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Benign and malignant tumors

Dr Sreeja C
Reader
Dept of Oral Pathology
• Definition by Willis(1952):
– A neoplasm can be defined as an abnormal mass
of tissue, the growth of which exceeds and is
uncoordinated with that of the normal tissue and
persists in the same excessive manner, even after
cessation of the stimulus that evoked the change.
Epithelial pathology
Connective tissue pathology
Classification of benign and malignant tumors

1.NEOPLASMS OF EPITHELIAL TISSUE ORIGIN


Malignant neoplasm
Benign neoplasm
1. Papiloma 1. Basal cell carcinoma
2. Keratoacanthoma 2. Squamous cell carcinoma
3. Pigmented cellular nevus 3. Verrucous carcinoma
4. Malignant melanoma
5. Spindle cell carcinoma
6. Primary intra-alveolar carcinoma
2.NEOPLASMS OF MESENCHYMAL ORIGIN
Benign neoplasm Malignant neoplasm

NEOPLASMS OF TISSUE FIBROUS


a.NEOPLASMS OF FIBROUS CONNECTIVE
CONNECTIVE TISSUE
Fibroma 1. Fibrosarcoma
Fibromatosis 2. Malignant fibrous Histiocytoma
Pyogenic granuloma
Giant cell fibroma
Peripheral ossifying fibroma
Central ossifying fibroma
Peripheral giant cell granuloma
Central giant cell granuloma
Benign fibrous histocytoma
b.NEOPLASM OF ADIPOSE NEOPLASM OF ADIPOSE
TISSUE TISSUE

1. Lipoma 1. Liposarcoma

c. NEOPLASM OF VASCULAR NEOPLASM OF


TISSUE VASCULAR TISSUE

1. Haemangioma 1. Haemangiopericytoma
2. Lymphangioma 2. Haemangioendothelioma
3. Angiosarcoma
d. NEOPLASM OF OSSEUS NEOPLASM OF OSSEUS
TISSUE TISSUE

1. Osteoma 1. Osteosarcoma
2. Osteoid osteoma 2. Parosteal osteosarcoma
3. Ewing’s sarcoma
3. Osteoblastoma
4. Osteoclastoma
5. Torus palatines
6. Torus mandibularis
e. NEOPLASM OF NEOPLASM OF
CARTILAGINOUS TISSUE CARTILAGINOUS TISSUE
1. Chondroma 1. Chrondrosarcoma
2. Chondroblastoma

f.NEOPLASM OF NEURAL NEOPLASM OF NEURAL


TISSUE TISSUE
1. Neurolemmoma 1. Neurosarcoma
2. Neurofibroma 2. Olfactory
Neuroblastoma
3. Neurofibromatosis
1. Peripheral nerve sheath tumor
4. Multiple endocrine Neoplasia syndrome
5. Traumatic neuroma
6. Plexiform neuroma
g. NEOPLASMS OF SMOOTH NEOPLASMS OF SMOOTH
MUSCLE TISSUE MUSCLE TISSUE

1. Leiomyoma 1. Leiomyosarcoma
2. angiomycoma 2. Angiomyosarcoma

h. NEOPLASM OF STRIATED NEOPLASM OF STRIATED


MUSCLE TISSUE MUSCLE TISSUE

1. Rhabdomyoma 1. Rhabdomyosarcoma
2. Granular cell myoblastoma
3. Congenital epulis of new born
i. NEOPLASM OF LYMPHOID NEOPLASM OF LYMPHOID
TISSUE TISSUE

No benign neoplasm 1. Hodgkin’s lymphoma


2. Non Hodgkin’s lymphoma
3. Burkitt’s lymphoma
4. Leukemias
5. Multiple myeloma
6. Plasmacytoma

j. NEOPLASM OF MIXED NEOPLASM OF MIXED


TISSUE TISSUE
1. Teratoma
k. NEOPLASM OF SALIVARY NEOPLASM OF SALIVARY
GLAND TISSUE GLAND TISSUE
SQUAMOUS
PAPILLOMA

•Papilloma virus HPV -6,11


•Exophytic, pedunculated,small finger like surface projections,
roughened cauliflower like surface
•Non contagious
•Tongue , lip and buccal mucosa
• Common wart or
verruca vulgaris –
skin
• HPV 2,4,40
• AUTO
INNOCULATION
• COWDENS
SYNDROME –
Multiple papillomas,
palmar plantar
keratosis,
haemangiomas,
xanthomas, lipomas
Treatment

• Surgical excision
KERATOACANTHOMA

Also called as self healing carcinoma


Clinically and pathologically resembles
epidermoid carcinoma
Starts as papule nodule with a
central crater with keratin plug

Grows static regression


Thickened layer of ortho or
parakeratin with central
plugging
Acanthosis of the marginal
epithelium and evelation
into center of crater
Treatment
• Surgical excision
NEVUS
• Hamartomas, developmental malformations
Benign proliferations of nevus cells in the epithelium or
connective tissue.
• Skin lesion with melanin pigmentation

Congenital (common in skin) Acquired


•Intradermal
•Junctional
•Compound
Small(3-5cm) Garment (10cm) •Spindle cell
•Macules to elevated hairy •Blue cell
Acquired nevi
• 8th month
• Increase with age (peak 3rd decade)
Intradermal nevus (common mole)
• Several lesion scattered over the body
• Most common
• Smooth flat or elevated
• Not seen in – soles of feet, palms and genetalia
Junctional nevus
• Distinct histologically and on prognosis
Compound nevus
• Intradermal and junctional
Spindle cell nevus /Blue nevus
• smooth and hair on surface
• Clinically benign and histologically malignant
• Not on mucous membrane
Other variants
Neural, balloon cell, halo nevi
NEVUS contd…
Oral manifestation
Except spindle cell all acquired nevi occur in oral cavity
All decades- except first
M:f = 1:2
Site: hard palate, bu mu , gingiva
Raised pigmented lesion , 20 %- flat
DD: melanotic macule, premalignant melanosis, amalgam tatoo
NEVUS contd…
Histopathology:

•Nevus cell
•Neural crest origin
•Resemble melanocytes but lack dentritic process
•Large cell with Ovoid shaped nucleus and pale cytoplasm
•Grouped in sheets or cords and contain granules of melanin
pigments in their cytoplasm
•Arranged in nests or theques
NEVUS contd…
Histopathology contd….
Intradermal nevus:
• Nevus cell within C.T
• Sep by a thick band of C.T from the overlying epithelium
Junctional nevus :
• No demarcation
• Nevus cell bled into the overlying epithelium
• Cross jn into C.T - abtropfung or dropping off effect
• Malignant change
Compound nevus :
• Nest of nevus cell dropping off from the epidermis, large nest also seen in
the dermis
Spindle cell nevus /Blue nevus:
• Pleomorphic cells – 3 types – spindle , oval , epithelioid
• Deeper dermis
• The reality is- Once we
make our move , we have
no control over the moves
the opponent will make.
• The opponent also has his
or her plan
• Whether its game of life or
game of chess , not
everything goes according
to what we had envisioned
in our lifes
• reason to go with the flow
• To not to be rigid about
what we had decided
To learn to change our strategies as
per the moment…..
• Adjust your plans
• Adapt to the challenges that life throws on
you
• Adopt new strategies to match those of your
opponent
• In life, apply the greatest virtue of flexibility
• Never be rigid
As she emanates from the Himalayan mountains with her plan
to move to reach her destination, shes not rigid
Montains through challenges in the
form of rock, zshe doesn’t stop
• Whatever challenges come on your path , just
keep moving…….
Potentially malignant disorders
(Precancerous lesions and
conditions)
Potentially malignant disorders
• " was defined by World Health Organization (WHO)
as the risk of malignancy being present in a lesion or
condition either during the time of initial diagnosis or
at a future date. Classified as….
• Precancerous lesion
• Precancerous condition
Precancerous lesion
• Also called Precancer, Premalignancy
• A benign, morphologically altered tissue in
which cancer is more likely to develop than its
apparently normal counterpart.
Precancerous condition
• A generalised state or disease which can be
associated with greater than normal risk of
cancer development.
CLASSIFICATION
Precancerous lesion Precancerous condition
• Leukoplakia • Oral submucous fibrosis
• Erythroplakia • Actinic keratosis/chelitis
• Palatal lesions in reverse • Erosive lichen planus
smokers • Discoid lupus
• Tobacco pouch or snuff erythematosus
dippers keratosis • Dyskeratosis congentia
• Epidermolysis bullosa
• Plummer wilson syndrome
Leukoedema :
• Is an abnormality of the buccal
mucosa which clinically resembles
early leukoplakia, but appears to
differ from it in certain aspects.
• ETIOLOGY: Developmental, smoking
C/F:
• Filmy opalescence of the mucosa in
early stages to a more definite
grayish-white coat with a coarsely
wrinkled surface in later stages.
• Usually occurs bilateral
• Buccal mucosa- along occlusal plane
• On stretching outward- lesion
disappear
H/F :
• Increase in thickness of epithelium, intracellular edema of the
spinous layer
• Broad rete pegs which appear irregularly elongated
• Characteristic edematous cells appear extremely large and
pale, present as reticular pattern.
• Cytoplasm appears lost
• Nuclei appear absent, clear or pyknotic.Inflammatory cell
infiltration.
Leukoplakia
• Leuko – white, plakia –
patch
• WHO def - a white patch or
plaque that cannot be
characterized clinically or
pathologically as any other
disease.
• Could be due to thickened
keratin layer or thick
spinous layer masking the
normal vascularity
• Considered to be a
precancerous lesion
Leukoplakia
• Etiology :
Predisposing factors are best remembered as 8 S
• Smoking (tobacco), Spirit , Sharp tooth , Spicy food ,
Syphilis, Sepsis (HSV-1,HPV,
Candidasis),sunlight(Actinic radiation), sanguinaria
• Vitamin deficiency- Both vitamin A and B deficiency
• Galvanism
Clinical features
• Male predilection
• Mostly occurs in 4th to 7th decade of life
• Site:
Buccal mucosa and commisures are
commonly involved, followed by alveolar
mucosa, lip, tongue, hard and soft palates,
floor of the mouth and gingiva.
Types:
• 1.Homogenous 2. Non-homogenous

a.Speckled
b.Nodular
c.Verrucous
d.Proliferative
verrucous
HOMOGENOUS
Uniform white patch
,Usually plaque like,slightly
raised mucosa
some are smooth, may be
wrinkled or criss-crossed by
small crack or fissure.
• Malignant transformation
– 1 to 7%.
Leukoplakia- Homogenous
NON-HOMOGENOUS LEUKOPLAKIA
TYPES –
1. Speckled (High
malignant
transformation)
2. Nodular
3. Verrucous
4. Proliferative
verrucous
leukoplakia
• NODULAR/GRANULAR
SPECKLED/ERYTHRO LEUKOPLAKIA

• Mixed red
and white
area
• Advanced
dysplasia in
biopsy
NON HOMOGENOUS- VERRUCOUS
PROLIFERATIVE VERRUCOUS LEUKOPLAKIA
• Multiple
keratotic
white plaques
with
exophytic and
verrucous
projections

• Strong female
prediliction

• No habits
Dysplasia
- defined as loss in uniformity of cells along with loss in oreintation
SMITH-PINDBORG CRITERIA:
1. Drop-shaped rete ridges.
2. Loss of epithelial stratification.
3. Keratinisation of the cells below the keratinised layer- dyskeratosis
4. Basal cell hyperplasia.
5. Acanthosis
6. Loss of intercellular adhesion.
7. Loss of polarity.
8. Hyperchromatic nuclei.
9. Increased nuclear-cytoplasmic ratio in basal and prickle cell layer.
10. Pleomorphism of cells and nuclei.
11. Anisocytosis of cell and nuclei
12. Mitotic activity.
13. Keratin pearl formation
14. Presence of bizarre mitosis
A clinical staging system for oral leukoplakia (OL-system) on the
lines of TNM staging was recommended by WHO in 2005 taking
the size (L)and the histopathological features (P) of the lesion
into consideration.

• L1: Single or multiple lesions together <2 cm.


• L2: Single or multiple lesions together 2-4 cm.
• L3: Single or multiple lesions together >4 cm.

• P0: No epithelial dysplasia.


• P1: Mild to moderate epithelial dysplasia.
• P2: Severe epithelial dysplasia.
• Stage I: L1 P0.
• Stage II: L2 P0.
• Stage III: L3 P0 or L1/ L2 P1.
• Stage IV: L3 P1
DIFFERENTIAL DIAGNOSIS
(Definable lesions)
• White sponge nevus
• Frictional keratosis
• Chemical burns
• Acute pseudomembranous candidiasis
• Leukoedema
• Lichen planus (plaque type)
• Lichenoid reaction
• Discoid lupus erythematosis
• Stomatitis nicotina palate
• Oral hairy leukoplakia
DD…
Oral hairy leukoplakia
• Hairy leukoplakia is a condition that is
characterised by irregular white patches on the
side of the tongue,bilaterally
Etiology -
• chronic irritation.
• Associated with Epstein-Barr virus (EBV) and
• occurs primarily in HIV-positive individuals.
• Male predilection
• Most common in 40 – 60 years of age
OHL
TREATMENT AND PROGNOSIS

• The first step in treatment is to arrive at a


definitive histopathologic diagnosis.
• Therefore, a biopsy is mandatory and will
guide the course of treatment. Tissue to be
obtained for biopsy, should be taken fromthe
clinically most "severe" areas of involvement .
• Multiple biopsies of large or multiple lesions
may be required.
1.Chemoprevention
• L-Ascorbic Acid (Vitamin C)
• α-Tocoferol (Vitamin E)
• Retinoic Acid (Vitamin A)
• Vitamin A derivative, isotretinoin, and 13-cis retinoic acid:
28,500IU per day.
• Beta-carotene 150,000 IU of beta-carotene twice per week for
six months.
• Bleomycin-Topical bleomycin in treatment of oral leukoplakia
was used in dosages of 0.5%/day for 12 to 15 days or 1%/day for
14 days.

2.surgical
PROGNOSIS
• Duration of lesion
• Gender
• Site
• Clinical appearance
• Habit association
• Degree of dysplasia
• ?????
????
• HOMOGENOUS LEUKOPLAKIA
????
• NODULAR LEUKOPLAKIA
????
• HAIRY LEUKOPLAKIA
???
???
???
????
ERYTHROPLAKIA/ERYTHROPLASIA OF QUEYRAT
• The word erythroplakia means
"red patch“
• Erythroplakia of the genital
mucosae - erythroplasia of
Queyrat.
• WHO-1978
Any lesion of the oral mucosa that
presents as bright red velvety
plaques which cannot be
characterized clinically or
pathologically as any other
recognizable lesion.
• Histologically- always dysplastic
change
CLINICAL FEATURE:
• Age:65-75
• Gender: men
• Site: floor of
mouth, tongue,
soft palate
• c/f:
well demarcated
erythematous
patch/plaque with
soft velvety texture.
Asymtomatic
DD
1.Inflammatory /immune disorders
• Desquamative gingivitis
• Erosive lichen planus
• Discoid lupus erythematosus
• Pemphigoid
• Allergic reactions

2.Infections:
• Erythematous candidasis
• Histoplasmosis

3. Hamartomas/neoplasia
• Haemangioma
• kaposi sarcoma
HISTOPATHOLOGY
• 90% REPRESENT- severe
dysplasia, ca in situ,
invasive SCC.
• EPITHELIUM- atrophic,
lack keratin production-
show through
underlying blood vessel
• CONNECTIVE TISSUE-
chronic inflammation
Treatment and prognosis
• Surgical excision
• Mutifocal oral involvement and recurrence
• Long term follow up
Tobacco pouch keratosis
• Two forms of smokeless tobacco-
1.chewing tobacco
2. Snuff
Two major carcinogen
1. Methyl nitrosamine
2. Nitrosonicotine
Lesion strongly influenced by:
Duration, brand, total hrs /day, site
Clinical features
• Gingival recession
• PDL destruction
• Attrtion
• Extrinsic stains

• ALTERED MUCOSA- soft velvety


feel on palapation or wrinkled
surface Sand on beach after
ebbing tide appearance
• pouch distinct on stretching
Sand on beach
after ebbing tide
appearance
classification
• Degree1: slight superficial wrinkling. Color
change- normal to grey. No thickening
• Degree2: wrinkling obvious, Whitish grey, no
thickening
• Degree3: Mucosa thickened with white patch,
deep furrows
Histopathology
• Hyperkeratinized
and acanthotic
epithelium
• Parakeratin
chevrons
• Sub ep vascularity
increased
• Amorphous
eosinophillic
material
• Mild dysplasia
treatment
• Habit cesation
• Low malignant transformation rate
4. Palatal lesions in reverse
smoking
• Specific to population(south american and
south east asian) who smoke with lighted end
of the cigar or cheroot inside the mouth
C/F
• MEN
• 45 YRS
• Palate
• Whitish grey---elevated papules----palatal
keratosis---fissured or dried mud appearance
• Present as- white, red and white or red lesion
HISTOPATHOLOGY
• Hyperkeratosis and
acanthosis of palatal ep
• Chr inflammation
Treatment and prognosis
• Habit cesation
• High malignant transformation
PREMALIGNANT CONDITION

ORAL SUBMUCOUS FIBROSIS


Condition – A generalized state associated with
a significant increase risk of cancer
Ex-
Oral submucous fibrosis
Actinic keratosis/chelitis
Erosive lichen planus
Discoid lupus erythematosus
Dyskeratosis congentia
Epidermolysis bullosa
Plummer wilson syndrome
Preceeded, associated, followed, leading
Definition
SCHWARTZ – atropica idiopathica mucosae oris
SIRSAT AND PINDBORG’S :
An insidious chronic disease affecting any part of oral
cavity and sometimes pharynx , occasionally
preceded by/associated with vesicle formation and
always associated with juxta epithelial inflammatory
reaction followed by hyalinization of lamina propria
with epithelial atrophy leading to stiffness of oral
mucosa and progressive limitation in mouth
opening
• Preceeded, associated, followed, leading
Epidemiology
• Affects up to 0.5% of Indian population

• Incidence is rising, especially amongst younger


population
ETIOLOGY
• ARECANUT
• CAPSACIN

• DEFICIENCY OF IRON/VIT B12- affect the


integrity of oral epithelium ,leading to
increase absorption of arecanut alkaloids into
mucosa

• GENETIC SUSCEPTIBILITY – HLA A10, B7, DR3.


TGF β
ROLE OF ARECANUT
Derived from endosperm of fruit of areca catechu t
• Arecanut- various forms-
• Betel quid-
arecanut+betel leaf+lime
with/out tobacco
• Raw arecanut –
seeval flakes, Kotta pakku
granules
• Pan masala- Powdered
arecanut+additives
• Gutka-Powdered
arecanut+tobacco
PATHOGENESIS –
OSMF

Increased decrease collagen Collagen


collagen degradation stabilization (Cu)
production (tannins)
(arecoline)
Increased collagen Increased cross
production linking of collagen

FIBROSIS
Increased collagen production Decreased collagen degradation
• Tannins --- inhibit
• Alkaloids collagenase
• TGF-β • TGF-β (as a response to
inflammation t cell)–
Increased cross linking 1.activation of
plasminogen activator
of collagen inhibitor- (PAI)---increase
Cu- increase salv in PAI---- plasminogen is
copper-diffusion through not converted to plasmin-
ep cells- reach c.t- --- Procollagenase not
increase lysyl oxidase- converted to collagenase-
-- decreased collagenase--
increase cross linking of - decreased degradation
collagen- fibrosis • 2.activation of TIMP
Normal values
Parameters Male Female
Mouth opening- 47.5 mm 44.6 mm
inter incisal
distance
Tongue 24.9 mm 24.8 mm
protrusion
Cheek flexibility 9.7 mm 9.0 mm
Clinical features
• GENDER :M:F – 4:1
• AGE : Young adults – older age group
• SITE: buccal mucosa, retromolar area, soft palate, uvula, labial
mucosa, floor of mouth
• Difficulty in mouth opening
• Burning sensation
• Pallor of mucosa
• Palpable vertical bands
• Initial stages: vesicles, petechiae, melanosis, xerostomia
Ranganathan et al
• Group1- only symptoms
without restriction in
mouth opening
• Group 2- limited mouth
opening, above 20mm
• Group 3- below 20mm
• Group4- OSMF with
precancerous /cancerous
changes throughout the
mucosa
Prodromal signs & Symptoms –
Rajendran et al(2003)
Early OSF

• Burning sensation
• vesicles- especially on the palate

• Dryness

• Defective gustatory sensation


Prodromal signs & Symptoms….. –
Rajendran et al(2003)
Advanced OSMF
• Blanched oral mucosa
• Fibrous band in buccal mucosa and labial
mucosa
• Shrunken bud like uvula
• Impairment in tongue movement
• Difficulty in mouth opening
HISTOPATHOLOGY
• Hyperkeratosis with marked
epithelial atrophy
• Rete pegs -flattened
• Sub epithelial hyalinization
• Dense connective tissue
• Variable no of inflammatory
cells
• Degeneration of muscle
Pindborg et al -four stages
• Very early stage
• Early stage
• Moderately advanced stage
• Advanced stage
OSMF DIAGRAM
Management
GENERAL MANAGEMENT:
• Reduction or even elimination of the habit of areca nut
chewing .At least in the early stage of OSMF, it could
probably slow the progress of the disease
• Vitamin B complex and iron
• Physiotheraphy – mouth opening with heat theraphy

SPECIFIC MANAGEMENT:
1.MILD CASES- Intralesional Corticosteroids(decrease TGF)
2. Moderate to Severe – Surgical splitting
• Excision of the fibrous bands
• Intralesional Injections- Interferon-g
Malignant transformation rate of OSMF 7–13%
recap
• Definition
• Etiology
• Pathogenesis
• Clinical features- Ranganathan and Rajendran
et al
• Histopathology- PINDBORG
• Management
• Malignant transformation
Case-1
• Advances in ISSN: 2573-2862 ACP Cytology & Pathology
• Case ReportVolume 2 Issue 1 - 2017
• Oral Submucous Fibrosis-A Case Report
• Asha Ml, Aprajita Dua*, Lekshmy L, Basetty Neelakantam Rajarathnam,
Mahesh Kumar HM and Ankita Gupta
• Department of Oral Medicine and Radiology, Syamala Reddy Dental
College, India
• Received: January 30, 2017 | Published: February 03, 2017
• *Corresponding author: Aprajita Dua, Department of Oral Medicine and
Radiology, Syamala Reddy Dental College, #111/1, SGR College Main Road
Munnekolala, Marathahalli (Post), Bangalore- 560037, India, Tel:
09972458292; Email:
• Citation: Asha ML, Dua A, Lekshmy J, Rajarathnam BN, Kumar MHM, et al.
(2017) Oral Submucous Fibrosis-A Case Report. Adv Cytol Pathol 2(1):
00011.
• Patient had sunken
cheeks with reduced
cheek blowing capacity
and tongue protrusion
and restricted mouth
opening
• Bud shaped uvula
• Inter
incisal
-
19mm
• Inspection: mucosa appeared blanched
• On palpation interincisal opening was limited to 19 mm. Vertical
bands were palpable in the buccal mucosa with respect to right
posterior molar region on right side and the retro molar area.
Case-2
• CASE REPORT
• Year : 2012 | Volume : 30 | Issue : 1 | Page : 85-88

• Oral submucous fibrosis: A report of two pediatric cases and a brief


review

• R Dhariwal1, JG Ray2, S (Mohanty) Pattanayak2, N Swain3


• 1 Department of Oral Pathology, M. M. C. D. S. R., Mullana, Ambala,
Haryana, India
• 2 Department of Oral Pathology, Dr. R. Ahmed Dental College and
Hospital, Kolkata, West Bengal, India
• 3 Department of Oral Pathology, M. G. M. Dental College and
Hospital, Navi Mumbai, Maharashtra, India
Case-2
• A 12-year-old local factory worker boy reported
with difficulty in opening mouth and taking
spicy food for the last 3 months.
• Both his parents were labourers. He was
reportedly chewing gutkha two to three times a
day for the last 1 year, as his colleagues at the
local factory encouraged him to take the habit.
• Intraoral
view
showing
difficulty in
mouth
opening
with
blanching
of oral
mucosa,
generalized
stains
• Inter
incisal-
15mm
Case-3
• A 12-year-old girl complained of burning sensation on
having food for the last 3-4 years, which has
aggravated recently.
• The girl's grandmother was a habitual pan masala
chewer and unaware of the consequences, used to
give her granddaughter a small amount of it almost
daily since she was 5 years old.
• Shrunken uvula and
generalized blanched
muco
• Inter-incisal
distance=1.9
cm
VERRUCOUS CARCINOMA/SNUFF DIPPERS
CANCER
HISTORY
• Verrucous carcinoma of the oral cavity was first reported by
Ackerman in 1948.

• In 1960, Rockand Fisher described a similar lesion, which they


named oral florid papillomatosis.

• It is now agreed that oral florid papillomatosis merely represents a


verrucous carcinoma of the oral cavity. It has also been referred to
as Ackerman tumor or verrucous carcinoma of Ackerman.
Verrucous carcinoma CONTD…

• Etiology –
• Tobacco - snuff dipping, and betel chewing, all of which
may cause leukoplakia
• HPV-16,18

• Preceded by leukoplakia- 57% of patients in one series.


• It may also be preceded by oral lichen planus, chronic
candidiasis, and chronic lupus erythematosus.
Verrucous carcinoma CONTD…
CLINICAL FEATURES
• Age/ gender elderly (65-70 yrs)
white men.
• Site buccal mucosa and the gingiva.
• Usually painless
• Clinical appearance
• Early stages- white keratotic patch.
• Later- it appears as a soft, rubbery,
papillary verruciform growth that
may have ulceration.
• Patients may have lymph
adenopathy due to secondary
infection simulating a metastatic
tumor
Verrucous carcinoma CONTD…

Histology
• Reveals a sharply circumscribed
tumor, with marked
papillomatosis and overlying
hyperkeratosis.
• Broad bulbous acanthotic
projections of epidermis may
extend deep into the stroma.
• Parakeratin plugging
• An associated dense
inflammatory cell infiltrate is
often present. Little atypia is
present inmost cases.
VERRUCOUS CARCINOMA
RADIOGRAPH
• Local
destruction may
occur, with
invasion into
bone.
Verrucous carcinoma CONTD…

Treatment
• Although distant metastases are rare, local
destruction may occur, with invasion into
bone.
• The treatment of choice is surgical excision.
• Radiation therapy should be avoided due to
the risk of anaplastic transformation to a more
aggressive form of SCC.
CASE REPORT -1

Mrs.NAVAMMA (OP.NO:1921434)

55Years /F

C/O Pain in the left lower back tooth

region for the past 1 week


PERSONAL HISTORY
• H/O betel quid (betel nut, lime chewing
with tobacco) use for 35 years

• Quids the betel quid in the left posterior


buccal vestibule
INTRA ORAL VIEW
SHOWING THE LESION
AN AXIAL VIEW
SHOWING THE LESION
A CLOSE UP OF THE LESION

Intra oral examination:

 two well defined


lesions.

 the posterior part of the


lesion showed white,
minute and numerous
finger like projections

 This lesion was encircled


by a homogeneous white
plaque with surface blebs
Intra oral
examination:

the borders of the

verrucous lesion in the


posterior part of the
lesion seems to invade
into the mucosa.
DIAGNOSTIC POINTS
 Female patient

 Fifth to sixth decade

 Use of smokeless form of tobacco

 Presence of multiple minute projections from the surface

 Borders invading into the mucosa

 A well defined lesion

 Homogenous white plaque encircling the central verrucous

lesion
PROVISIONAL DIAGNOSIS

Verrucous Carcinoma

Left Buccal Mucosa

Associated With

Leukoplakia!!!
DIFFERENTIAL DIAGNOSIS:

VERRUCOUS HYPERPLASIA

– Similar in appearance

– Borders evade out of the surface


Investigations

• Routine haemogram

• OPG
INVESTIGATION: Advised OPG
CROPPED OPG • An ill- defined saucer shaped

radiolucency

• In relation to the left mandibular

body

• Borders of the radiolucency had a

wide margin of transition with the

surrounding bone.

• Loss of considerable amount of

bone in relation to the root of 36

• 36 had a floating tooth

appearance
SO WE ADVISED BIOPSY:

• INCISIONAL
BIOPSY :
• SITE : L
Buccal
mucosa
• 1x1cm
HISTOPATHOLOGY
REPORT
The H&E section shows
cleft with
Parakeratin plugging.

The underlying
connective tissue shows
Collagen
fibers,adipocytes and
muscles
• The surface epithelium shows hyper para-

keratinisation with intact basement

membrane and juxta epithelial inflammatory

reaction also seen.

• The retepegs showing pushing effect with

dysplastic features.
H/P DIAGNOSIS

VERRUCOUS CARCINOMA
DIAGNOSIS

VERRUCOUS
CARCINOMA
(OR)
ACKERMANS
TUMOR!!!!
TREATMENT

• slow growing

• late to metastasize

• normally advised surgical excision.

• Reccurence is uncommon

• prognosis is much better than OSCC.


CASE -2
• Journal of Skin Cancer
Volume 2011 (2011), Article ID 370605, 4 pages
http://dx.doi.org/10.1155/2011/370605Case Report
• A Troubling Diagnosis of Verrucous Squamous Cell Carcinoma (“the Bad
Kind” of Keratosis) and the Need of Clinical and Pathological Correlations:
A Review of the Literature with a Case Report
• A. Santoro,1 G. Pannone,1 M. Contaldo,2 F. Sanguedolce,1 V. Esposito,2 R.
Serpico,2 L. Lo Muzio,3 S. Papagerakis,4 and P. Bufo1
• 1Section of Anatomic Pathology and Cytopathology, Department of
Surgical Sciences, University of Foggia, Viale L Pinto 1, 71100 Foggia, Italy
2Department of Odontostomatological, Orthodontical and Surgical

Sciences, Second University of Naples, Via De Crecchio 1, 80138 Naples,


Italy
3Section of Oral Pathology, University of Foggia, Viale L Pinto 1, 71100

Foggia, Italy
4Division of Head and Neck Surgery and Oncology, Department of

Otolaryngology, University of Michigan Medical School, Ann Arbor, MI


48109, USA
77 YR MALE
CASE-3
• Verrucous Carcinoma with Dysplasia or
Minimal Invasion:
• A Variant of Verrucous Carcinoma with
Extremely Favorable Prognosis
• Kalyani R. Patel • Rebecca D. Chernock •
• Parul Sinha • Susan Mu¨ller • Samir K. El-
Mofty •
• James S. Lewis Jr.

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