BENIGN

SKIN LESIONS
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 Most skin lesions are benign; however, some concern
has caused the patient to make an inquiry, and a correct
diagnosis is important.
 The following 3 general types of characteristics must
been considered when defining a benign lesion:
1. Characteristics outside of the lesion e.g. patient age, ethnicity,
presence of associated symptoms, related systemic disorders, and
location.
2. Physical characteristics of the lesion
3. Histologic characteristics of the lesion
 Initially, benign lesions must be differentiated from
malignant lesions. This is best done by being familiar
with characteristics of common malignant lesions.
 The clinician should try to categorize any skin lesion
as one of the following:
a. most likely benign,
b. most likely malignant,
c. or unclear.
the last 2 categories should be biopsied.
 Benign lesions of the surface epithelium.
 Cutaneous Cysts.
 Benign Melanocytic Neoplasms
 Neoplasms and proliferations of follicular lineage
 Neoplasms and proliferations with sebaceous
differentiation
 Neoplasms and proliferations with apocrine
differentiation
 Neoplasms and proliferations with eccrine differentiation
 Fibrous and Fibrohistiocytic Proliferations of the Skin
and Tendons
 Muscle, Adipose and Cartilage Neoplasms
 Vascular Neoplasms
 MULTIPLE SOLITARY LINEAR
1. Seborrheic keratosis 1. Inverted follicular 1. Epidermal nevus
2. DPN keratosis 2. ILVEN
3. Stucco keratosis 2. Keratoacanthoma 3. Linear porokeratosis
4. Disseminated superficial 3. Cutaneous horn 4. Nevus comedonicus
actinic porokeratosis 4. Clear cell acanthoma 5. Mosaic form of Darier
5. Porokeratosis palmaris 5. Warty dyskeratoma disease
et plantaris disseminata 6. Lichenoid keratosis
6. Acrokeratosis
verruciformis of Hopf
 SKs usually begin to appear during and
after the fourth decade and continue to
arise throughout life.
 An apparent familial predisposition with a
postulated autosomal dominant inheritance.
 They only occur on hair bearing skin. Can
arise on all body surfaces except mucosa,
palms and soles.
 Though harmless, SKs can occasionally
become irritated or can be cosmetically
bothersome.
 The exact cause of seborrhoeic keratoses is not known may be;
1. There is a familial predisposition in those with hundreds of lesions.
2. Sun exposure (Although SKs are common in areas covered by
clothing) higher prevalence of SKs within sun-exposed areas such
as the head and neck in contrast to non-sun exposed areas in the
same subjects.
3. Very rarely, eruptive SKs may denote an underlying internal
malignancy. The syndrome is known as the sign of Leser-Trélat.
4. Neoplastic origin (somatic mutations).
5. HPV may be implicated.
 Typically appear as sharply marginated, pigmented lesions.
 They may be macules, papules, plaques or even
pedunculated, depending on their stage of development.
 Color is variable even within the same lesion (pink, yellow,
flesh colored, tan, brown, black).
 Surface is usually waxy and the texture can vary from
smooth, velvety to verrucous.
 Often multiple & can be extensive.
 Keratotic plugging with follicular prominence.
 They have a stuck-on quality.
 SKs can develop on the face, neck and trunk (especially the
upper back), as well as the extremities.
 Usually measure about 1 cm in diameter but they can
become quite large, i.e. > 5 cm in diameter.
 Lesions may become inflamed due to rupture of the small
pseudocysts they contain or from trauma, or rarely from
infection with microorganisms such as Staphylococcus
aureus.
 Conditions associated with an abrupt “flare” of lesions
followed by regression include pregnancy, coexisting
inflammatory dermatoses (in particular erythroderma) and
malignancy.
Velvety, dark brown Light tan or Verrucous, tan
almost skin
colored
Multiple SKs
Multiple SKs
 If you are in doubt of the diagnosis, try gently picking
or scratching the lesion. It may crumble,
hyperkeratotic scale, or lift off, revealing that
superficial waxy character.
This SK has been partially picked off (If picked off
or curetted, SKs will leave a pink moist base with
minimal bleeding)
• Use dermoscopy to look for
keratin pseudocysts.
• These are small white spots
commonly found in seborrheic
keratoses.
Seborrheic keratosis
clinical white spots are directly comparable with the horn pseudocysts
which is it histological equivalent.
Dermoscopy of SKs showing horny pseudocysts
Leser-Trélat sign
 It is not precancerous.
 SCC cutaneous melanoma, BCC, keratoacanthoma, and SCC in situ have all
been rarely observed in association with SKs. This represents a coincidental
neoplasm developing in adjacent skin.
 The sign of Leser–Trélat is a rare cutaneous marker of internal malignancy (in
particular gastric (60%) or colonic adenocarcinoma, breast carcinoma, and
lymphoma). It is considered to be a paraneoplastic cutaneous syndrome
characterized by an abrupt and striking  in the number and/or size of SKs
occurring before, during or after an internal malignancy has been detected
majority and of the lesions are located on the back, followed by the extremities,
face and abdomen and usually associated with pruritus. Neoplasm may secrete
TGF-alpha  epithelial hyperplasia.
I. IRRITATED SEBORRHOEIC KERATOSIS
II. DERMATOSIS PAPULOSA NIGRA
III. STUCCO KERATOSES
IV. INVERTED FOLLICULAR KERATOSES
• Inflamed lesion, often red, edematous
and crusted.
Irritated SKs
erythematous, edematous and crusty
 Multiple, small, symmetric hyperpigmented,
sessile to filiform, smooth-surfaced papules
measuring from 1 to 5 mm.
 Arise in darker skin types, usually on the cheeks,
temples. Less often, lesions are on the neck,
chest and back.
 It has a strong familial predisposition. Women
are twice as likely to be affected as men.
 It tends to have an earlier age of onset (during
adolescence) than that of SKs.
 HP pattern quite similar to the acanthotic type of
SK.
DPN
 Small white-gray papules or plaques scattered on
dorsal feet and ankles of older fair-skinned
individuals.
 Lesions are “stuck on”, and when scraped off, with a
fingernail and there is usually minimal, if any,
bleeding. A collarette of dry scale may remain
 The papules may number in the hundreds. They are
usually small, measuring from 1 to 4 mm, but rarely
individual plaques may be as large as a few centim-
eters.
 There is no familial predilection.
 Men are four times more likely to be affected than
women.
 It displays prominent orthokeratotic hyperkeratosis
and papillomatosis, often showing “church spire”
pattern.
 Asymptomatic solitary firm, white to light-tan
or pinkish papules usually less than 1 cm in
diameter on face or neck of middle-aged and
older adults.
 They are typically stable and persistent
lesions, but may regress.
 Benign endophytic variant of irritated SK.
 It is derived from the infundibulum of the hair
follicle.
 Histologically, The keratinocyte
proliferation seems to surround one or
several follicular canals that open to the
surface. squamous eddies and inflammation
are common.
Histopathology of IFK
 There are at least six histologic types of SK but different histologic
features are often present in the same lesion:
1. Acanthotic: the most common.
2. Hyperkeratotic: more prominent hyperkeratosis and papillomatosis.
3. Reticulated: delicate strands of epithelium that extend from the
epidermis in an interlacing pattern.
4. Irritated: perivascular, diffuse or lichenoid lymphoid infiltrate.
Squamous eddies are common findings.
5. Clonal: well defined nests of loosely packed uniform cells in the
epithelium.
6. Melanoacanthoma: shows dendritic melanocytes packed with melanin
which is absent in keratinocytes.
 Usually presents as a smooth surfaced, dome -
shaped papule. Slight hyperkeratosis and
papillomatosis are often present, while the
greatly thickened epidermis typically contains a
preponderance of basaloid cells.
 Sharply demarcated horizontal base called
“string”.
 Papillae may be narrow in some lesions.
 Invaginated horn pseudocysts are most
prevalent in this variant.
 This type often contains an amount of pigment
superior in quantity than others; it is primarily
concentrated in keratinocytes and is transferred
from neighboring melanocytes and deeply
pigmented lesions contain abundant melanin in
basaloid cells.
Acanthotic type
Hyperkeratotic type
with church spires of papillomatosis and hyperkeratosis & preponderance
of squamous cells relative to basaloid cells
Reticulated type
with delicate, lace-like strands of interconnecting epithelium composed of a double
row or more of hyperpigmented basaloid cells and interspersed horn pseudocysts
Reticulated type
Irritated type
exophytic lesion with papillomatosis, hyperkeratosis, hemorrhagic crust
and dermal inflammation
Clonal type
with Borst–Jadassohn phenomenon* characterized by well-demarcated nests
of keratinocytes within the epidermis
* ‘clones’ of basaloid, squamatized, or pale keratinocytes in epidermis appear different than their neighbors
 Assurance.
 Superficial destructive means mainly for
cosmetic reasons;
1. Cryotherapy: The most commonly used method but
can result in hypopigmentation in dark individuals.
2. Curettage.
3. Electrodessication (very light) is often safe.
4. Shave excision
5. Scissor snip (pedunculated lesions & DPN).
6. Laser ablation (pulsed CO2, erbium: YAG)
 Full thickness excision: if melanoma is
considered in the differential diagnosis for
histology.
 They are due to an hamartoma of the epidermis present at
birth (50%) or develop during childhood (mostly in the first
year of life) and persist indefinitely.
 The abnormality arises from a defect in the ectoderm (outer
layer of the embryo that gives rise to epidermis and neural
tissue).
 Most commonly, hyperpigmented papillomatous papules
and plaques appear in a linear array along Blaschko’s lines.
 The incidence of epidermal nevus is estimated to be 1 in
1000 infants.
 Sporadic rarely inherited.
Blaschko’s lines
 Originate from pluripotent cells in the basal layer
of the embryonic epidermis.
 Mosaicism (skin cells that have the active
abnormal gene spread out to form the epidermal
naevus, whereas the remaining skin cells form the
other areas of apparently normal skin) for
activating mutations in the gene that encodes
fibroblast growth factor receptor 3 (FGFR3) was
demonstrated in “common” epidermal nevi.
 While these lesions are classically referred to as
“epidermal” nevi, the hamartomatous process
also involves at least some portion of the dermis,
especially the papillary dermis.
Epidermal Naevi
Epidermal Naevi
 Epidermal nevi most commonly present as a
single linear lesion, but sometimes multiple
unilateral or bilateral linear plaques are seen.
 Asymptomatic well circumscribed,
hyperpigmented, papillomatous papules or
plaques.
 The earliest lesions may be macular once
developed, it become thickened and more
verrucous, especially over joints and in
flexural areas.
 Occur most commonly on trunk, extremities
or neck following Blaschko’s lines.
TYPES OF EPIDERMAL NAEVI:
1. Localized Linear Epidermal Naevus (Nevus
Verrucosus)
2. Naevus Unius Lateris
3. Systematised Epidermal Naevus (Ichthyosis Hystrix)
4. ILVEN
5. Epidermolytic Epidermal Naevus
6. Acantholytic Epidermal Naevus
NEVUS UNIUS LATERIS:
 It is a variant in which there are extensive
unilateral plaques, often involving the
trunk.
SYSTEMATIZED EPIDERMAL
NEVUS (ICHTHYOSIS HYSTRIX)
 It is a variant with extensive
bilateral involvement, also
usually on the trunk.
 EPIDERMAL NEVUS
SYNDROME is diagnosed
when epidermal nevi occur
in combination with other
developmental anomalies.
 These abnormalities most
commonly involve the
neurologic or musculoskel-
etal systems.
 All epidermal nevi are
characterized by epidermal
hyperplasia, hyperkeratosis,
acanthosis, papillomatosis, and
variable parakeratosis.
 Other findings such as
epidermolytic hyperkeratosis
and focal acantholytic dyskerato-
sis may be prominent features.
 Neoplasms such as BCC, SCC
and keratoacanthoma may rarely
develop in association with
epidermal nevi.
 Infants and children with epidermal nevi, particularly multiple or extensive
lesions, require a thorough evaluation for systemic abnormalities.
 MEDICAL:
1. Topical therapies such as corticosteroids, retinoic acid, tars, anthralin, 5-fluorouracil
and podophyllin have all been used, but they are of limited benefit.
2. Oral therapy with systemic retinoids for long term has been reported to be effective at
decreasing the thickness of systematized epidermal nevi, although it does not result in
resolution.
 SURGICAL:
1. Superficial destructive means (e.g. by cryotherapy, shave excision or curettage)
recurrence is common as only the epidermis is removed. Laser ablation may also be
undertaken, but, to be effective, it must induce scarring and fibrosis of at least the
papillary dermis. Therefore, this treatment is often not cosmetically acceptable to
patients and test sites are recommended.
2. Full thickness surgical excision is curative but can be complicated by hypertrophic
scars or keloid formation.
 It is relatively rare, linear, psoriasiform
plaque that usually presents on one
extremity and appears before the age of 5
years in 75% of patients.
 Four times more common in girls.
 The definitive cause is unknown. As it
bears some resemblance to psoriasis
histologically, some believe that the two
conditions share a common pathogenesis.
 Rarely arthritis may be associated with
ILVEN.
ILVEN
 Psoriasiform appearance.
 Significant pruritus.
 Scaly, erythematous papules
coalesce to form a linear plaque,
almost always unilateral on a limb of
a child.
 Most lesions spontaneously resolve
by adulthood.
 Psoriasiform histology.
 Elongated rete ridges.
 Broad zones of parakeratosis without
an underlying granular layer alternate
abruptly with depressed regions of
orthokeratosis and hypergranulosis.
 There is often exocytosis of
lymphocytes and neutrophils into the
spongiotic papillomatous epidermis
and occasionally Munro’s
microabscesses may be seen.
 ILVEN is difficult to treat. Treatments that are successful in psoriasis
are only partially effective for ILVEN.
 MEDICAL:
1. Combination therapy with topical tretinoin and 5-fluorouracil creams
has been employed with beneficial results, but long-term success can
only be achieved with maintenance therapy.
2. Calcipotriol may be partially effective.
 SURGICAL:
1. Pulsed dye laser has been used successfully in some cases.
2. Surgical excision is effective but results in scarring.
 Rare benign hamartoma of the
pilosebaceous unit resulting in
numerous dilated, keratin filled
comedones usually arising before the
age of 10 years.
 It is due to genetic mosaicism with
FGFR2 mutation.
 Sometimes follow the lines of Blaschko.
 Hormonal influences of puberty often
worsen the condition.
Nevus Comedonicus
 Usually a single circumscribed
area or linear streak composed of
clusters of dilated follicular ostia
with central keratinous plugs
contain firm, darkly pigmented,
cornified material.
 Their size is variable and they can
range from a few centimeters in
diameter to extensive lesions
affecting half of the body.
 The site most commonly affected is the face,
followed by the trunk, neck and upper
extremity.
 These nevi may also arise in areas that are
devoid of hair follicles such as the palms,
soles and glans penis. When present on the
elbows and knees, lesions can be
verrucous in appearance.
 Rarely, at puberty or later, it may develop
inflammatory acne-like lesions within it.
These can lead to cysts, recurrent bacterial
infections, abscesses, and scarring.
 Grouped
undeveloped hair
follicles, presenting
as dilated
invaginations filled
with cornified debris
devoid of hair shafts.
 MEDICAL:
1. Keratolytic agents e.g. salicylic acid, tretinoin and ammonium lactate
may be helpful, but they are not curative.
2. Isotretinoin is not usually recommended owing to the long term
treatment required, but it may be beneficial in preventing cyst formation.
3. Antibiotics may be necessary to treat secondary infections.
 SURGICAL:
1. Manual comedo extraction, laser, dermabrasion may be done but it
is not curative.
2. Excision of localized lesions, although it is often difficult to excise
larger lesions.
 KA is a rapidly growing skin tumor that
considered by some to be a variant of
SCC and by others to represent benign
tumors (i.e. pseudomalignancy) this
remains in question, although based on a
systematic review keratoacanthoma
cannot be considered malignant.
Comparing the clinical behaviors of both
KA and SCC found that none of KA
resulted in distant metastases or death*.
* Savage JA, Maize JC Sr. Keratoacanthoma clinical behavior: a systematic review. Am J
Dermatopathol. May 2014;36(5):422-9.
 It tends to occur in males more
often than in females, with a male-
to-female ratio of 3-4:1.
 The peak incidence of KA is
between ages 50 and 70. This
tumour is rare before 40 years of
age.
 More common in fair skinned
people.
 The most common denominator appears
to be sun exposure.
 Some KAs appear to be related to infection
with HPV but the majority of KAs are not
found to be due to HPV.
 Genetic predisposition in case of multiple
KAs e.g. KAs associated with Muir–Torre
syndrome, Multiple spontaneously
regressing KAs of Ferguson-Smith.
KA
 A predictable clinical sequence
occurs, which consists first of the
development of a spontaneous dome-
shaped papule that is red to flesh
colored. The papule undergoes an
rapid growth phase over a few weeks,
forming a large sharply
circumscribed crater-like nodule with
a keratotic core. Over the next few
months, the tumor may slowly resolve
to leave an atrophic scar.
 Size usually 1-2 cm in diameter.
 Most lesions occur on the head and
neck or in sun-exposed areas of the
extremities, with or without symptoms
of pain or tenderness.
 Most common presentation is the
solitary KA.
 Three growth phases are described:

1. Proliferative phase: a solitary papule appears

suddenly and then rapidly grows to its maximum
size over 2 to 4 weeks.
2. Mature phase: the lesion is stable in size and
appearance for weeks to months; it may appear
crateriform if the core has been partially removed.
3. Resolving phase: the base becomes indurated,
the central core is expelled, and the base resorbs,
leaving a atrophic scar. This phase may last several
months.
Keratoacanthoma centrifugum marginatum
Progressive peripheral expansion and central involution with residual atrophy
Grzybowski syndrome
Multiple spontaneously regressing KAs of Ferguson-Smith
The patient had approximately 40 firm, 1- to 2-cm, dome-shaped, red-to-flesh
colored, hyperkeratotic nodules on the lateral upper arm and extensor forearms.
Giant keratoacanthoma
with a yellow–red color and a history of rapid growth
 SEVERAL DISTINCT CLINICAL PRESENTATIONS OF KA
CLINICAL VARIETIES FEATURES
1. Generalized eruptive severely itchy multiple non-regressing KAs hundreds
KA (of Gryzbowski) of papules resembling milia or early eruptive xanthomas
2. Multiple spontaneously autosomal dominant condition, where multiple KAs appear in
regressing KAs of patients aged 20-30 ys typically regress over weeks to months.
Ferguson-Smith
3. KA centrifugum is characterized by multiple grouped keratoacanthomas may
marginatum reach several cms in diameter resolve more slowly than solitary KA
4. Actinic KAs when KAs develop in sun-exposed skin associated with AK
5. KAs associated with may have sebaceous differentiation [“seboacanthoma”].
Muir–Torre syndrome
6. Giant KA several centimeters in diameter
7. Subugual KA associated with underlying bony destruction
8. Intraoral KA
9. KAs associated with immunosuppression
10. KAs associated with HPV infection
 Typically has a “volcano-like” architecture with
overall hemispheric shape with a keratin-filled
crater and overhanging edges.
 Mitotic figures are present, secondary to the
accelerated growth.
 Basaloid cells are found toward the periphery.
 Inflammatory cells eosinophils, lymphocytes
and neutrophils also may be common.
 Cytologic atypia is usually minimal. An overall
slight mild pleomorphism is detected.
 In general, the squamous epithelium is well
differentiated and has an abundant glassy
eosinophilic cytoplasm.
KA Histologic features
 Pseudocarcinomatous infiltration in
keratoacanthoma typically presents a
smooth, regular, well-demarcated front
that does not extend beyond the level
of the sweat glands.
 Perineural and vascular invasion also
can be observed.
 As the lesion regresses, the dome-
shaped architecture flattens and
fibrosis develops at the base of the
lesion.
 Immunohistochemical staining can help differentiate
KA from other epidermal carcinomas.
 Filaggrin is ubiquitous in KA but uncommon in
carcinoma.
 While the lesion is generally self-limited it should be treated for
several reasons;
1. To obtain pathology: KA can be difficult to distinguish from invasive SCC.
2. To be rid of an unsightly, tender or worrisome lesion
3. To minimize the scar, due to potential cosmetic compromise with the healing of
the lesion.
 Treatment requires destruction of the lesion. Options include:
1. Surgical Excision (the treatment of choice)
2. Cryotherapy
3. Curettage and Electrodesiccation
4. Laser
5. Radiotherapy
 Treatment of Multiple KAs:
1. Acitretin
2. Isotretinoin
3. 5-Fluorouracil
4. Methotrexate
5. Cyclophosphamide
 Clinical term for a hard conical white
to yellow brown projection from the
skin, made of compact keratin.
 So named as it resemble an animal’s
horn.
 It arise from benign, premalignant or
malignant skin lesions.
 Sun-exposed areas are the most
common locations.
Cutaneous Horn
Cutaneous Horn
Cutaneous Horn
 Cutaneous horns are more common in older patients,
with the peak incidence in those between 60 and 70.
 Men are affected more frequently than women and
there is a higher risk of the lesion being malignant in
men.
 They are more common in people with fairer skins (skin
phototype I and II).
SYMPTOMS:

 Cutaneous horns are usually asymptomatic, however

as they are protuberant, they can be injured causing
pain and inflammation.
APPEARANCE:
 Cutaneous horns generally present as
curved hard yellow brown horns.
 They can be surrounded by normal skin
or have a border of thickened skin.
 The side of the horn may be terrace-like
with horizontal ridges.
 The base of the horn may be flat,
protruding, or like a crater.
 Inflammation may be present, due to
recurrent injury.
SIZE:
 Typically, the horn is taller than twice the width at the base.
 It may vary from a few millimeters to several centimetres in
size.
LOCATION:
 Cutaneous horns are usually single, but can be multiple.
 They can occur anywhere on the body, but are more
common on sun-exposed areas especially the head and
ears, dorsum of hands and forearms.
 They may also occur on the chest, neck, shoulder and penis.
Dermoscopy of Cutaneous Horn
Terrace morphology is an orderly structural dermoscopic feature
 It shows hyperkeratosis, parakeratosis
associated with variable acanthosis.
Orderly horizontal parallel layers of
keratin are associated more with benign
lesions. Rapidly growing malignant lesions
exhibit a more erratic growth.
 The base of the lesion shows features of the
underlying lesion e.g. atypical
keratinocytes of actinic keratosis.
 BENIGN PREMALIGNANT AND MALIGNANT
1. Seborrhoeic keratosis 1. Actinic keratosis
2. Viral warts 2. SCC in situ or invasive
3. Epidermal naevus 3. Malignant melanoma (rare)
4. Molluscum contagiosum
5. Psoriasis
6. Hypertrophic lichen planus
7. Keratoacanthoma
8. Tumors derived from follicular
epithelium, especially tricholemmoma.
1. Excision biopsy with local destruction;
– It is the most common treatment.
– This must be done deeply enough to allow the pathologist to see the
dermis beneath the horn in order to evaluate the possibility of dermal
involvement by invasive carcinoma.
– Excision to adipose is best when invasion is suspected. In that case,
induration of the dermis is detected, as opposed to the thickness related
only to the horn.
2. Cryotherapy after paring of the horn.
 It is uncommon, usually solitary
lesion of unknown etiology appearing
on the lower legs but there have been
rare cases of multiple lesions occurring.
 They occur mostly in adults of middle-
age or older.
 It may be suspected by astute clini-
cians, but usually a biopsy is required
to establish the diagnosis.
 Lesions are almost always asymptomatic.
 Slightly elevated to dome-shaped rounded
papule, plaque or nodule.
 Colour varies from pink to brown, but is most
commonly blood red and shiny.
 Lesions are blanchable.
 Usually develop slowly, most commonly over
a period of 2–10 years. Can be from 0.3 to 2
cm in diameter.
 Wafer-like scale may be stuck round the
edges of the lesion. A moist or bleeding
surface may result if scale is removed.
Dermoscopic view of Clear Cell Acanthoma
characteristic looped blood vessels within the dermal papillae create red dots
in lines.
 Psoriasiform histology i.e.
acanthosis with elongation of rete
ridges with well-demarcated zone
containing characteristic
accumulation of clear to pale
glycogen-containing
keratinocytes that stain positively
with PAS.
 The epidermis is eroded and neu-
trophils extend from the papillary
dermis into the stratum spinosum,
aggregating in the overlying thin
crust.
 They may persist for years and years without changing
or causing any complications.
 Simple destruction or excision is adequate for removal.
Shave excision or curettage combined with
electrofulguration is a common form of treatment.
 Most lesions do not recur.
 Uncommon, usually solitary papule
or nodule with a central keratotic plug.
 Usually located on the head or neck.
 It is more prevalent in men, usually
appearing between the fifth and
seventh decades of life.
 Acantholytic dyskeratosis seen at the
base and side of a cup-like epidermal
invagination.
 Lesions should be biopsied to exclude
the possibility of a malignancy.
 Excision is curative.
 It presents as a solitary, rarely multiple,
verrucous, often crusted, skin-colored to red–
brown papule or nodule with a central pore and a
keratotic plug.
 Lesions grow slowly, and they are located most
commonly on the scalp, cheek, temple, forehead,
postauricular area and nose.
 Lesions have been found beneath the nail plate and
in the mouth, especially on the hard palate and
alveolar ridge.
 It typically range in size from several millimeters to
2 cm in diameter.
 Most warty dyskeratomas are asymptomatic, but
patients may rarely complain of pruritus or
burning. Bleeding and discharge of foulsmelling
cornified material may occur.
 Usually involves at least one dilated
folliculosebaceous unit. There is a
central cuplike invagination lined with
epithelium displaying acantholysis
and individual cell necrosis, corps
ronds and grains, most closely
resembling Darier disease.
 The central crater is filled with
cornified debris.
 The wall has multiple villi, sometimes
composed of only a single layer of
basal cells, often project upward from
the invaginated hyperplastic base.
Warty Dyskeratoma
 Bolognia 3rd ed.
 dermnetnz.org
 http://emedicine.medscape.com
 http://www.globalskinatlas.com
 AAD; Benign Skin Lesions (Presentation)
 Skin Tumors by Seyed Morteza Mahmoodi
(Presentation)