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460 Non-neoplastic Lesions of the Vulva
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and lacks the surface keratin layer. Nuclear
enlargement, hyperchromasia, loss of maturation, and increased mitotic activity may be evident in the basal layer. Both patterns may be
seen in the same patient and/or biopsy. Erosive
lichen planus may show nonspecificfeatures,
which may present a challeng e in making a
definitive diagnosis (Hoang et al. 2014;Lewis
and Bogliatto 2013).
Classic-type vulvar lichen planus is similar
histologically to lichen planus involving other
sites. Histologic findings include compact
hyperkeratosis, wedge-shaped hypergranulosis
with saw-tooth acanthosis of the epidermis
(Fig. 55a–c). A band-like infiltrate of lymphocytes is present in close proximity to the dermal-
epidermal junction with vacuolar changes and
dyskeratosis of the basal keratinocytes. Melanin
incontinence can be seen.
Hypertrophic lichen planus is similar to classic
lichen planus with more pronounced, irregular
acanthosis (Fig. 56a). Basal layer degeneration,
including vacuolar changes and dyskeratotic
keratinocytes may be restricted to the tips of the
rete ridges (Fig. 56b, c). Parakeratosis and
pseudoepitheliomatous hyperplasia may be seen.
Differential Diagnosis
Lichen sclerosus is a primary differential diagnostic consideration, especially in the absence of sclerosis. To distinguish early lichen sclerosus from
early lichen planus, Fung and LeBoit found that
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 55 Histologically, classic-type vulvar
lichen planus displays at low power compact hyperkeratosis, wedge-shaped hypergranulosis, and a band like
chronic inflammation (a). Squamous acanthosis with
saw-tooth rete ridges is seen (arrow) (b). The band-like
infiltrate of lymphocytes is presentin close proximityto the
dermal-epidermal junction with vacuolar changes and
dyskeratosis of the basal keratinocytes (c)
Non-neoplastic Lesions of the Vulva 461
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Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 56 Histologically, hypertrophic lichen
planus is characterized by more pronounced, irregular
psoriasiform lichenoid pattern, basilar
epidermotropism, basement membrane thickening,
absence of basal squamatization, absence of
wedge-shaped hypergranulosis, absence of cytoid
bodies, and absence of saw-tooth rete ridges all
favored lichen sclerosus over lichen planus (Fung
and LeBoit 1998). Niamh et al. found that sclerosis,
acanthosis, ectatic vessels, intraepidermal lymphocytes, and abnormal collagen were the most common features in early lichen sclerosus (Niamh et al.
2009). The presence of columnar parakeratosis in
association with thinning of the suprapapillary epidermis with presence of dyskeratotic cells with
tendency to group points to the diagnosis of lichen
sclerosus (Weyers 2013, 2015). In the absence of
sclerosis, all the abovementioned histologic clues
are less distinctive; however, a constellation of
acanthosis (a). Basal layer degeneration, including vacuolar changes and dyskeratotic keratinocytes, may be
restricted to the tips of the rete ridges (b, c)
these histologic features allows to support in the
right clinical scenario the diagnosis of lichen
sclerosus. When there are no features specificto
lichen sclerosus or lichen planus present in the
biopsy, a diagnosis of “lichenoid dermatitis” can
be rendered with recommendation to correlate with
the clinical findings.
Due to the presence of nuclear enlargement,
hyperchromasia, and increased mitotic activity in
the basal layer of regenerative-type erosive lichen
planus, dysplasia (both dVIN and high-grade
squamous intraepithelial lesion (HSIL)) is in the
differential diagnosis. Block p16 positivity supports a diagnosis of HSIL. Both erosive lichen
planus and dVIN can overexpress p53 in the basilar nuclei. Complete absence of p53 expression
excludes a diagnosis of lichen planus and supports
N
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a diagnosis of dVIN. This is a challenging differential, and careful clinicopathologic correlation is
necessary (Day et al. 2020).
Squamous cell carcinoma may need to be differentiated from hypertrophic lichen planus. Features favoring squamous cell carcinoma include
adjacent dysplasia (dVIN or HSIL), atypical
nuclei, and abnormal mitoses (Day et al. 2020).
Graft-versus-host disease (GVHD) can mimic
lichen planus histologically and requires correlation with a history of transplant. Lichenoid drug
eruption can be favored when excessive eosinophils, presence of parakeratosis, or multiple
inflammatory patterns are present (Day et al.
2020). If immunobullous disease is a consider-
ation, direct immunofluorescence will be of value.
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Non-trophoblastic Tumors of the Placenta, Pathology of the Placenta 469
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• Sex
Non-trophoblastic Tumors of
the Placenta, Pathology of the
Placenta
Joseph T. Rabban
University of California – San Francisco,
San Francisco, CA, USA
Synonyms
Metastatic fetal malignancy involving placenta;
Metastatic maternal malignancy involving
placenta.
Definition
Metastasis of malignant tumors of maternal origin
or fetal origin may involve the placenta. Uterine
mesenchymal tumors may adhere to the placenta
during delivery, simulating a primary placental
tumor.
Not applicable.
• Site
Not applicable.
• Treatment
Not applicable.
• Outcome
Both the maternal and fetal outcome of metastasis of maternal malignancy to the placenta is
generally poor, particularly for maternal melanoma and hematological malignancies. Vertical transmission to the fetus can occur.
Metastasis of fetal hematological malignancy
to the placenta portends poor prognosis for the
fetus though the maternal outcome is good.
Transplacental transmission of fetal malignancy to the mother has not been welldocumented. Uterine mesenchymal tumors,
such as inflammatory myofibroblastic tumor,
which adhere to the placenta are not of true
placental origin and are thought to carry the
same prognosis as those that are occur outside
of pregnancy.
Macroscopy
Clinical Features
• Incidence
Metastasis of primary maternal or fetal malig-
nancy to the placenta is exceedingly rare. The
incidence is unknown. The most common
maternal malignancies to involve the placenta
are melanoma, hematological malignancies,
breast cancer, lung cancer, and cervical cancer.
The most common fetal malignancies to
involve the placenta are hematological malig-
nancies and neuroblastoma. Small case series
of uterine inflammatory myofibroblastic tumor
adherent to the placenta have been reported;
these are not truly of placental origin, as con-
firmed by molecular evidence, but are coinci-
dental co-existing uterine tumors that are
identified at the time of delivery.
• Age
Not applicable.
Maternal malignancies may be visible by macroscopic examination in some cases or only microscopically evident in other cases. Maternal
melanoma may be pigmented or nonpigmented.
Fetal malignancies involving the placenta are typically seen only on microscopic examination.
Uterine mesenchymal tumors adherent to the placenta appear similar to their counterparts in the
nonpregnant setting.
Microscopy
Metastasis of maternal malignancies may
involve the intervillous space and/or invade villous stroma and fetal vessels. Fetal hematologic
malignancies may extensively involve the fetal
vessels throughout the placenta and may be present in the intervillous space. Uterine mesenchymal tumors adherent to the placenta appear
N
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