BENIGN

EPITHELIAL
PATHOLOGIES
OF ORAL
CAVITY.
Presented by: Madhura Shekatkar MDS II
Guided by: Dr. Supriya Kheur
Prof and HOD
Dept of Oral Pathology
Date: 02/08/2021
 CONTENTS
• Squamous Papilloma
• Verruca Vulgaris
• Condyloma Acuminatum
• Focal epithelial hyperplasia
• Molluscum Contagiosum
• Verruciform Xanthoma
• Oral Melanotic Macule
• Oral Melanoacanthoma
• Acquired Melanocytic Nevus
• Congenital Melanocytic Nevus
• Halo Nevus
• Spitz Nevus
• Blue Nevus
VERRUCA VULGARIS
(COMMON WART)
 INTRODUCTION
• Verruca vulgaris is a benign lesion of skin and mucous membranes caused by human papillomavirus (HPV).

• The lesions are typically self-limited but may vary in size and number. It is also known as common warts and the

lesion tends to affect epithelial tissues and mucous membranes.

• Verruca vulgaris is a benign epidermal proliferation with infrequent malignant change.

• The clinical presentations of verruca vulgaris vary according to the viral type and the anatomical site infected.

• The benign VV include squamous papilloma with verruca vulgaris, focal epithelial hyperplasia and condyloma.

• Verruca vulgaris is most commonly induced by HPV-2, HPV-4 or HPV-40 and it rarely occurs on the tongue.

Ural, Ahmet et al. “Verruca vulgaris of the tongue: a case report with a literature review.” Bosnian journal of basic medical
sciences vol. 14,3 136-8. 16 Aug. 2014, doi:10.17305/bjbms.2014.3.29
• Differential diagnosis of oral warts includes:
• verrucous leukoplakia,
• squamous papilloma,
• condyloma acuminatum,
• focal epithelial hyperplasia,
• exophytic squamous cell carcinoma,
• keratoacanthoma,
• exophytic verrucous carcinoma
• verruciform xanthoma
• They share similar clinical impression but can only be differentiated
on the basis of histopathological examination.
 TREATMENT

• Conservative surgical excision with safe margins is the treatment of

choice.

• Frequently similar lesions if left untreated may resolve spontaneously

and those that persist should be removed surgically either by routine
excision or laser ablation.

• Intra-lesional injections should be used as a last resort.

Condyloma acuminatum is an infectious lesion that is
characteristically located in the anogenital region but
may also involve the oral mucosa.
Common to these sites is a warm, moist squamous
epithelial surface.
An increasing frequency of this lesion has been noted in
HIV-infected patients, reflecting an aspect of
opportunistic infection.
 ETIOPATHOGENESIS

Condyloma acuminatum is a verrucous or papillary growth that

has been etiologically related to HPV subtypes 6 and 11.
The maturation of the various subtypes of HPV within oral and
genital mucosal cells is essentially the same.
The keratinized cells act as the hosts for the virus, with
replication linked to the process of keratinization.
CLINICAL
FEATURES
Papillary projections extending from the base
of each lesion are covered by stratified
squamous epithelium that is often
parakeratotic but at times may be
nonkeratinized.

Koilocytosis of upper level epithelial cells is

usually found.
The epithelial layer itself is hyperplastic
without evidence of dysplastic change.
The underlying stroma is well vascularized
and may contain a trace of chronic
inflammatory cells.
 FOCAL
EPITHELIAL
HYPERPLASIA
 HECK’S
DISEASE

MULTIFOCAL
PAPILLOMA

VIRUS
EPITHELIAL
HYPERPLASIA
HECK’S
DISEASE
 Associated with HPV 13 and 32 and was
originally diagnosed in the Inuit population.

Frequently affects children but is increasingly

seen in the HIV-associated population as well.

The lesion is typically located in the labial,

buccal and lingual mucosa.

Lesions usually resemble the normal mucosal

color but may occasionally appear white and
papillary.
A differential diagnosis would include
verruca vulgaris and multiple squamous
Papillomas.
The oral mucosal lesions of Cowden's
(multiple hamartoma) syndrome may present
similarly and should be ruled out.
In addition, oral manifestations of Crohn’s
disease and pyostomatitis-vegetans might be
considered.
No particular treatment is indicated, especially
with widespread involvement.
Surgical removal may be used if few lesions are
present.
Spontaneous regression has been noted in many
cases, perhaps as an expression of viral
recognition and cell-mediated immunity.
• Keratoacanthoma (KA) is a low-grade, rapidly growing, 1 to 2 cm dome-shaped skin tumor with a
centralized keratinous plug.

• Over the past hundred years, this tumor has been reclassified and reported differently throughout
literature. 

• Before 1917, keratoacanthoma were regarded as skin cancer. In the 1920s, reports labeled the tumor
as verrucae or vegetating sebaceous cyst.

• Between 1936 and the 1950s the lesion was labeled and reported in the literature as molluscum
sebaceum.

• Keratoacanthoma is characterized by initial rapid growth followed by a period of variable tumor

stability and spontaneous regression.

• Although recognized as benign, KA shares histopathological features with squamous cell carcinoma
(SCC) requiring treatment.
 CLASSIFICATION

Keratoacanthoma
Giant Multiple
Centrifugum
Keratoacanthoma Keratoacanthomas
Marginatum
• In some instances • Characterized by • Ferguson-Smith
may reach multiple tumors syndrome.
dimensions of growing in a • Multiple
several centimeters. localized area. keratoacanthomas.
 Ultraviolet (UV)
radiation

Recent trauma Exposure to

or surgery to chemical
the location carcinogens

ETIOLOGY

Viral exposure
including
Immuno-
human
suppression
papillomavirus
(HPV)
Genetic
predisposition
including
mutations of
p53 or H-Ras

Ranglani H, Pai VV, Shukla P. Keratoacanthoma-like cutaneous metastases in a case of squamous cell carcinoma of the tongue. Indian J Dermatol Venereol
Leprol. 2019 Sep-Oct;85(5):568.
 Autosomal dominant Muir-Torre
syndrome

Autosomal dominant Ferguson-

Smith syndrome

Autosomal recessive xeroderma

pigmentosum

X-linked dominant incontinentia

pigmenti

Autosomal dominant Witten-Zak

Fujimura T, Lyu C, Tsukada A, Sato Y, Kambayashi Y, Aiba S. Eruptive keratoacanthoma with spontaneous regression arising from a cervical
squamous cell carcinoma patient treated with nivolumab. J Dermatol. 2019 May;46(5):e177-e178.
 PATHOPHYSIOLOGY
Originating in the pilosebaceous unit, keratoacanthomas are derived from an abnormality leading to hyperkeratosis of the
infundibulum. 
Although associated with hair-bearing areas and sunlight, these tumors can develop in other areas including within the mouth, lip,
gingiva, hard palate, and other mucosal surfaces.

3 STAGES
These stages include proliferation, maturation, and involution. In the proliferative phase, rapid growth occurs up to approximately 6 to 8 weeks.
The maturation phase lasts several weeks to months where the keratoacanthoma maintains its crateriform appearance.
Involution is the final stage where the keratoacanthoma regresses into an atrophic scar. 

RISK FACTORS

Ultraviolet light, trauma, human papillomavirus (HPV), genetic factors, immune status, use of hedgehog pathway inhibitors for
basal cell carcinoma (BCC), and use of BRAF inhibitors in patients with melanoma have been implicated as risk factors.
 CLINICAL FEATURES

Solitary or multiple. Rapid enlargement of the Fully developed, it contains

papule occurs, ultimately a core of keratin
Begins as a small red resulting into a surrounded by a concentric
macule turning to firm hemispheric, firm, elevated, collar of raised skin or
papule. asymptomatic nodule. mucosa.

Multiple lesions: Muir-Torre

Spontaneous regression
syndrome, an autosomal
occurs, central keratin is
dominant skin condition of
exfoliated, leaving a cup
genetic origin, consists of
shaped lesion, heals with
cutaneous tumors of
superficial scar formation.
sebaceous gland.
CLINICA
L
PICTURE
1. Squamous cell carcinoma
2. Amelanotic melanoma
3. Molluscum contagiosum
4. Prurigo nodularis
5. Metastatic lesion to the skin
6. Merkel cell carcinoma
7. Nodular basal cell carcinoma
8. Ulcerative basal cell DIFFERENTIAL
carcinoma DIAGNOSIS
9. Nodular Kaposi sarcoma
10. Hypertrophic lichen planus
11. Deep fungal infection
12. Atypical mycobacterial
infection
13. Foreign body reaction
14. Verruca vulgaris.

 Keratoacanthomas of the neck and face have the potential to metastasize.

 INTRODUCTION
 Virus-induced epithelial hyperplasia.
 Caused by: Molluscum contagiosum virus (member of DNA poxvirus
group)
 Incubation: 14 to 50 days.
ROUTES OF Lesions have
TRANSMISSION:
1. SEXUAL CONTACTS (IN predilection for warm
ADULTS) portions of the skin
2. NON SEXUAL CONTACT: and sites of recent
sharing clothing,
wrestling, swimming. injury; florid cases
have been reported in
immunocompromised
Active phase: Virus is patients.
sloughed from a central
core in each papule.
 • Hyperplastic condition of epithelium
VERRUCIFORM of mouth, skin and genitalia.
• Characteristic accumulation of lipid-
XANTHOMA laden histiocytes beneath the
epithelium.

• No role of HPV.

CAUSE • Unusual reaction or immune

response to localized epithelial
trauma or damage.

• Histopathologically similar to other

dermal xanthomas.
ASSOCIATION • Not associated with diabetes,
hyperlipidemia or any other
metabolic disorder.
Intra-oral lesions occur on Well-demarcated, soft, Yellow-white, or red color,
gingiva and alveolar painless, sessile, slightly papillary or roughened
mucosa. elevated mass. surface.

Similar to squamous
papilloma, condyloma
acuminatum or early
carcinoma.
SPEAKS IT ALL
 ORAL MELANOTIC MACULE
(FOCAL MELANOSIS)
Flat, brown mucosal discoloration produced by focal increase in melanin deposition and a
concomitant increase in the number of melanocytes.
May represent intra-oral freckle, post-inflammatory pigmentation or macules associated with Peutz-
Jeghers syndrome, Bandler syndrome or Addison’s disease.

Vermilion zone of the lower lip is the most common site, followed by buccal mucosa, gingiva and
tongue.
Solitary, well-demarcated, uniformly tan to dark brown, asymptomatic, round or oval macule.
No malignant potential.
Peutz-Jeghers
Syndrome/
Addison’s
Disease.
 Increase in melanin in the Lesion does not show
basal and para-basal layers of elongated rete ridges like Melanin incontinence.
the epithelium. those seen in actinic lentigo.
 ORAL MELANOACANTHOMA (MELANOACANTHOSIS)

Benign and uncommon acquired pigmentation of the oral mucosa,

characterized by dendritic melanocytes dispersed throughout the epithelium.

Blacks, Female, Third and fourth decades of life.

M/c: Buccal mucosa.

C/P: Smooth, flat or slightly raised, dark-brown to black in color.

Demonstrate rapid increase in size.
 Numerous Mild acanthosis. Dispersion of
benign dendritic Mild to moderate pigment laden
melanocytes chronic dendritic
scattered inflammation . melanocytes.
throughout the
lesional
epithelium.
 ORAL NEVI

ORAL MELANOTIC NEVUS

NEVOCELLULAR NEVUS

MOLE

MUCOSAL MELANOCYTIC NEVI

 Categorized as hamartomas,
developmental
In 1943, Ackermann and Field King et al, adopted the less
malformations, the nevi are
have reported the first case of anatomically specific term,
benign proliferations of nevus
an oral nevus. intramucosal nevus.
cells in either epithelium or
connective tissue.

Adult whites harbor this lesion

Nevi may also be classified as
rather commonly but intraoral
congenital or acquired
lesions are much less
(Buchner and Hansen).
common.
 On the basis of the histologic location of the nevus cells, cutaneous
acquired nevi can be classified into three categories:

• When nevus cells • Nevus cells are in • Nests of nevus

are limited to the the epidermis cells are entirely
basal cell layer of and dermis. in the dermis.
the epithelium.

Junctional Compound Intraderma

Nevus Nevus l Nevus
Junctional Compound Intramucos
Nevus Nevus al Nevus
Nests of nevus cells are
theques of nevus cells Nevus cells proliferate
no longer found within
are found only along the and group of cells begin
the epithelium but are
basal cell layer of the to drop off into the
found only within the
epithelium, especially at underlying lamina
underlying connective
the tips of rete ridges. propria.
tissue.

Cells are now present

The lesional cells are
both along the junction The skin counterpart is
found at the junction
of epithelium and termed as intradermal
between the epithelium
underlying connective nevus.
and connective tissue.
tissue.
 CLINICAL FEATURES

Ainsworth and her colleagues separate the congenital nevi of the skin into ‘small’ and ‘garment’ nevi.
The ‘small’ nevi are greater than 1 cm in diameter and usually 3–5 cm.
The ‘garment’ nevi are greater than 10 cm in diameter and can cover large areas of the skin.

Acquired nevi are extremely common. They appear in bout the eighth month of life and increase in number
with age.
Reaching their peak numerically in the late third decade of life.

Clark has stated that the number of nevi which a person has is genetically determined.
The number of nevi begin to decrease as one ages, so that elderly persons average far fewer nevi than younger
adults.
INTRADERMAL NEVUS

JUNCTIONAL NEVUS

COMPOUND NEVUS
• The intradermal nevus • The junctional nevus may • The compound nevus is a
(common mole) is one of appear clinically similar to lesion composed of two
the most common lesions the intradermal nevus, the elements: an intradermal
of the skin, most persons distinction being chiefly nevus and an overlying
exhibiting several, often histologic. junctional nevus.
dozens, scattered over the • It is extremely important;
body. however, that a distinction
• The common mole may be be drawn, since the
a smooth flat lesion or may prognosis of the two
be elevated above the lesions is different.
surface; it may or may not
exhibit brown
pigmentation, and it often
shows strands of hair
growing from its surface.
• This form of mole seldom
occurs on the soles of the
feet, the palms of the
hands or the genitalia.
SPITZ NEVUS
(BENIGN
JUVENILE
MELANOMA;
SPINDLE AND
EPITHELOID
CELL NEVUS)
 INTRODUCTION:
• Uncommon type of melanocytic nevus.
• Shares histopathological features with melanoma.
• Benign biologic behavior of the lesion was first emphasized by Spitz in 1948.

CLINICAL FEATURES
• During childhood.
• Solitary, dome shaped, pink to reddish-brown papule, smaller than 6mm in diameter.

HISTOLOGICAL FEATURES:
• Overall: like compound nevus.
• Lesional cells are: spindle shaped or plump (epithelioid).
• Epithelioid cells are multinucleated, bizzare, lacking cell cohesiveness.
• Mitotic figures present in superficial layers.
• Ectatic superficial blood vessels impart the color.
 BLUE NEVUS
(DERMAL
MELANOCYTOMA;
JADASSOHN-
TIEcHE NEVUS)
 • Benign proliferation of dermal melanocytes,
deep within the sub-epithelial connective tissue.
INTRODUCTION • 2 types: common and cellular.
• Blue color: Tyndall effect.

• Common Nevus:
• Palate.
• Children and young adults.
• Female predilection.
• Macular or dome shaped, blue or black lesion, smaller than 1cm.
CLINICAL
FEATURES
• Cellular Nevus:
• Second to fourth decades.
• Slow growing, blue or black papule or nodule.
• Occasional lesions remain macular.
 • Pale hypo-pigmented border or
“halo” of the surrounding
HALO epithelium, apparently due to
destruction of nevus cell by the
NEVU immune system.
• Development of multiple halo

S nevi has been seen in patients

who have had a recent excision
of a melanoma.
 ORAL MANIFESTATIONS
Oral nevi most commonly Most oral nevi are
occur on the hard palate, asymptomatic, and the
with almost 40% presenting lesions are usually detected Approximately 85% of oral
in that location. as an incidental finding on nevi are pigmented.
The second most common routine dental examination. Pigmentation usually varies
location is the buccal mucosa Nevi are often mistaken for from brown to black or blue.
(20% of cases). melanotic macules, amalgam Nevi are well circumscribed,
Other common locations tattoos, physiologic ethnic round, or oval, and are raised
include the vermilion border pigmentation, smoker’s or slightly raised.
of the lip and the labial melanosis, or other vascular
mucosa. or pigmented lesions.
 DIFFERENTIAL DIAGNOSIS

Sr. No Differential Diagnosis Differential Features Features seen in Oral Nevi

1. Melanotic Macules Flat mucosal surface. Elevated mucosal surface.
2. Amalgam Tattoos
3. Ethnic pigmentation Always symmetric and rarely affects the surface Stippling of gingiva is lost.
topography or disturbs the normal stippling in the
gingiva.
4. Smoker’s Melanosis Involves only the anterior gingiva and most often Involves mainly the hard
occurs in women who smoke and take oral palate.
contraceptives.
5. Vascular lesions Usually blanch with compression No blanching visible on
compression.
6. Malignant melanoma Associated with diffuse areas of pigmentation, Well circumscribed lesion.
possible ulceration, nodularity, variegation in color,
and an irregular outline.
 Intramucosal nevi are
distributed almost
equally between the
hard palate and
buccal mucosa, with
almost 25% in each
location. 17% of intramucosal
nevi are on the
Two-thirds of blue
gingiva, 12% on the
nevi occur in hard
vermilion border of
palate.
the lip, and almost 9%
on the labial mucosa.

ANATOMIC
DISTRIBUTION
• The nevus cells are assumed to be derived
from neural crest.
• Nevus cells are large ovoid, rounded, or
spindle-shaped cells with pale cytoplasm;
and may contain granules of melanin
pigment in their cytoplasm.
• The nucleus is vesicular and lacks the
dendritic processes typical of
melanocytes.
• They either lack contact inhibition or lose
it shortly after the proliferation process
begins.
• Melanosomes are retained by nevus cells
and are not transferred to adjacent
keratinocytes.
• They tend to be grouped in sheets or cords
which are called nest or thèque.
• Nevus cells also have the ability to
migrate from the basal cell layer into the
underlying connective tissue.
In the intradermal
nevus, the nevus cells
are situated within
the connective tissue
and are separated
from the
overlying epithelium
by a well defined
band of connective
tissue. Thus, in the
intradermal nevus,
the nevus cells are
not in contact with
the surface
epithelium.
In the junctional nevus, this zone of
demarcation is absent, and the nevus
cells contact and seem to blend into
the surface epithelium.
This overlying epithelium is usually thin
and irregular and shows cells apparently
crossing the junction and growing down
into the connective tissue—the so-called
abtropfung or ‘dropping off ’ effect.
This ‘junctional activity’ has serious
implications because junctional nevi
have been known to undergo
transformation into malignant
Melanomas.
The compound nevus shows
features of both the
junctional and intradermal
nevus.
Nests of nevus cells are
dropping off from the
epidermis, while large nests
of nevus cells are also present
in the dermis.
The spindle cell and/or epithelioid cell
nevus is commonly composed of
pleomorphic cells of three basic types:
spindle cells, oval or ‘epithelioid’ cells,
and both mononuclear and multinucleated
giant cells. These are arranged in well
circumscribed sheets and there is
generally considerable
junctional activity.
The blue nevus is of two types: the
common blue nevus and the cellular
blue nevus.
In the common blue nevus, elongated
melanocytes with long branching
dendritic processes lie in bundles,
usually oriented parallel to the
epidermis, in the middle and lower third
of the dermis.
There is no junctional activity.
The melanocytes are typically packed
with melanin granules, sometimes
obscuring the nucleus, and these
granules may extend into the dendritic
processes.
In the cellular
blue nevus, an
additional cell
type is present: a
large, round or
spindle cell with
a pale vacuolated
cytoplasm. These
cells commonly
are arranged in an
alveolar pattern.
 TREATMENT & MALIGNANT
TRANSFORMATION

 It has become customary to recommend removal of pigmented moles if they occur in areas which are

irritated by clothing, such as at the belt or collar line, or if they suddenly begin to increase in size,

deepen in color, or become ulcerated.

 Allen and Spitz have stated that it is fairly certain that trauma to an intradermal nevus will not induce

malignancy. Whether simple trauma to a junctional nevus will produce malignancy is not known.

 Congenital nevi have a great risk for transformation to malignant melanoma.

 Kaplan reported seven cases which were seen at the Stanford University Hospital and discussed 49

other cases. It is estimated that 14% of the large congenital nevi may undergo malignant

transformation.