosis orientedperpendicular to the surface, while
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 44 Well-demarcated plaques with
heavy white scale classic for psoriasis vulgaris on
keratinized, dry skin. (Courtesy of Dr. Libby Edwards)
psoriasis classically present regular epidermal
hyperplasia associated with hypogranulosis and
confluent parakeratosis. However, in chronic
lesions of psoriasis, features of lichen simplex
chronicus can be superimposed in psoriatic lesions
Early lesions show minimal psoriasiform epidermal hyperplasia with spongiosis associated
with neutr ophil-rich parakeratosis mounds.
Basal layer mitotic figures can be seen. The
papillary dermis shows vascular congestion,
edema, and sparse perivascular infiltrate with
rare neutro phils. The spongiosis seen in early
stages of a psoriatic lesion is also marked in
lesions involving the intertriginous area or
inverse psoriasis. Established lesions are char-
as secondary changes due to itchiness. Although
psoriasis shows spongiosis, mainly in early lesions
and intertriginous areas, chronic eczematous dermatitis shows in addition to the spongiosis hypergranulosis and absence of neutrophils and
parakeratosis. Numerous eosinophils in the dermal
inflammatory reaction favor a psoriasiform
drug reaction. Accurate diagnosis may need multiple biopsies with careful clinicopathologic
correlation.
acterized by variable epidermal hyperplasia
with elongation of the rete ridges in a regular,
club-shaped pattern also known as regular
Syphilis
psoriasiform hyperplasia (Fig. 45a). The latter
is accompanied by thinning of the suprapapillary epidermal plates and increased mito-
Synonyms
Lues.
ses in the basal layer. Premature keratinization
of the epidermis leads to confluent parakeratosis
and diminishment o f the granular layer
(Fig. 45b). Intra corneal collections of
Definition
Sexually transmitted disease caused by infection
with the spirochete Treponema pallidum
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454 Non-neoplastic Lesions of the Vulva
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Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 45 Histologically, established lesions
of psoriasis are characterized by epidermal hyperplasia
with elongation of the rete ridges in a regular, club-shaped
pattern also known as regular psoriasiform hyperplasia (a).
The latter is accompanied by thinning of the suprapapillary
Clinical Features
• Incidence
Historically, the incidenc e of syphilis has
decreased significantly after the introduction
of penicillin treatment in the 1940s to reach
an all-time low in the USA of 2.1 cases/
100,000 persons (Centers for Disease and
Prevention 2006). Since then, the incidence
has increased steadily in recent years to 5.3
cases/100,000 persons in 2013 (Patton et al.
2014). Over 60% of the new cases are detected
in men having sex with other men although
increases have been also noted in women and
epidermal plates (arrow) and increased mitoses (arrow).
Premature keratinization of the epidermis leads to confluent parakeratosis and diminishment of the granular layer
(b). Intracorneal collections of neutrophils or Munro
microabscesses are also part of the spectrum of histologic
features (c)
all age groups and ethnicities (Patton et al.
2014). There has been also an increase in con-
genital syphilis in the recent years (Miller and
Karras 2010).
• Age
Syphilis affects usually young adults;however,
recently an increased incidence has been
documented in all age groups including older
individuals (Mattei et al. 2012).
• Site
Primary infection can occur anywhere on the
anogenital skin but is more commonly seen on
the labia majora or minora.
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• Treatment
Penicillin represents the first line of treatment
for all forms of syphilis. Alternative regimens
for nonpregnant patients with no evidence of
central nervous system involvement include
doxycycline, tetracycline, ceftriaxone, and
azithromycin (Brown and Frank 2003).
• Outcome
Good outcome for treated cases. Untreated
syphilis can progress from primary to second-
ary, and latent to tertiary phases.
Macroscopy
Syphilis has several phases of infection: primary,
secondary, latent, and tertiary. Primary phase of
infection results in a chancre, presenting
20–30 days after exposure as an indurated,
punched-out painless ulcer (Mattei et al. 2012).
Unilateral inguinal lymph node involvement can
be seen. Chancres can be painful due to superinfection which is common on vulvar lesions. The
primary chancre resolves in 1–4 weeks, faster
when treated.
Secondary syphilis presents at 6 weeks to
6 months after untreated primary infection as a
maculopapular eruption involving the trunk, face,
and extremities (Baughn and Musher 2005;
Mattei et al. 2012). Clinical presentation of secondary syphilis can be subtle which makes it
prone for underdiagnosis. Condyloma lata represents a type of secondary syphilis involving the
vulva, characterized by a verrucous morphology
that resembles condyloma acuminatum. Secondary lesions resolve usually in 2 weeks to 3 months
even without treatment. Tertiary syphilis develops
in about one-third of untreated patients and manifests as noduloulcerative cutaneous lesions
(gumma), cardiovascular syphilis, and
neurosyphilis (Chung et al. 1991). Finally, latent
phase occurs in asymptomatic but seropositive
patients.
lymphocytes, histiocytes, and a variable number
of plasma cells (Figs. 46 and 47). Small vessels
may show endothelial swelling and perivascular
plasma cells (Fig. 48). The spirochetes can be
identified with a Warthin-Starry special stain or
with a specific immunohistochemical stain often
in a perivascular distribution and in the epidermis
or mucosa (Fig. 49). Lesions of secondary syphilis
have a more variable constellation of histologic
findings. Most will show irregular epidermal
acanthosis and elongated rete ridges with a superficial and deep perivascular and often lichenoid
inflammatory infiltrate containing lymphocytes,
histiocytes, and plasma cells. Endothelial swelling
can also be appreciated (Puavilai et al. 1993).
Neutrophils are less common in late lesions.
N
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 46 Primary chancre showing irregular
epidermal acanthosis with ulceration and a dense inflammatory infiltrate
Microscopy
Lesions of syphilis commonly encountered on the
vulva are primary chancre and condyloma lata.
Primary syphilis is characterized by epidermal
hyperplasia accompanied by a dense inflammatory infiltrate composed of neutrophils
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 47 Primary chancre demonstrating a
lymphoplasmacytic inflammatory infiltrate with
intraepidermal neutrophils
456 Non-neoplastic Lesions of the Vulva
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Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 48 Endothelial swelling accompanied
by a perivascular plasmacytic infiltrate
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 49 Immunohistochemical stain for
Treponema pallidum demonstrating spirochetes in a perivascular distribution
Other histologic features include vacuolarinterface dermatitis, epidermal effacement, and
lymphocytes with ample cytoplasm. Cases with
only a few histologic findings occur and are prone
to misdiagnosis (Flamm et al. 2015). In contrast to
primary lesions, in secondary syphilis the spirochetes are mainly located intraepidermal/
intramucosal and not as much around the vessels
(Martin-Ezquerra et al. 2009). Condyloma lata
lesions demonstrate marked epidermal acanthosis
often with pseudoepitheliomatous hyperplasia
and numerous plasma cells in a perivascular distribution (Figs. 50 and 51). Similar to other cases
of secondary syphilis, the spirochetes are mainly
located intraepidermal or intramucosal (Fig. 52).
Lesions of tertiary syphilis have a granulomatous
histology.
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 50 A lesion of condyloma lata show-
ing pseudoepitheliomatous hyperplasia anda dense inflammatory infiltrate
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 51 At higher magnification, there are
numerous plasma cells surrounding vessels with endothelial swelling
Immunophenotype
An immunohistochemical stain specific for Treponema pallidum is available, and it is the preferred
ancillary test currently due to higher specificity
and sensitivity compared to Warthin-Starry special stain.
Differential Diagnosis
As the histologic features of primary and secondary syphilis are not specific, correct diagnosis
requires good clinicopathologic correlations and
a high index of suspicion. In thevulva, differential
diagnosis is with other entities presenting with
ulceration including chancroid, granuloma
inguinale, and lymphogranuloma venereum.
Another entity in the differential diagnosis is
Non-neoplastic Lesions of the Vulva 457
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most common presenting symptom is pruritus
with a minority of patients reporting pain or no
symptoms.
Erosive lichen planus is the most common
type th at affects the vulva. In a recent consensus, the diagnosis of erosive lichen planus can
be made with at least three of the following
clinical and histologic features: (1) welldemarcated erosions at vaginal introitus,
(2) hyperkeratotic border or Wickhams striae
in surroundin g skin, (3) scarring or loss of archi-
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 52 Immunohistochemical stain for
Treponema pallidum demonstrating spirochetes within
the epidermis
tecture, (4) pain or burning, (5) other mucosal
involvement, (6) vaginal inflammation,
(7) band-like infiltrate at the dermal-epidermal
junction, (8) lymphocyte predominance, (9) and
evidence of basal layer degeneration (Simpson
Zoon (plasma cell) vulvitis which is a rare disease
et al. 2013).
characterized by a plasma cell-rich infiltrate.
Performing a spirochete stain is advised when
there is a suspicion of spirochete infection.
Clinical Features
• Incidence
The general incidence of vulvar lichen planus
is unknown. In a study of women in a specialty
Lichen Planus
vulvar clinic, 3.7% had histologically con-
firmed lichen planus (Micheletti et al. 2000).
Definition
Lichen planus is a chronic inflammatory T-cellmediated skin disorder that has been reported in
association with immune deficiency, malignancy,
cirrhosis, peptic ulcer d isease, hepatitis C,
hepatitis B, and ulcerative colitis. An association
with other autoimmune diseases including alopecia areata, vitiligo, and thyroid disease has also
been reported (Lewis and Bogliatto 2013).
Approximately half of women with lichen planus
have genital involvement (Lewis et al. 1996).
Three types of lichen planus involve the vulva:
erosive lichen planus, hypertrophic lichen planus,
and classic lichen planus. Vulvovaginal-gingival
syndrome is a subtype of erosive lichen planus
that involves the vulva, vagina, and gingival
margins.
The clinical symptomatology of vulvar lichen
planus patients varies somewhat depending on
type. In erosive lichen planus, patients may present with pain, pruritus, and dyspareunia.
A minority of patients may also have blood-tinged
vaginal discharge and/or dysuria. In nonerosive
lichen planus (hypertrophic and classic types), the
• Age (Day et al. 2020)
Vulvar lichen planus most commonly affects
postmenopausal women. The mean age of
women affected by erosive lichen planus is
57–67 years; however, it occasionally presents
in reproductive-age women as young as
26 years of age. The mean age of women
affected by nonerosive lichen planus is 63;
however, a wide age range of 21–88 years
can be affected. In contrast, vulvovaginalgingival syndrome typically has an earlier age
of onset and may present in adolescence.
• Site (Day et al. 2020; Regauer et al. 2014;
Hoang et al. 2014)
Erosive lichen planus may involve the labia
minora, vestibule, a nd/or vagina. Lesions are
often bilateral or demonstrate a horseshoe
morphology affecting the inner labia minora,
clitoral frenulum, and/or posterior fourchette.
Hair-bearing skin is not involved in this type.
Anywhere on the vulvar can be the site for
presentation of classic vulvar lichen planus.
In hypertrophic lichen planus, the vulvar and
perianal areas are frequently affected.
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• Treatment
Vulvar lichen planus can be challenging to
treat and tends to recur after treatment is
discontinued. Treatment goals include reduction of symptoms and prevention of scarring.
Potent topical steroids are considered first-line
therapy. Topical calcineurin inhibitors have
also been used. There is no consensus regarding the utility of systemic therapy in vulvar
lichen planus. More rapid initial control and
better maintenance of control have been
reported with a combination of oral and topical
therapy; however, another study did not find
any consistently effective systemic treatments
(Bradford and Fischer 2013; Cooper and
Wojnarowska 2006). Oral therapies that have
been used include oral steroids and methotrexate. Other anecdotally report ed effective therapies in corticosteroid-resistant patients include
griseofulvin, ciclosporin, dapsone, and
hydroxychloroquine (Lewis and Bogliatto
2013). Surgical management may be needed
for correction of introital stenosis and division
of vulval adhesions.
• Outcome
Erosive lichen planus is associated with scarring and architectural changes including loss of
labia minora, sealing of clitoral hood,
narrowing of the introitus, and burial of the
clitoris (Hoang et al. 2014; Lewis and
Bogliatto 2013; Day et al. 2020). Vaginal
involvement by erosive lichen planus can
cause vaginal synechiae and stenosis (Lewis
and Bogliatto 2013). Classic lichen planus is
not associated with distortion of the normal
anatomy of the vulva. It is unknown whether
hypertrophic lichen planus is associated with
architectural changes (Day et al. 2020).
Controversy exists whether there is an
increased risk of squamous cell carcinoma in
patients with vulvar lichen planus. In a study
by Regauer et al. of 38 patients with primary
lichen planus-associated vulvar SCC, vulvar
lichen planus was associated with an increased
risk of squamous cell carcinoma (SCC) arising
in a background of differentiated vulvar
intraepithelial neoplasia (dVIN). In their
study population, SCC, which was seen in
patients with both erosive and nonerosive
lichen planus, behaved aggressively with high
rates of regional lymph node metastasis at presentation (nearly 50%) and recurrence (40%
within the first post-operative year). Total
30% of disease-related deaths were reported
(Regauer et al. 2014). In contrast, a study by
Day et al. did not identify an association
between lichen planus and HPV-independentsquamous cell carcinoma in vulvar excisions
over an 11 year period. All non-HPV related
squamous cell carcinoma excisions were associated with lichen sclerosus either at the time of
excision (95%) or on follow-up biopsies (5%)
(Day et al. 2018). In a recent review of
127 women with vulvar lichen planus from
Portugal, 1.6% developed vulvar SCC after a
mean follow-up of 4 years. The authors concluded that malignant transformation in
women with vulvar LP under surveillance and
treatment is low (Lyra et al. 2021). They also
emphasized the need of closely following up
these patients with biopsy of any suspicious
lesion. The prevalence of malignancy in
women with vulvar lichen planus in Portugal
is similar to that reported in a multicentric audit
in the United Kingdom (2.3% in a total of
175 cases) (Simpson et al. 2012), in a vulvar
clinic in Rotterdam with 2.1% in 95 cases
(Santegoets et al. 2010), and 0.14% of vulvar
cancer in 13,100 women from Finland
(Halonin et al. 2018).
Macroscopy
In erosive lichen planus, the physical exam demonstrates well-demarcated, bright red to purple
erosions (Fig. 53). There may be a superimposed
white lacy pattern at the periphery, lateral white
papules, or a white border around the red patch/
erosion. As described above, scarring with architectural changes can develop.
In classic type vulvar lichen planus, the physical exam is similar to that seen at other sites.
Lesions are moderately to well-demarcated
plaques or papules with a smooth surface co ntour.
Color may vary from gray-white to pink-red to
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purple-brown. Overlying lacy reticulation, known
as Wickhams striae, may be present.
In hypertrophic lichen planus, lesions are moderately demarcated thickened, warty pink-red
plaques with a purplish to violaceous edge (Day
et al. 2020; Lewis and Bogliatto 2013).
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 53 Clinically, the patients suffering
from erosive lichen planus demonstrate well-demarcated
bright red erosions with surrounding white epithelium and
typical scarring with loss of the labia minora and near loss
of the clitoral hood. (Courtesy of Dr. Libby Edwards)
Microscopy
All types of vulvar lichen planus demonstrate a
lichenoid tissue reaction characterized by a bandlike lymphocytic infiltrate at the dermalepidermal junction with basal layer damage in
the form of vacuolar changes and dyskeratotic
basal keratinocytes (Fig. 54a, b). There is variability in the histopathologic findings depending on
type.
The basal layer degeneration in erosive
lichen planus is divided into two categories:
degenerative and regenerativ e. In both types,
there is a band-like lymphocytic infiltrate at
the dermal-epidermal junction with absent or
reduced rete ridges. In degenerative type, there
is absent or minimal acanthosis w ith
squamatization, vacuolar de generation, and/or
dyskeratosis of the basal layer. Scattered plasma
cells and eosinophils may be present among the
dermal in filtrate (Day et al. 2020). Areas that a re
histologically indistinguishable from classic
lichen planus may correspond to white reticulation adjacent to or within the erosive area; therefore, a biopsy from this clinical area may
increase diagnostic accuracy. Regenerativetype erosive lichen planus has a thin epidermis
N
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 54 Histologically, erosive lichen
planus like the other variants shows a lichenoid tissue
reaction characterized by a band-like lymphocytic infiltrate
at the dermal-epidermal junction (a) with basal layer damage in the form of vacuolar changes and dyskeratotic basal
keratinocytes (arrows) (b)
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