NON-ODONTOGENIC TUMORS

OF EPITHELIAL TISSUE ORIGIN

GUIDED BY- PRESENTED BY-

DR. ASHISTARU SAHA DR. POOJA AGRAWAL
DR. TUSHAR TANWANI
DR. ANUPAM PURWAR
DR. NEHA NAVLANI
 CONTENT
 Introduction
 Contrasting features of benign and malignant tumors
 Cellular adaptations
 Carcinoma in situ
 Metastasis
 Diagnosis
 TNM staging
 Classification of non- odontogenic tumors
 Benign tumors of epithelial tissue origin-
1. Squamous papilloma
2. Squamous acanthoma
3. Keratoacanthoma
4. Oral nevi
 Malignant tumors of epithelial tissue origin-
1.Basal Cell Carcinoma
2.Squamous cell carcinoma
3.Verrucous Carcinoma
4.Spindle Cell Carcinoma
5.Adenoid Squamous cell Carcinoma
6.Lmphoepithelioma and Transitional cell carcinoma
7.Malignant Melanoma
 Conclusion
 References
 INTRODUCTION
 The study of tumors of the oral cavity and adjacent
structures constitutes an important phase of
dentistry because of the role which the dentist plays
in the diagnosis and treatment of these lesions.

 A tumor, by definition, is simply a swelling of the

tissue in the strict sense, the word does not imploy a
neoplastic process.
 NEOPLASM- The term ‘neoplasia’ means new
growth.But all new growths are not neoplasm.
 “ a mass of tissue formed as a result of abnormal,
excessive, uncoordinated, autonomous and
purposeless proliferation of cells.”

 Neoplasm may be BENIGN or MALIGNANT.

 All tumors ,benign as well as malignant, have 2
basic components:
 Parenchyma-comprised by proliferating tumor cells.
 Supportive stroma- composed of fibrous connective
tissue and blood vessels; it provides the framework
on which the parenchymal tumor cells grow.
 Constrasting features of benign and
malignant tumors
Benign Malignant
1. Clinical features
Boundaries Well- circumscribed Poorly-circumscribed
Size Usually small Often larger
2. Microscopic features
Pattern Usually resembles the Often poor resemblence to
tissue of origin closely tissue of origin
Basal polarity Retained Often lost
Pleomorphism Usually not present Often present
Nucleo-cytoplasmic ratio Normal Increased
Anisonucleosis absent Generally present
Hyperchromatism absent Often present
Mitosis May be present but are Mitotic figures increased
always typical mitosis and are generally atypical
and abnormal
 Benign
Tumor giant cells May be present but without
nuclear atypia
Chromosomal abnormalities Infrequent
Function Usually well maintained
3. Growth rate Usually slow
4. Local invasion Often compresses the
surrounding tissues without
invading or infiltrating them
5. Metastasis Absent
6.Prognosis Local complications
Malignant
Present with nuclear
atypia
Invariably present
May be retained, lost or
become abnormal
Usually rapid
Usually infiltrates and
invades the adjacent
tissues
Frequently present
Death by local and
metastatic complications
CELLULAR ADAPTATIONS
 ATROPHY- Reduction of the number and size of
parenchymal cells of an organ or its parts which eas
once normal is called atrophy.
 HYPERTROPHY- Hypertrophy is an increase in
the size of parenchymal cells resulting in
enlargement of the organ or tissue, without any
change in the number of cells.
 HYPERPLASIA- Hyperplasia is an increase in the
number of parenchymal cells resulting in
enlargement of the organ or tissue.
 METAPLASIA-Change of one type of epithelial or
mesenchymal cell to another type of epithelial or
mesenchymal cell.
 DYSPLASIA- Disordered cellular development,
may be accompanied with hyperplasia or
metaplasia.
 CARCINOMA IN SITU
 It is also called intrepithelial carcinoma.
 Carcinoma in situ (Cis), also known as in situ neoplasm, is
a group of abnormal cells.While they are a form of neoplasm
there is disagreement over whether Cis should be classified
as cancer. Some authors do not classify them as cancer,
however, recognizing that they can potentially become
cancer.
 Carcinoma in situ is defined as dysplastic epithelial cells that
extend from the basal layer to surface of the mucosa (top-to-
bottom change).The epithelium may be hyperplastic or
atrophic. There may or may not be a thin layer of keratin on
the surface.
 Highly dysplastic
epithelium (top to
bottom )
Altered nuclear
Cytoplasmic ratio

Connective tissue
stroma
 METASTASIS
 Spread of tumor by invasion in such a way that
discontinuous secondary tumor mass/masses are
formed at the site of lodgement.
 ROUTES OF METASTASIS-
 1. Lymphatic spread- Carcinomas
 2. Haematogenous spread- Sarcomas
 3. Other routes
 DIAGNOSIS
 BIOPSY- Biopsy is the removal of tissue from the
living organism for the purposes of microscopic
examination and diagnosis.
 TYPES OF BIOPSY-
 1. Excisional biopsy
 2. Incisional biopsy
 3. Intraosseous biopsy
 4. Punch biopsy
 5. Frozen section biopsy
 EXCISIONAL BIOPSY- If the pathologically
altered mucosa is small (0.8-1 cm in diameter or
smaller), the entire lesion including a rim of
adjacent normal tissue is removed in toto.
 INCISIONAL BIOPSY- If the diameter of
pathologic alteration is larger than 1 cm, a
representative sample of tissue from the boundary
zone where normal and pathologically altered tissue
adjoin should be harvested.
 EXFOLIATIVE CYTOLOGY- the surface of lesion
is either wiped with some sponge material or
scraped to make a smear. It is the microscopic
examination of the cells shed from an epithelium.

 FINE NEEDLE ASPIRATION CYTOLOGY

(FNAC)- It is the microscopic examination of an
aspirate obtained by inserting a fine needle into the
lesion.
 TNM STAGING
TNM is based on 3 components

LETTER STANDS FOR DESCRIPTION

T Tumor
N Lymph nodes
M Metastasis
indicates the size of the primary (The site or
area in the body where cancer started.)
tumour and the degree of spread into nearby
tissues (local invasion)
indicates whether or not the cancer has
spread to nearby lymph nodes, the size of the
nodes that contain cancer and how many
lymph nodes contain cancer.
indicates whether or not cancer has spread
(metastasized) to distant organs.
 Primary tumor (T)-
 Tx- Main tumor can not be measured.
 T0- Main tumor can not be found.
 Tis- Carcinoma in situ
 T1- Tumor 2 cm or less in diameter.
 T2- Tumor 2 to 4 cm in diameter.
 T3- tumor more than 4 cm in greatest diameter
 T4- Tumor of any size in which tumor invades
adjacent structures(eg- cortical bone, inferior alveolar
nerve, floor of mouth)
 REGIONAL LYMPH NODES (N)-
 NX- Cancer in nearby lymph nodes can not be measured.
 N0- There is no cancer in near by lymph nodes.
 N1- Metastasis in single ipsilateral lymph node less than 3
cm in diameter.
 N2- Single lymph node, no more than 6 cm in greatest
dimension, of bilateral /contralateral lymph node, no more
than 6 cm
 N2a- Single ipsilateral lymph node more than 3 but less than
6 cm.
 N2b- Multiple ipsilateral lymph nodes less than 6 cm.
 N2c- Bilateral or contralateral lymph node less than 6 cm in
greatest dimension.
 N3- Metastasis in a node more than 6 cm in greatest
dimension
  DISTANT METASTASIS(M)-
 Mx- Distant metastasis can not be assessed
 M0- No evidence of distant metastasis
 M1- Distant metastasis is present
STAGE TNM CLASSIFICATION

Stage1 T1 N0 M0

Stage 2 T2 N0 M0

Stage 3 T3 N0 M0 or T1,T2 orT3 N1 M0

Stage4 Any T4 lesion, any N2, N3 lesion, or any

M1 lesion
 Classification of Non Odontogenic
Tumors
Epithelial tissue origin

Benign Malignant
1. Squamous papilloma 1.Basal Cell Carcinoma
2. Squamous acanthoma 2.Squamous cell carcinoma
3. Keratoacanthoma 3.Verrucous Carcinoma
4.Spindle Cell Carcinoma
4. Oral nevi
5.Adenoid Squamous cell
Carcinoma
6.Lmphoepithelioma and
Transitional cell carcinoma
7.Malignant Melanoma
BENIGN TUMORS OF
EPITHELIAL TISSUE
ORIGIN
 SQUAMOUS PAPILLOMA
 Benign proliferation of stratified squamous
epithelium, resulting in a papillary or verruciform
mass.

 Lesion is induced by human papilloma virus(HPV)

 CLINICAL FEATURES-
 Equal frequency in both men and women.
 Common in 30 to 50 year age group.
 Most common site- Tongue, lips and soft palate.
 Soft, painless, usually pedunculated , exophytic
nodule with numerous finger like projections that
impart a “ cauliflower” or wartlike appearance.
 Maximum size of lesion- 0.5 cm
 HISTOPATHOLOGIC FEATURES- Proliferation
of kerarinized stratified squamous epithelium
arrayed in finger like projections with fibrovascular
connective tissue cores.
 Connective tissue cores may show inflammatory
changes.
 Koilocytes, virus altered epithelial clear cells with
small dark pyknotic nuclei, are sometimes seen high
in prickle cell layer.
Multiple finger like
Projections lined by
Keratinized stratified
Squamous epithelium

Thin connective
Tissue core
 TREATMENT-
Conservative surgical excision, including the base
of the lesion.
 If the tumor is properly excised, recurrence is rare.
 SQUAMOUS ACANTHOMA
 Uncommon lesion which probably represents a
reactive phenomenon of the epithelium rather than a
true neoplasm.
 It is generally described as a small flat or elevated,
white, sessile or pedunculated lesion on the mucosa.
 KERATOACANTHOMA
 Also called as Self healing carcinoma,
 Molluscum pseudocarcinomatosum
 Molluscum sebacceum
 Verrucoma
 A lesion which clinically and pathologically resembles
squamous cell carcinoma, keratoacanthoma is a relatively
common low grade malignancy that originates in the
pilosebaceous glands.
 Keratoacanthoma is characterized by rapid growth over a
few weeks to months, followed by spontaneous resolution
over 4-6 months in most cases. 
 CLINICAL FEATURES-
 It is dome-shaped, symmetrical, surrounded by a
smooth wall of inflamed skin, and capped with
keratin scales and debris.
 KA is commonly found on sun-exposed skin, often
face, forearms and hands.
 M>F
 Common sites- Lips, vermilion border of lip
 Incidence increases with age.
 HISTOLOGIC FEATURE-
 The lesion consists of hyperplastic squamous
epithelium growing into the underlying connective
tissue.
 The surface is covered by a thickened layer of
parakeratin or orthokeratin with central plugging.

 TREATMENT- Surgical excision. Prognosis is

excellent following excisional surgery.
Central keratin plug

Hyperplastic
squamous
epithelium

Connective tissue
stroma
 ORAL NEVI
 Oral melanocytic nevi are benign proliferations of
nevus cells in the epithelial layer, the submucosal
layer, or both.
 As such, they are classified as junctional,
intramucosal, and compound nevi. Nevi may also be
classified as congenital or acquired.
 Unlike their cutaneous counterparts, oral
melanocytic nevi are rare.
 Intramucosal nevi are typically light brown and
dome-shaped. These are the most common type,
accounting for 64% of all reported oral nevi.

Intramucosal nevus on the lower lip. This

brown papule measured 0.6 cm in diameter and
was only slightly raised
 The common blue nevus is the second most
common type found in the oral cavity, accounting
for 16.5-36% of all oral nevi.

Blue nevus on the gingiva. This 1-cm saucer-shaped tan macule on the gingiva
has histologic features consistent with those of a blue nevus, which is the
second most common type of oral nevus. This location is atypical because
most blue nevi occur on the palate
 Junctional and compound nevi are uncommon,
accounting for only 3-6% and 5.9-16.5%,
respectively.
 Oral nevi most commonly occur on the hard palate,
buccal mucosa, vermilion border of the lip and the
labial mucosa.
 Most oral nevi are asymptomatic and the lesions are
usually detected as an incidental finding on routine
dental examination.
 HISTOLOGIC FEATURE-
 The nevus cells are assumed to be derived from
neural crest cells.
 Nevus cells are large ovoid, rounded, or spindle
shaped cells with pale cytoplasm; and may contain
granules of melanin pigment in their cytoplasm.
 Melanin pigment

Nevus cells restricted

To epithelium
Nevus cells proliferating
To form theques

Connective tissue
Melanin pigment

Proliferating nevus
Cells both in
epithelium and
Connective tissue
 Epithelium

Melanin pigment

Zone of normal
Connective tissue
Separating overlying
Epithelium from
Nevus cell
collection

Proliferating nevus
Cells in connective
tissue
 TREATMENT- Surgical excision of all intraoral
pigmented nevi is recommended as a prophylactic
measure.
 MALIGNANT TUMORS
OF EPITHELIAL TISSUE
ORIGIN
 BASAL CELL CARCINOMA
 Most common skin cancer, is a locally invasive,
slowly spreading primary epithelial malignancy that
arises from the basal cell layer of the skin and it’s
appendages.

 About 80% are found on the skin of the head and

neck. Also called Rodent ulcer.

 This cancer mainly results from chronic exposure to

ultraviolet radiation.
 CLINICAL FEATURES-
 Age- 40 years
 Common form- Nodular (Noduloulcerative) BCC
begins as a firm, painless papule that slowly
enlarges and gradually develops a central depression
and an umbilicated appearance.
 Destruction of underlying bone or cartilage may
ooccur, but metastasis is extremely rare.
 Other Variety- Pigmented BCC
 Sclerosing BCC
 Superficial BCC
 HISTOLOGIC FEATURES-
 Uniform ovoid, dark staining basaloid cells with
moderate sized nuclei and relatively little
cytoplasm.
 The cells are arranged into well demarcated islands
and strands, which appear to arise from basal cell
layer of the overlying epidermis and invade into
underlying dermal connective tissue.
 Overlying
epithelium

Islands of
Epithelial cells
Resembling basal
cells

Peripheral cells
Having palisading
Arrangement
Of nuclei

Connective tissue
stroma
 TREATMENT AND PROGNOSIS-
 Small lesion- <1 cm- Surgical excision with 5 mm
margins of clinically normal appearing skin.

 Large lesion- Radical surgical excision

Radiation therapy

 Recurrence rate- 30%

SQUAMOUS CELL CARCINOMA
 Approximately 94% of all oral malignancies are
squamous cell carcinoma.
 M:F- 3:1
 ETIOLOGY- Multifactorial, extrinsic and intrinsic
factors
 Tobacco smoking
 Smokeless tobacco
 Betel quid(paan)
 Alcohol
 Phenols
 Radiation
 Iron deficiency
 Vitamin A deficiency
 Syphillis
 Candidal infection
 Oncogenic virus
 Immunosuppression
 Oncogenes and tumour suppressor genes
 CLINICAL FEATURES-
 Exophytic- mass forming, Fungating, Papillary,
Verruciform
 Endophytic- Invasive, burrowing, Ulcerative
 Leukoplakic- White patch
 Erythroplakic- red patch
 Erythroleukoplakic- combined red and white patch

 Most common site- Tongue-posterior lateral and

ventral surfaces, Oral floor, Soft palate, gingiva,
buccal mucosa, labial mucosa, hard palate
 METASTASIS-through the lymphatics to ipsilateral
cervial lymph nodes. A cervical lymph node that
contains a metastatic deposit of carcinoma- firm to
stony hard, nontender and enlarged.
 HISTOLOGIC FEATURES- SCC arises from
dysplastic surface epithelium , invasive ,islands and
cords of malignant squamous epithelial cells.
 Lesional cells show abundant eosinophillic
cytoplasm with large, often darkly staining nuclei
with an increased nuclear to cytoplasmic ratio.
 Highly dysplastic
epithelium
Break in basement
membrane
Dysplastic cells
Invading connective
tissue
Multiple keratin
pearls

Connective tissue
with dense lymphocytic
Infiltration

SCC- Well differentiated

Dysplastic epithelial cells

Connective tissue with

inflammatory cells
Highly dysplastic
epithelium

Keratin formation
Highly dysplastic
Cells in connectice
tissue

Connective tissue
 TREATMENT AND PROGNOSIS-
 Intraoral SCC is guided by clinical stage of disease
and consists of wide surgical excision, radiation
therapy or combination of surgery and radiation
therapy.

 Prognosis for survival from oral cancer depends on

tumour stage, 5 year disease free survival rate
 76% if no metastasis
 41% if cervical node involved
 9% when metastasis below clavicle is present.
 VERRUCOUS CARCINOMA
 Also called- Snuff dipper’s cancer
 Ackerman’s tumor
 Verrucous carcinoma is a low grade variant of oral
squamous cell carcinoma.
 Reported first by Ackerman in 1948 as a spit
tobacco associated malignancy.
 Many verrucous carcinomas arise from the oral
mucosa in people, who chronically use chewing
tobacco or snuff, typically in area where the tobacco
is habitually placed.
 CLINICAL FEATURES-
 M>F
 Age- 65 to 70 years.
 Common site- mandibular vestibule, buccal mucosa,
Hard palate
 Diffuse, well demarcated ,painless, thick plaque
with papillary or verruciform surface projections.
 Lesions are typically white but may also appear
erythematous or pink.
 HISTOLOGIC FEATURES-
 Wide and elongated rete ridges that appear to push
into the underlying connective tissue.
 Parakeratin typically fills the numerous clefts
between the surface projections(Parakeratin plugs).
 An intense infiltrate of chronic inflammatory cells
in subjacent connective tissue.
Wide and
elongated rete ridges

chronic inflammatory
Cells

connective tissue
 TREATMENT AND PROGNOSIS-
 Surgical excision
 90% of patients are disease free after 5 years, some
patients require additional surgical procedures.
 SPINDLE CELL CARCINOMA
 Also called- Sarcomatoid Squamous cell carcinoma
 Polypoid squamous cell carcinoma

 Spindle cell carcinoma is a rare variant of squamous

cell carcinoma characterized by dysplastic surface
squamous epithelium in conjunction with an
invasive spindle cell element.
 CLINICAL FEATURES-
 Age range- 29- 93 years
 Common site- larynx, Oral cavity, esophagus
 In oral cavity- lower lip, lateral posterior togue,
alveolar ridges
 Pedunculated, polypoid mass
 Occasionally appear as sessile, nodular or fungating
mass or an ulcer.
 Pain and paresthesia.
 HISTOLOGIC FEATURES-
 Composed of fascicles of anaplastic spindle shaped
cells.
 Metastatic lesions may show only spindle cells, only
squamous cells or a combination of spindle and
squamous cells.

Spindle cells
 TREATMENT AND PROGNOSIS-
 Radical surgery with neck dissection.
 5 year disease free survival rate is approximately
30% for oral lesions.
ADENOID SQUAMOUS CELL CARCINOMA

 Also called as adenocanthoma,

 Pseudoglandular squamous cell carcinoma
 A squamous cell carcinoma containing
pseudoglandular spaces or lumina.
 This variant is produced as a result of acantholysis
and degenration within islands of a SCC. The result
is a pseudoadenocarcinomatous appearance but
there is no evidence of glandular differentiation or
of secretory activity or products.
 CLINICAL FEATURES-
 Common age- 50 years
 Common site- head and neck region
 Lip lesions- Ulcerated, hyperkeratotic, Exophytic

 HISTOLOGIC FEATURES-Proliferation of surface

dysplastic epithelium into the connective tissues.
 Lateral or deep extensions of epithelium show solid
and tubular ductal structures which typify the lesion.

 TREATMENT AND PROGNOSIS-

 Surgical excision, Recurrence rate- 38%
 LYMPHOEPITHELIOMA AND
TRANSITIONAL CELL CARCINOMA
 Unusual group of malignant neoplasms exhibiting
many features in common which involves
nasopharynx, oropharynx, tongue, tonsil and
anatomically asssociated structures such as the nasal
chamber and paranasal sinuses.

 This group of neoplasms consists of

lymphoepithelioma and transitional cell carcinoma
 CLINICAL FEATURES-
 Primary lesion- Very small, completely hidden.
 The tumor is indurated and appears as exophytic or
fungating growth.

 HISTOLOGIC FEATURES- Transitional cell

carcinoma consists of cells growing in solid sheets
in cords and nests.
 Lymphoepithelioma is made up of cells growing in
a syncytial pattern with the stroma infiltrated by
varying numbers of lymphocytes.

 TREATMENT- Radiation therapy

 undifferentiated cells

lymphoid cells

LYMPHOEPITHELIOMA
 MALIGNANT MELANOMA
 Also termed- melanocarcinoma, melanoma
 Malignant neoplasm of melanocytic origin that arises
from a benign melanocytic lesion or de novo from
melanocytes within normal skin or mucosa.
 ETIOLOGY- UV Radiation, Sun exposure
 Third most common Skin cancer
 25%- Head and neck area
 40%- Extremities
 Rest on trunk
 Oral mucosal melanoma-rare
 CLINICAL FEATURES-
 Age- 50-55 years
 4 types- Superficial spreading
 Nodular
 Lentigo maligna
 Acral lentiginous
 ABCD of malignant melanoma-
 A- Asymmetry
 B- Border irregularity
 C- Colour variation
 D- Diameter greater than 6 mm
 ORAL MELANOMA- Brown to black macule
with irregular borders.
 The macule extends laterally and a lobulated ,
exophytic mass develops once the vertical growth is
initiated.

 HISTOLOGIC FEATURES- Atypical

melanocytes are initially seen at the epithelial and
connective tissue junction.
 They have potential to proliferate throughout the
epithelium laterally along the basal cell layer and
downward into the connective tissue.
Malignant melanocytes
Invading connective tissue

Melanin pigments
 TREATMENT AND PROGNOSIS-
 Surgical excision with 3 to 5 cm margin for large
lesion and 1 cm for small early lesion.
 Prognosis for oral melanoma- poor
 CONCLUSION
 There are various benign and malignant
nonodontogenic tumors affecting oral cavity and
head and neck region. Prosthodontist play an
important role in rehabiliation of such patients; So
knowledge about different nonodontogenic tumors
is essential.
 REFRENCES
 Neville. Oral and maxillofacial pathology. Third
edition. Elsevier publication.
 Shafer’s Textbook of oral pathology. Fifth edition.
Elsevier publication.
 Harsh mohan. Essential Pathology for dental
students. Third edition. Jaypee publication.