Chapter 8

Oral malignant neoplasms

& premalignant lesion

1
 I . Oral Malignant Neoplasm
Classification according to the tissue of
origin:
1- Squamous cell carcinoma
2- Lymphoepithelioma
3- Basal cell carcinoma
4- Malignant melanoma
5- Sarcomas

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All white & red
lesions be submitted
for M/E in order to
determine their true
nature

High-risk sites for development of oral carcinoma. The shaded

U-shaped area accounts for only about 20% of the whole area of the
interior of the mouth but is the site of over 70% of oral cancers.
3
1- Squamous cell carcinoma
- Definition : A common epithelial malignancy of the oral
mucosa appearing as red , white , or ulcerated area. SCC is the
most common oral cancer.
- Etiology : While the cause of oral SCC is not known with
certainly , several risk factors have been identified : Tobacco ,
alcohol , viruses & sunlight .
1) Tobacco : Oral SCC occurs 5-10 times more commonly in
cigarette smokers. A number of studies have shown that
patients with oral SCC are far more common likely to use
tobacco products than the general population. The risk of
developing oral SCC 5-10 times in cigarette smokers than in
non-smokers .

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• As might be expected , the risk of cancer development increases with the
number of cigarettes consumed each day & the number of years that the
habit has been pursued . After cessation of tobacco use the risk of
developing oral SCC declines.
• Oral SCC is more common in those who use other forms of tobacco .
• Unlike lung cancer where cigarette smoking is the primary etiologic culprit
, pipe & cigar smoking as well as using chewing tobacco & snuff has be
implicated in the cause of oral SCC ,. The heat generated from the stems
of pipes has been suggested as causing some lip & palate cancers.
• Smokeless tobacco ( chewing tobacco & snuff) is associated with cancers
of the buccal mucosa & gingiva.
• The use of these of these products is of particular concern because of
their use by youngsters as they emulate tobacco – chewing professional
baseball players.

5
 2- Alcohol :
• Oral SCC is more common in heavy users of alcohol. It has been long
recognized that alcohol abuse & development of oral SCC are related .
• Here again , several studies have provided the basis for this linkage. . It is
postulated that excessive alcohol use dries the oral mucous membrane
somehow making it susceptible to cancer development . Like cigarette
smoking , the incidence of oral SCC declines with cessation of alcohol use.
It has been confirmed in later studies heavy alcohol use is the major risk
factor for development of oral SCC. Oral SCC is often found in those who
both smoke & drink.
• Cigarette & alcohol are , therefore , associated with the development of
most oral SCCs . It is a common observation that heavy alcohol users are
also heavy smokers. The two combined are a powerful risk factor for
development of this disease.

6
 3- HPV & HSV may participate in oral SCC
formation : There has been considerable
interest in the role of the human papilloma
virus ( HPV) & the herpes simplex (HSV) in the
development of oral SCC. Serologic or E/M
studies of oral SCC has demonstrated the
presence of these viruses in some cases.
While it is doubtfull that these organisms
acting alone can initiate a cancer , they may
act along with other ( alcohol ? Cigarette
smoke ? ) to cause malignant transformation “
cocarcinogen”
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 4- Sunlight exposure is associated in development of lip
SCC : Exposure to actinic radiation is clearly associated
with development of cancer ( SCC) of the lip. That this cancer
affects the lower , not the upper , lip & occurs commonly in
those in outdoor occupations , lead to the observation
5- Syphilis : syphilitic leukoplakia developing late in the
syphilitic patients . This leukoplakia has high malignant
potential .
6- Aging : It has already been mentioned that the incidence of
oral SCC becomes more common with increasing age.
Clinical picture : old age , sex: male than female , Site : not
affect all mouth areas equally . Incidence of SCC by location

8
 incidence Specific location General location

26% -Lateral surface Tongue

-Ventral surface

23% -Soft palate Oral pharynx

-Tonsillar pillars

20% - Vermilion surface Lip

17% - Floor of mouth Floor of mouth

9% -Gingiva Gingiva

3% - Buccal mucosa Buccal mucosa

2% - Hard palate Hard palate

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Relative risks of developing oral cancer
in consumers (males
in a western population) of tobacco and
alcohol. The relative risk for a
non-smoker and non-alcohol consumer is
taken as
1. A smoker consuming 30 cigarettes a
day and 20 alcoholic drinks a week is
seven times more likely to develop
carcinoma.

10
 - Commonly affected areas are “ high risk areas” for SCC.
- Review of the locations listed in the following table clearly demonstrate
that it is the lateral tongue , the ventral tongue , the soft palate , the
tonsillar pillars , & the floor of the mouth account for two thirds ( 66%) of
the cases of intraoral SCC.
-The lips are excluded from this figure because they are not within the
mouth ( not intraoral) & because the cure from lip SCC is very high.
- On the other hand , the cure rates for intraoral SCC is much lower.
- The risks associated with intraoral SCC are so high that “ high risk
areas” have been identified .
- These high risk areas are 1) the lateral tongue , 2) the ventral tongue , 3)
the floor of the mouth , 4) the soft palate , & 5) the tonsillar pillars.
- It is essential that dentists & dental hygienists include these areas in
intraoral clinical examination.

11
 High risk areas :
- Tongue , lateral
- Tongue , ventral
Intraoral high risk areas for SCC
- Floor of mouth
- Soft palate
- Tonsillar pillars

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Characters :
- Oral SCC can be recognised by changes in color &
texture in the oral mucosa.
- Oral SCC arises in the epithelium of the oral
mucous membrane.
-The changes associated with the development of this
malignancy produce changes that can be seen by an
observant clinician.
- These changes include alterations in colour , texture
, & shape of the oral mucous membrane.
- The appearance of oral SCC is variable.

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 -It is dependent on the stage in which it is discovered , how
aggressively the neoplasm behaves , & from what part of the
mucosa did it arise.
- Oral SCC often manifests as a painless , indurated ulcer :
-As will be seen later , once a cancer originating in the
mucosal epithelium invades the underlying C.T. ( lamina
propria) it is designated as being : invasive “ .
-In the remainder of that is a centimeter or larger in diameter
-The rolled & raised edges of the lesion surround a depressed
central region.
-The lesion is usually redder than the surrounding mucosa &
easily bleeded.
-Palpation reveals the lesion to be firm & “ fixed” to the
surrounding tissues , a property known as “ induration” .

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 The margins of ulcer is glazed , the floor is papillomatous
with foul odour.
- Red , white , or ulcerated lesions :
By the time oral SCC becomes a 1cm crated ulcer ,
invasion has surely occurred & the possibility of
metastasis is real.
The way to prevent this tragedy , of course , is to
discover oral SCC before invasion & metastasis occurs.
It turns out , that early changes manifest in a number of
different ways.
Some lesions are white , some are red & some are
speckled red & white.
Some are raised above the surface as smooth or
papillary or warty projections . And some are small non-
indurated ulcers.
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 Clinical designation Appearance

Indurated ulcer Indurated ulcer

Leukoplakia White patch

Erythroplakia Red patch

Speckled lesion Red/white patch

Exophytic papillary growth Papillary projection

Exophytic polypoid growth Smooth projection

Exophytic verrucous growth Warty projection

Non- indurated ulcer Soft ulcer

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Microscopic features :
• Microscopically oral SCC usually shows abnormal
keratinization.
• As it is name was designed to covey , oral “
squamous cell carcinoma “ is malignant neoplasm
that arises from covering & lining epithelium ( oral
mucous membrane).
• The disease probably arises from malignant
transformation of “ reserve keratinocytes “ located in
the stratum basalis or the stratum spinosum .
• Such transformation usually produces a neoplasm
that is able to produce some abnormal keratin.

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• The capability is sign of differentiation ; it is retention
means that the neoplasm is a “ moderately – well-
differentiated” one.
• Epithelial dysplasia = it means abnormal formation of
epithelium.
Signs of epithelial dysplasia :
1- basilar hyperplasia
2- loss of polarity & disorientation of cells.
3- cell nest formation
4- epithelial pearl & individual cell keratinization
5- abnormal mitosis
6- hyperchromatism of the nuclei
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7- alteration of N/C ratio
8- dyskeratosis ( nuclear atypia)
9- poikoilo karynosis ( division of the nucleus without division of
the cytoplasm) .
10- large prominent nucleoli.
• Keratinization is equated with a “ moderate “ level of
differentiation.
• Because most oral squamous cell carcinomas are moderately
to well differentiated neoplasms & retain some features of
keratinization , it is not surprising that most are composed of
polyhedral cells displaying “ intercellular bridges” &
abnormal keratinization.

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• Abnormal keratin manifests as whorls of flat keratinized cells
called “ keratin pearls” & as orange – staining cells indicating
“ individual cell keratinization “ .
• The identification of these features are important because
they identify the neoplasm as being 1) derived from covering
& lining epithelium & being 2) moderately to well –
differentiated .
• While this pattern is the common theme , from time to time
variations occur.
• Most of these do not show keratinization & are , therefore ,
less differentiated forms of the disease. Microscopically , the
invasive qualities of SCC can be seen clearly . Despite the level
of differentiation , virtually lesions demonstrate invasion of
the underlying tissues by groups of epithelial cells , a feature
that is

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 Obvious to the experienced eye. Such invasion may
penetrate lymphatic vessels , blood vessels , & nerve
sheaths providing metastatic pathway .
Treatment : Surgery ; radical surgery may be
necessary . - may be treated by radiation with or without
surgery , - Chemotherapy : to control dissemination
Prognosis : The prognosis depends on it is stage when
treated
1- the size tumour T ,
2- whether lymph nodes are involved N
3- whether distant has occurred M
Staging is accomplished by the TNM systems ,in the
following table :

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Prognosis Stage Definition TNM
100% 0 Tis = No invasion TIS , N0 , Mo
64% I T1= less than 2cm in diameter T1 , N0 , Mo
55% II T2= 2-4cm in diameter T2 , N0 , Mo
33% III T3=greater than 4cm in diameter T3, N0 ,M0
T1 , N1 , M0
T2 , N1 , M0
9% IV T4= greater than 4cm in diameter & T4 , N0 , M0
obvious invasion Any T , N2-3 , M0
Any T , any N , M1

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 Complications
complications Treatment
-Incomplete removal Surgery
-Deformity
-Osteoradionecrosis Radiation
-Radiation caries
-Xerostomia
-Mucositis
-Candida

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Squamous cell carcinoma of the lip :
• The lip is the most common site of oral cancer
Defintion : it is a malignant neoplasm arising from stratified squamous
epithelium
Clinically : age : middle & old age , sex : male more than female 2:1
Site : lower lip > upper lip ( 95% lower lip – 5% upper lip .
• Usually begin on the vermilion border to one side of the middle , it starts
as a small thickening , induration & ulceration covered with a crust , later ;
hard prominent mass , or crater like ulcer
• Crater like ulcer : Everted raised edges , Glazed margins , Papillomatous
floor , bleeding Foul odour , indurated base.
• Rate of growth & histopathology :
• Slow or rapid forming a large fungating mass. Most lip carcinomas are
grade : & II so : late metastasis to submental or submandibular L.N. ,
ipsilateral (same side ) or contrlateral

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Advanced carcinoma of lip. There is extensive Squamous carcinoma of lip. There is an indurated,
ulceration and necrosis and distortion. Nowadays crusted ulcer with keratosis at one margin in the
such extensive lesions are unusual. centre of the lower lip.

25
 Squamous carcinoma. Higher power shows strands of
malignant epithelium invading the connective tissue.

A small squamous carcinoma. At low

power the epithelium is seen to invade
deeply into the connective tissue and
underlying muscle. At this early stage
there is no ulceration.

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Squamous carcinoma. In this moderately well-differentiated Squamous carcinoma. At high power a group of
tumour many of the neoplastic epithelial cells are forming tumour cells shows typical cytologic irregularity.
keratin pearl Surrounding and beneath the tumour, muscle
fibres are being destroyed.

Squamous carcinoma. In this poorly-differentiated

carcinoma
there is little or no keratin formation and the malignant cells
show great pleomorphism with variably-sized nuclei, many
of which are hyperchromatic, and frequent mitotic figures.

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Squamous carcinoma. Less frequent than Squamous carcinoma. In this carcinoma malignant
perineural invasion is vascular invasion. Here epithelium is invading around nerve sheaths. Although
a cluster of poorly-differentiated malignant this is infrequent, occasionally carcinoma may spread
epithelial cells have eroded the wall of the some distance from the main tumour mass along nerve
vessel and entered the circulation. trunks.

28
29
 Histological variants of squamous cell carcinoma of the lip

Adenoid SCC Pseudoglandular Spindle cell carcinoma

Ca
-It follows senile keratosis of the lip . -Clinically similar to the common SCC but
-It starts as an elevated nodule that may be follows : X ray radiation , thermal burn , or
crusted or ulcerated . physical trauma
Rarely metastasize. -It is highly malignant it has :
-Good prognosis . -Early metastasis , grave prognosis ( cause
-It is least malignant death )
-Histologically : -Histologically : The tumour cells are :
It resembles the common SCC but deeper spindle –shaped , spindle or oval
epithelial extensions form : hyperchromatic nuclei , grouped in strands or
Solid & tubular duct – like structures which bundles in direct continuity with overlying
are lined by a layer of cuboidal cells & epithelium , exhibit mitosis & invade deeper
contain degenerating or dyskeratotic cells. tissue.

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Carcinoma of the tongue :
Malignant epithelial neoplasm of the tongue
• Etiology : Sepsis , spicy food , syphilis , Spirits ( alcohol) , smoking
• Clinical picture : Age : middle & old age , sex : male more than female ,
• Site : lateral border of the anterior part of tongue.
• Characters :
1) Exophytic or
2) Ulcer , which infiltrates the deep layers of the tongue , producing
fixation & induration , The ulcer has : irregular raised edges , glazed
margins , inflammed granulating floor , bleeding , foul odour , indurated
base due to infiltration of the surrounding by the tumour & to fibrosis.
• The tongue becomes stiff & more painful ( severe pain difficulty in eating ,
swallowing & talking ) as the growth is fixed & infiltrates the tongue .
Involvement of L.Ns is common.
• Hidden carcinoma of the tongue : Affect the posterior portion of the
tongue & are usually more malignant , metastasis early & offer a poor
prognosis.

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 Signs of hidden Ca of the tongue :
1- Slight deviation of the tongue to the affected side on protrusion ( Deviation ) due
to : a- restricted mobility of muscles ( tumour invasion )
b- paralysis of motor nerve
2- Slight defect in speech ( Defective speech )
3- Slight surface dimpling ( Dimpling ) , or other evidence of mucous membrane
retraction.
4- A minute ulcer at the most superficial point ( Defective surfaces )
5- Bleeding with a disagreeable fetid exudate ( Discharge )
6- Induration at the base ( Hardness )
Lymphatic drainage :
1- Tip of tongue – submental L.N.
2- Dorsum & sides of tongue – submandibular L.N.
3- Abnormal routes of cancer spread may occur
So all L.N of neck must be examined ( L.N become enlarged , hard & fixed )
Metastasis :
A- same side ( ipsilateral
B- bilateral ( contralateral)

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Local spread : Destruction of adjacent parts tongue becomes
fixed . Severe pain so swallowing & speech are difficult.
Cause of death :
1- Pain & infection cause difficulty in eating.
2- Aspiration of septic material from the mouth
( bronchopneumonia)
3- Haemorrhage
4- Metastasis to vital organs.
Histopathology : Poorly differentiated SCC Grade II & grade V

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Carcinoma of Maxillary sinus :
• It is a very serious disease as it is often advanced before the
patient discover it.
• Carcinoma of the maxillary sinus may be :
• SCC or adenocarcinoma ( originating from the glands in the
lining of the sinus ).
Clinical features :
1- Swelling of the maxillary alveolar ridge , palate or
mucobuccal fold.
2- loosens or elongation of the maxillary molars.
3- Swelling of the face inferior & lateral to the eye.
4- Unilateral nasal bleeding or discharge.
5- Difficulty of wear denture.

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• VERRUCOUS CARCINOMA : it is a form of SCC of the oral
cavity which was defined as an entity. It differs from usual SCC in :
1- slow growth 2- Exophytic growth 3- invade superficially
4- low tendency & late metastasis 5- not aggressive , needs local excision.
6- Always good prognosis.
Clinical features : Age : old age 60-70 y , Sex : 75% of lesions develop in males
( tobacco chewing ) , Site : Buccal mucosa , gingiva or alveolar mucosa .
Occasionally involves the palate or floor of the mouth.
Characters : Papillary or warty lesion covered by a white film. Patient complain of
pain & difficulty in mastication .
Histopathology :
1- Down growth of proliferating rete ridges.
2- Blunt rete pegs “ push down” but do not invade the underlying tissues.
3- Well differentiated epith. & shows little mitotic activity.
4- Cleft like spaces lined by a thick layer of parkeratin extend from the surface
deeply into the lesion.
5- Marked chronic inflammatory cell infiltration in the underlying C.T.
Prognosis : much better than usual SCC

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 Verrucous carcinoma. An extensive lesion covering most
of the buccal mucosa and starting to involve the skin at
the commissure. Such longstanding lesions are likely to
develop invasive squamous carcinoma and may then
metastasis.

Verrucous carcinoma. The epithelium is thickened and

thrown into a series of folds with a spiky parakeratotic
surface. Deeply the carcinoma retains a broad pushing front.

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2-Transitional cell carcinoma or
lymphoepithelioma :
- It is very malignant neoplasm.
- It runs a rapid clinical course , metastasize rapidly & widely & causes very early
death.
Clinical pictures : Age : old age , Sex : male more than female.
Site : the posterior part of the tongue , the tonsil or the nasopharynx & on the palate.
Characters : it may be
Very small hidden or slightly elevated or ulcerated . Sore throat , nasal obstruction ,
defective hearing or ear pain , headach , dysphagia & epistaxis. Metastasis to the
regional L.Ns occurs early before medical advice.
Histopathology :
sheets or cords & nests of : large round or polyhedral cells , with indistinct outlines
& large , round nuclei , variable degrees of mitotic activity.
The stroma is infiltrated by lymphocytes ( it is very radiosensitive).
Treatment : radiation.
Prognosis : poor because of early widespread metastasis & early recurrence.

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Basal cell carcinoma ( Rodent ulcer ) :
It is a locally malignant epithelial neoplasm .It arises from the basal cells.
Aetiology : - Ultraviolet rays of sunlight - Commonly affect blond people
Clinical features : Age : middle & old age , Sex : more common in males , site :
exposed skin surface , scalp & middle third of face . It may reach oral mucosa as it
extends from the skin.
Characters : Small elevated papule which ulcerate & heals over. Break down again &
later on superficial ulcer with smooth rolled border . The lesion invades locally all
tissue so it can erode the skull & kill the patient.
Histopathology : Nests with indistinct cell membranes or islands of cells with large
deeply stained nuclei or sheets with some mitotic figures.
- The peripheral cells of each cell nests are well polarized cells that resemble basal
cells.
- There is no or little tendency to differentiate .
- No metastasis
- But as the basal cells are pluripotential cells which form hair , sebaceous glands
sweat gland. Multiple basal cell carcinoma of the skin are a feature of the jaw cyst ,
bifid rib , basal cell naevus , syndrome

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39
40
4- Malignant melanoma
• It is the most deadly neoplasm , it arise from junctional nevus
Clinical features : Age : after 30 years of age , Sex : equal , Site : skin , eye ,
vaginal mucosa.
• Uncommon oral mucosa ( maxillary alveolar ridge & palate ) , cheek ,
tongue & floor of mouth.
Characters : It appears as enlarging pigmented area often surrounded by an
erythematous zone , frequently shows crusting , bleeding or ulceration .
• Oral lesion : appears as deeply pigmented area , often ulcerates & bleeds &
tend to increase in size..
• Metastasis are common to regional lymph node & to distant sites such as
liver & lung.
Histopathology : Closely packed cuboidal or fusiform cells arranged in an
alveolar pattern , reaching deep in the C.T. , mitotic activity & melanin
pigmentation.
Treatment : radical surgical resection.

41
42
 ?What kind of malignant cell would have pigment in it
43
44
Malignant C.T. neoplasms ( Sarcoma)
1- Fibrosarcoma : it is a malignant fibrous C.T. neoplasm
Clinical features : Age : 20-40 years , Sex L equal ,Site : buccal mucosa ,
palate , lip & jaw
Characters : It appears as a fleshy swelling , ulceration , haemorrhage &
secondary infection.
- it destroys the surrounding structures .
- Asymmetric swelling & distortion
- Metastasis are not frequent.
Histologic features :
- Proliferating malignant fibroblasts show anaplasia & mitosis.
- Interlacing collagen & reticulin fibers show spiral arrangement .
-Thin walled blood vessels.
- Giant cells & numerous abnormal mitotic figures in tumours.

45
Fibrosarcoma of the tongue. There are
streams of neoplastic fibroblasts, but the
striking feature is the spindle-shaped,
darkly staining nuclei and their variation in
size and mitoses.

46
2- Osteogenic sarcoma
• It is a primary malignant neoplasm of bone
• Unknown etiology but few cases follow irradiation of Paget,s disease of bone.
• Age : 10-20 years or old age if associated with Paget,s disease of bone., Sex : male
more than female , Site : body of mandible is more than maxilla.
• Radiographic : osteoblastic appear as radioopaque
osteolytic appear as irregular radiolucent area
3- Chondrosarcoma
• It is a malignant neoplasm of cartilage.
• Primary chondrosarcoma from the start or secondary from chondroma
• Age : 30-60 years , male more than female , site : mandible or maxilla
• X ray : radiolucent with radioopaque.
3- Ewing ,s sarcoma :
• It is a malignant neoplasm arising from bone marrow endothelium.
• Age : 5-25 years , male more than female , site : long bone , skull , clavicle ,
mandible & maxilla.
• Radiograph : onion skin appearance ( due to subperiosteal bone formation )

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The most common subtype is osteosarcoma that arises in the metaphysis of
long bones; is primary, solitary, intramedullary, and poorly differentiated;
and produces a predominantly bony matrix
48
 CHONDROSARCOMA

49
 Ewing sarcoma

50
Kaposi,s sarcoma : ( multiple idiopathic
haemorrhagic sarcoma of kaposi)
- It is the most common intra oral sarcoma after the
outbreak of AIDs ( acquired immune deficiency
syndrome ) .
• It is neoplastic disease of blood vessels.
• It mainly affects male homosexuals affected with
AIDS or immunosuppressed patient with organ
transplants.
• Site : multiple lesion on : extremities , face , oral
cavity , visceral organs.

51
 Kaposi's sarcoma. Lesions are red, maroon or
bluish and highly vascular. They may be flat or
form tumour masses and the gingivae or palate are
characteristic sites.

Kaposi's sarcoma. The tumour is composed of

spindled and plump cells with cytological atypia and
frequent mitoses. Many of the small holes visible
are the result of formation of capillaries.

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Non- invasive diseases preceding oral cancer :
General features of premalignancy & preinvasion :
- The first step in premalignant change is the development of dysplasia
( disorganisation of epithelial cells ) in oral cavity it is called mucosal
dysplasia
- In second step : malignant transformation has taken place stopping short of
invasion , this is called carcinoma in situ means malignant cells without
invasion
- the third lesion : benign keratosis .
There are several terms :
1- Benign keratosis
2- Mucosal dysplasia
3- Carcinoma in situ
4- Nicotine stomatitis
5- Actinic cheilosis
6- Oral submucous fibrosis

53
 Terms used concerning early oral SCC
Definition Term
A lesion caused by increased keratin production Keratosis
A red patch Erythroplakia
A white patch ( usually keratotic Leukoplakia
Normal keratosis Orthokeratosis
Increased thickness of the stratum corneum Hyperkeratosis
Retension of nuclei in the stratum corneum Parakeratosis
Cellular changes indicating anaplasia will follow Dysplasia
Cellular changes indicating malignancy Anaplasia
Spread of malignant cells into underlying C.T Invasion

54
MACRO- scopic (clinical) TERMS micro-scopic (histologic) TERMS

• macule • hyperkeratosis
• patch • parakeratosis
• papule • hypergranulosis
• nodule • acanthosis
• plaque • papillomatosis
• vesicle
• acantholysis
• bulla
• blister • spongiosis
• pustule • hydropic swelling
• wheal (ballooning)
• scale • exocytosis
• lichenification • erosion
• excoriation • ulceration
• onycholysis • vacuolization
• lentiginous
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MACROSCOPIC TERMS
Macule: Circumscribed lesion of up to 5 mm in diameter characterized by flatness and
usually discolored (often red)
Patch: Circumscribed lesion of more than 5 mm in diameter characterized by flatness
and usually discolored (often red)
Papule: Elevated dome-shaped or flat-topped lesion 5 mm or less across.
Nodule: Elevated lesion with spherical contour greater than 5 mm across.
Plaque: Elevated flat-topped lesion, usually greater than 5 mm across (may be caused
by coalescent papules).
Vesicle: Fluid-filled raised lesion 5 mm or less across.
Bulla: Fluid-filled raised lesion greater than 5 mm across.
Blister: Common term used for vesicle or bulla.
Pustule: Discrete, pus-filled, raised lesion.
Wheal: Itchy, transient, elevated lesion with variable blanching and erythema formed as
the result of dermal edema.
Scale: Dry, horny, platelike excrescence; usually the result of imperfect cornification
(i.e., keratinization).
Lichenification: Thickened and rough skin characterized by prominent skin markings;
usually the result of repeated rubbing in susceptible persons.
Excoriation: Traumatic lesion characterized by breakage of the epidermis, causing a
raw linear area (i.e., a deep scratch)
Onycholysis: Separation of nail plate from nail bed.
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MICROSCOPIC TERMS
Hyperkeratosis: Thickening of the stratum corneum, often associated with a qualitative
abnormality of the keratin.
Parakeratosis: Modes of keratinization characterized by the retention of the nuclei in the stratum
corneum. On mucous membranes, parakeratosis is normal.
Hypergranulosis: Hyperplasia of the stratum granulosum, often due to intense rubbing.
Acanthosis: Diffuse epidermal hyperplasia.
Papillomatosis: Surface elevation caused by hyperplasia and enlargement of contiguous dermal
papillae.
Dyskeratosis: Abnormal keratinization occurring prematurely within individual cells or groups of
cells below the stratum granulosum. Generally the same as DYSPLASIA.
Acantholysis: Loss of intercellular connections resulting in loss of cohesion between
keratinocytes.
Spongiosis: Intercellular edema of the epidermis.
Hydropic swelling (ballooning): Intracellular edema of keratinocytes.
Exocytosis: Infiltration of the epidermis by inflammatory or circulating blood cells.
Erosion: Discontinuity of the skin exhibiting incomplete loss of the epidermis.
Ulceration: Discontinuity of the skin exhibiting complete loss of the epidermis and often of portions
of the dermis and even subcutaneous fat.
Vacuolization: Formation of vacuoles within or adjacent to cells; often refers to basal cell-
basement membrane zone area.
Lentiginous: Referring to a linear pattern of melanocyte proliferation within the epidermal basal cell
layer. Lentiginous melanocytic hyperplasia can occur as a reactive change or as part of a neoplasm
of melanocytes.
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1- Benign Keratosis :
• It is a common lesion appearing as a white patch that is usually associated with
tobacco & /or alcohol use or with repeated frictional trauma.
• Atiology : - Toboacco - Alcohol - Chronic infection
• Benign keratosis is a common response of the oral epithelium to some irritant .
• Long term use of toboacco & /or alcohol as well as chronic traumatic irritation
( e.g. cheek biting may produce this lesion.
• The epithelial responds to such irritation by becoming thicker ( acanthotic) & by
producing keratin.
• It is these changes that make the lesion appear white ( leukoplakia) .
• While some etiologic factors of this condition are shared with oral SCC , it is not
all certain if benign keratosis is the earliest state in cancer development.
• Clinical features : Age : old age , Sex : male more than female , Site : cheek
( chronic irritation.
• Characters : The lesion may arise anywhere on masticatory or lining mucosa .
• The lesion is invariably white & may be flat ( macule ) or slightly elevated
( plaque)

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 Frictional keratosis. A poorly-defined patch of
keratosis on the buccal mucosa is due to friction from
the sharp buccal cusp of a grossly carious upper
molar.

Frictional keratosis. There is a slight hyperplasia of the basal

cells and a thick layer of orthokeratin at the surface.

59
 Oral keratosis of renal failure. Microscopy shows
acanthosis and a picture somewhat similar to hairy
leukoplakia.

60
• Histopathology :
• -Hyperkeratosis without dysplasia or anaplasia.
• - Bening keratosis shows thickening of the stratum spinosum
( acanthosis) & a prominent stratum corneum that may be
orthokeratinized or parakeratinized .
• - Other than these changes the epithelium is normal i.e. no
dysplasia , anaplasia , or penetration of the basement
membrane & invasion of the underlying C.T. .
• Treatment : complete excision will cure benign keratosis
• if small & send for M/E , if large , incisional biopsy & the
send for M/E

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2- Mucosal dysplasia ( premalignant )
• A common mucosal lesion appearing as a white or red patch or as soft
ulcer
Atiology :
• - Usually associated with toboacco & / or alcohol use
• - While chronic traumatic irritation may play a role , mucosal dysplasia is
most commonly associated with toboacco & alcohol abuse.
Clinical features : old age , male more than female site : high risk areas
Characters : A white / red patch or soft ulcer.
• The lesion may appear as a white patch ( leukoplakia) , or red patch
( erythroplasia) , a white , red patch ( speckled ) or a soft ulcer .
• It usually occurs in an area at high risk for oral SCC but may be seen
elsewhere ( e.g gingiva & buccal mucosa )

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Histopathology : Dysplasia without anaplasia .
- Keratinization may or may not be prominent in mucosal
dysplasia ; if it is , the lesion white , if not , it is red.
- The characteristic M/E is the presence of dysplasia in the
stratum basale & lower layers of the stratum spinosum. -
While dysplasia is present , there is no anaplasia , no
permeation of the basement membrane , & no invasion of
underlying tissues.

Treatment : complete excision will cure mucosal dysplasia .

• Because it is impossible to diagnose mucosal dysplasia from
clinical examination , it is necessary to biopsy all lesions of
the oral mucosa.

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 Homogeneous leukoplakia
Speckled leukoplakia

Red lesion
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Ulcer lesion
 Hairy leukoplakia

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 Mild dysplasia. In this lesion there is Mild dysplasia. In this lesion there is a
prominent orthokeratosis and a keratohyaline thin layer of parakeratin and the
layer immediately below it. Dysplasia is more structure, maturation and orderly
prominent than in the previous figure, with differentiation of the epithelial cells is
enlarged hyperchromatic and bizarre cells in largely unaffected. However, there is a
the basal and lower prickle cell layers. degree of irregularity of basal cells with
variation in size and hyperchromatism.

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 Moderate dysplasia. The dermal papillae extend close to the
surface and there are elongated rete processes, some of which
are broader deeply. Enlarged and hyperchromatic cells are
visible at this low power in rete processes and in most of the
prickle cell layer.

Severe dysplasia. This rete process is

composed almost entirely of cells with dark
and irregularly shaped nuclei. Only the most
superficial layers of cells show maturation to
squamous cells and the orderly maturation
and differentiation of epithelial cells has been
lost.

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3- Carcinoma – in situ ( preinvasive condition =
intraepithelial carcinoma ) :
- Lesion appearing as a white & / or red patch or as soft ulcer.
- Like dysplasia associated with toboacco & alcohol abuse & to a
lesser degree repeated irritation.
Clinical features : Age : old age , Sex : male more than female ,
site : high risk areas
Characters : - A red patch or soft ulcer
- As a general rule , carcinoma in situ manifests as
velvety red patch while increased keratin production
production & a resulting leukoplakia is a possibility , it is
biopsy erythroplasia that so often returns a diagnosis of “
carcinoma in situ “ .This lesion is generally found in the high
risk areas for oral SCC however , it may occur elsewhere.

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Histopathology : Much anaplasia but no invasion ,
intact basement membrane.
As just mentioned , keratinization is not a usual feature
of this condition.
The unique features of carcinoma in situ are :
1) anaplasia that affects the entire stratum spinosum &
2) the lack of invasion through & below the basement
membrane.
The presence of anaplasia confirms that the lesion is
malignant ( carcinoma) but the absence of invasion
warrants it is designation as “ preinvasive “.

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Nicotinic Stomatitis :
An uncommon condition caused by smoking tobacco
Etiology : Smoking pipes , cigars & cigarettes which are directed
toward the mucosa of hard palate that produces this lesion.
Clinical picture : Old age , male more than female , site : hard
palate.
Characters : Leukoplakia of the hard palate
- The hard palate takes on a grey to white colour depending on
the amount of smoke directed toward it.
Scattered raised areas with red centers complete the clinical
picture.

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• The raised areas are clumps of minor salivary glands & the
central red dots are the openings of their ducts.
• It is because ducts are lined with nonkeratinizing epithelium
that they appear red.
Histopathology :
- Hyperkeratosis with or without dysplasia.
- As the white nature of the lesion suggest , the stratum
corneum is prominent.
- The remainder of the epithelial layers are usually ; however ,
it is possible for dysplasia or anaplasia to be present.
Treatment : Cessation of smoking .

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 Stomatitis nicotina (smoker's palate). There is a generalised
whitening with sparing of the gingival margin. The inflamed
openings of the minor salivary glands form red spots on the
white background.

Stomatitis nicotina (smoker's palate). The epithelium is

hyperplastic and hyperkeratotic, especially around the orifice of
the duct where there is a concentration of inflammatory cells.

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5- Actinic Cheilosis :
• Caused by excessive exposure to sunlight & manifesting as
crusting lesion of the lower lip.
• Etiology : unprotected excessive exposure to sunlight .
• The condition is caused by chronic over exposure to actinic
radiation ( sunlight) .
• The lesion is commonly found in those following outdoor
occupations .
• Because of this relationship , the lesion is most commonly
seen in males ; while females are also pursuing outdoor
occupations , their use of lip coverings may protect them from
the disease.

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• The heat generated in pipe smoking & the
carcinogenic materials found in cigar wrappings may
also cause the condition.
Clinical picture : Age : old age , Sex: male more than
female , Site : lower lip
Characters : As a crusting lesion of the lower lip .
Actinic cheilosis is recognized crusting of the lower
lip . It may manifest as a small single lesion or may
transform the entire lip. The lesion is dry & crusting .
Palpation usually reveals that the lesion has caused a
thickening of the lip ( induration ).

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Histopathology :
• Dysplasia , anaplasia , or invasion.
• The stratum corneum is very thick & is composed of many
layers of keratin. Their may be dysplasia or anaplasia in the
stratum spinosum a finding that means , of course , the lesion
may be as ominous as mucosal dysplasia or carcinoma in situ.
While dysplasia & anaplasia may be present , it is very
uncommon for invasion to occur. The underlying C.T. often
shows an abnormal staining reaction attributed to action of
sunlight ( solar elastosis ) .
Treatment : complete surgical excision will cure actinic
cheilosis.

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 Contact cheilitis

.Actinic cheilitis
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6- Oral submucous fibrosis :
• It is a chronic disease affecting oral mucous membrane
Etiology : unknown , but may be due to 1- chilis 2 – spicy food.
Clinical picture : Age : over 40 years , Sex : female
Site : Buccal mucosa , soft palate , tongue & lips.
Race : Indian people.
Character : burning sensation , vesicle , ulceration of the vesicles , excessive salivation
firstly then xerostomia , defective taste sensation , stiffness of the oral mucosa ,
inability to eat , swallowing , difficulty in opening the mouth
Histopathology :
- Atrophy of the epithelium
- Flattened rete ridges.
- Dysplastic epithelium.
- Hyalinization in C.T.
- Homogenous collagen fibers
- Chronic inflammatory cells.
- less fibroblasts & narrow blood vessels

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