....

2.  Willis defined neoplasia as
‘An abnormal mass of tissue, the growth of
which exceeds that of normal tissues and
persists in the same excessive manner after
the cessation of the stimuli which evoked the
change.’

3.  A focal malformation that resembles a
neoplasm, grossly and even microscopically
 A mass of histologically normal tissue in an
abnormal location
 There is an abnormal mixture of tissue
elements normally present at the site.
 It develops and grows at the same rate as
normal tissue and is not likely to compress or
invade adjacent structures (in contrast to a
neoplasm).

4.  A rare benign tumour consisting of
microscopically normal tissue derived from
germ cell layers foreign to that body site
 A mass of histologically normal tissue in an
abnormal location

5.  A true neoplasm made up of different types
of tissue, which may not belong to the area
in which it occurs; usually found in the ovary
or testis
 It develops from multipotent cells of more
than one primitive embryonic layer
(ectoderm, endoderm, mesoderm), which
differs in prognosis according to the organ
involved and degree of maturation of the
tissues
 Benign or malignant

6. Benign
1. Epithelial origin
 Papilloma
 Keratoacanthoma
 Pigmented cellular
nevus
2. Fibrous connective
tissue
 Fibroma.
 Giant cell fibroma.
 Ossifying fibroma.
 Myxoma
Malignant
1. Epithelial origin
 Basal cell carcinoma.
 Squamous cell
carcinoma.
 Verrucous carcinoma.
 Melanoma
2. Fibrous connective
tissue
 Fibrosarcoma

7. Benign
3. Adipose tissue
• Lipoma
4. Blood vessels.
• Hemangioma,
• Heridetary hemorrhagic
telangiectasia
5. Lymphatic vessels
• Lymphangioma
6. Bone
• Osteoma.
• Osteoid osteoma,
• Osteoblastoma
Malignant
3. Adipose tissue
• Liposarcoma.
4. Blood vessels.
• Hemangiopericytoma
• Hemangioendotheliom
• Kaposi’s sarcoma.
5. Lymphatic vessels.
• Lymphangiosarcoma
6. Bone
• Osteosarcoma,
• Parostealosteosarcoma,
• Ewing’s sarcoma

8. Benign
7. Cartilage
• Chondroma,
• Benign
chondroblastoma.
8. Lymphoid tissue
No benign tumours.
9. Plasma cells.
No benign tumous
Malignant
7. Cartilage
• Chondrosarcoma
8. Lymphoid tissue
• Hodgkin’s lymphoma
• Non-Hodgkins
lymphoma,
• Burkitt’s lymphoma,
• Mycosis fungoides.
9. Plasma cells.
• Multiple myeloma

9. Benign
10. WBC’s
 No benign tumours
11. Nerve tissue
 Traumatic neuroma,
 Schwannoma,
 Neurofibroma,
 Melanotic neuroectodermal
tumour of infancy.
12. Smooth muscle
 Leiomyoma,
 Angiomyoma
Malignant
10. WBC’s
 Leukemias
11. Nerve tissue
 Malignant
schwannoma.
 Neurofibrosarcoma.
 Neuroblastoma
12. Smooth muscle
 Leiomyosarcoma,
 Angiomyosarcoma.

10. Benign
13. Striated muscle
Rhabdomyoma.
Granular cell
myoblastoma
Congenital epulis of the
newborn.
Malignant
13. Striated muscle
Rhabdomyosarcoma.
14. Metastatic tumours
Carcinomas
Sarcomas

11. Feature Benign Malignant
Size of tumour Usually small Usually large
Rate of growth Slow Very Fast
Pain Absent or rare Mostly present
Haemorrhage Rare Very common
Ulceration Absent Present
Paresthesia Does not occur Commonly occurs
Fixation to surrounding
tissues
Absent Often fixed to
neighbouring structures

12. Feature Benign Malignant
1. Metastasis Absent Common
2. Cell multiplication
rate
Slow Very fast
3. Cell maturation Near normal Immature cells
4. Cell morphology Not altered Morphology is lost
5. Cell function Normal Altered or lost
6. Tissue
architecture
Mantained Mostly destroyed
7. Superadded
infection
Absent Very common
8. Prognosis Good Bad

13.  Benign
1. Papilloma
2. Keratoacanthoma
3. Pigmented cellular nevus or pigmented
mole
 Malignant
1. Squamous cell carcinoma
2. Basal cell carcinoma
3. Verrucous carcinoma
4. Malignant melanoma

14.  Generic disease process representing
localized epithelial proliferations that typically
have a roughened surface (exophytic
growth).
 Usually associated with HPV
 Oral papillomas include:
1. Squamous Papilloma
2. Verruca Vulgaris
3. Condyloma Acuminatum

15.  Benign proliferation of stratified squamous
epithelium.
 It produces a papillary or verruciform mass.
 It the fourth most common oral mucosal mass .
 Common lesion .( 3% of all oral lesions) ( 7-8% of
oral lesions in children are squamous papillomas)
 The growth may be induced by HPV virus; usually
Type 6 and 11.
 HPV 6 and 11 have been identified in 50% of
squamous. HPV 6 and 11 have very low
infectivity or virulence rates.

16.  Double stranded DNA virus of papovirus family
 Buccal epithelial cells of 81% normal adults
have at least one type of HPV
 Higher levels are present in disease and lower
in normal cells
 The exact mode of transmission is not known
but person to person spread by sexual and non
sexual routes transmission has been proposed

17.  Equally in males and females.
 Any age but more common in persons
between 30 and 50 years
 May develop at any intraoral site; tongue,
lips, buccal musosa, soft palate

18.  It appears as soft, painless, pedunculated
exophytic nodule with numerous finger like
projections on its surface
 This is termed as a verruciform or cauliflower
like growth
 The growth is white, red or of normal colour,
depending on the amount of keratin present
 Papillomas are generally solitary and enlarge to
a maximum size of about 0.5 cms

20.  Proliferation of keratinized stratified
squamous epithelium, in the form of
rounded finger like projections
 Each epithelial projection has a central core
of fibrovascular connective tissue
 The surface keratin layer is thickened in
lesions with a whiter clinical appearance
 Features of mild atypia like basilar
hyperplasia and few mitotic figures may be
seen in the epithlium
 Koilocytes, (virus altered epithelial cells)
appear as clear cells with small dark
pyknotic nuclei in the spinous cell layer

22.  Common wart, associated primarily with
HPV types 2, 4,6 & 40
 Very common on the skin, uncommon on
oral mucosa
 Usually occurs in the anterior aspect of the
oral cavity due to autoinoculation
 Oral lesions are always white in colour
indicating heavy keratinization.
 Very contagious lesion

23. Differences from squamous papilloma
1. The epithelial projections are pointed and
narrow.
2. The elongated reteridges converge towards
the centre ‘cupping effect’
3. Keratin layer is very thick
4. Stratum granulosum is prominent with
eosinophilic intranuclear inclusions
5. Significant number of koilocytes are seen

25.  Venereal/genital wart, typically associated with
HPV 6,11,16,18,53,54. Oncogenic HPV 16 & 18
are common in anogenital lesions but less
common in the oral cavity
 Typically seen in the anterior aspects of the
mouth and on the lingual frenulum .
 This is a STD with lesions developing at site of
sexual contact or trauma
 When seen in children, indicative of child
abuse.
 Incubation period is 1 -3 months
 The lesion is highly contagious

26.  Condylomas may be multiple, are typically
non-keratinized, and are thus the same
colour as surrounding tissue.
 Histologically, shows broader papillomas
than the squamous papilloma
 Koilocytes are prominent in cervical lesions.

28.  Surgical excision , including the base of the
lesion
 Recurrence is unlikely
 No reports of malignant transformation
 Non surgical modes of excision like laser
ablation, cryotherapy, topical agents like
podophyllotoxin are also used
 Anogenital lesions are at high risk for
malignant transformation

29.  Role of HPV vaccine against HPV 6,11,16
and 18 is recommended by CDC(centre for
disease control)to prevent cervical cancer
and anogenital papillomas
 This vaccine may also prevent lesions in H &
N region
 However there is no guideline for this
vaccine to be used to prevent oral lesions

30.  Familial occurrence is reported.
 HPV 13, 32 related
 Familial occurrence due to genetic
susceptibility or HPV transmission
 Poor hygiene, lower socio economic status
are risk factors
 Increased frequency in AIDS

31.  Multiple soft, non tender
papules. (cobblestone
appearance)
 Same colour as normal
mucosa.
 Does not recur after
removal
 No risk of malignant
transformation

32.  Sinonasal papillomas
 Molluscum contagiosum (poxvirus group),
(molluscum bodies / Henderson-Paterson
bodies)
 Verruciform xanthomas (lipid laden
histiocytes in the connective tissue)

33.  Verruca vulgaris
 Condyloma acuminatum
 Verruciform xanthoma
 Focal epithelial hyperplasia

34. Tumour HPV type Contagious Sites affected
1. Squamous
papilloma
Type 6 and 11 •Not contagious.
•Low infectivity
and virulence
Mucosal
2. Verruca
vulgaris
Type 2,4,6,40 •Contagious Skin
3. Condyloma
Acuminatum
Types
6,11,16,18,53,54
•Contagious .
•Sexually
transmitted
Mucosal
4. Hecks
disease
Type 32,13 •Not contagious Mucosal

35.  Also called as self healing cancer.
 Clinically and histopathologically, it
resembles a squamous cell carcinoma.
 It originates in the pilosebaceous glands.
 It is relatively common low grade malignancy
that originates in pilosebaceous gland.

36.  Exposure to sunlight.
 Exposure to coal tar.
 Trauma.
 HPV (9,11,13,16,18,24,25,33,37,57)
 Genetic factors.
 Immunocompromised state.

38.  Solitary firm, round papules, which rapidly
progress to dome shaped nodules, with
central crateriform ulceration or keratin plug
which projects like a horn.

39.  Clinical course is very typical.
 It starts as a small firm nodule which grows in
size over 4-8 weeks.
 It remains static for next 4-8 weeks.
 It then undergoes spontaneous regression over
next 4-8 weeks by expulsion of the keratin and
resorption of the mass.
 Overall duration of the lesion as long as 2 yrs.
 The rapid growth which is seen leads to
suspicion of malignancy.

41.  Hyperplastic squamous epithelium which grows
into the underlying connective tissue.
 The epithelium shows hyper parakeratosis or
hyper orthokeratosis.
 Central plugging of keratin is seen.
 At the deep epithelial margin, the islands of
epithelium appears to be invading the
connective tissue.
 This leads to suspicion of squamous cell
carcinoma.

42.  Clinical features and histologic features
suggestive of malignancy.
 However it heals on its own without any
treatment.
 Thus termed as ‘Self healing cancer’.

45.  Rolled out margins with central ulceration.
 The most common skin cancer.
 80% of BCC occur on the skin of head and neck
region.
 Locally invasive malignancy, which does not
metastasize.
 Pathogenesis- BCC is believed to arise
from pleuripotent stem cell compartments of
basal layer of epidermis as well as follicular
structures(hair follicle stem cell just below the
sebaceous gland duct)

47.  Mutation in the p53 tumour suppressor gene.
 Mutations in PTCH I gene and dysregulation
of the sonic hedgehog signaling pathway are
responsible for development of BCA.

48.  It is usually seen in adults with a fair
complexion (FOURTH DECADE OF LIFE).
 Male to female ratio 3:2.
 Most frequently seen in middle third of face.
 Persons with red hair and blue eyes are
particularly susceptible to this form of
malignancy.
 It is a locally invasive, slow growing epithelial
malignancy which does not metastasize.
 BCA does not occur on oral mucosa except
by extension

49. The clinical types include- NPSSCMM
 Nodular basal cell carcinoma (most common
type)
 Pigmented BCA (contains several normal
melanocytes, therefore appears brown, black
or blue)
 Sclerosing BCA (can be mistaken for scar
tissue)
 Superficial BCA (appears as multiple scaly
lesions)

51.  Most common variety .Begins as a firm
painless papule with a central
depression(Umblicated appearance).
 One or more telangiectatic blood vessels are
seen coursing over the border around the
central depression.
 Ulceration starts in the centre.
 Intermittent bleeding and healing is reported.
 If untreated, it keeps enlarging slowly with
destruction of the underlying structures bone
and cartilage.

52.  The different clinical types have variable
histopathologic appearances
 In the nodular BCA, the tumour cell is an
ovoid, dark staining basaloid cell with
moderate sized nuclei and little cytoplasm
 The cells are arranged in well demarcated
islands and strands.
 The cells appear to arise from the basal cell
layer of overlying epidermis
 Palisading of peripheral cells is evident

53.  Cleft formation,known as artifactual
retraction may be seen between the
epithelial islands and the connective tissue
 This is due to shrinkage of mucin during
tissue processing
 In pigmented BCC,benign melanocytes are
present around the tumour produces large
amount of melanin.
 In superficial BCC,buds of basaloid cells
attached to the undersurface of epidermis.

54.  Nests of various sizes are seen in upper dermis.
 In morpheaform and infilterating type,strands of tumour
cells embedded in dense fibrous c.t stroma.

55.  Sometimes a BCA of skin can develop
simultaneously with SCC of underlying oral
mucosa.
 This has been termed as baso squamous
carcinoma
 It can be considered as a basal cell
carcinoma with squamous metaplasia

56.  Depends on the site and size of the lesion
 Small lesions< 1cm are treated by surgical
excision and laser ablation(X-ray radiation)
 At least 5 mm margin of normal tissue is
excised.
 Recurrence and metastasis are rare
 In patients with large lesions, death may be due
to local invasion into vital structures
 Treated patients should be reviewed at regular
intervals as there is 30% chance of second
tumour developing within 3 years of treatment

57.  Malignancy of epidermal melanocytes
 Can develop de novo or from a benign
melanocytic lesion
 This is the third most common skin cancer.
 Most deaths are caused by this form of skin
malignancy .
 Oral mucosal melanoma is rare as compared
to skin melanomas.
 The mucosal melanomas are diagnosed at a
later stage and are more aggressive than the
skin lesion .

60.  Environmental -
 Sun exposure
 Relative with history of melanomas
 Fair complexion
 Light coloured hair
 Tendency to sunburn easily and history of
several episodes of blistering sunburn in
childhood
 Personal history of congenital or dysplastic
nevus

62. Two growth phases.
•Radial .
•Initial phase.
•Spreads horizontally in
the epidermis.
•This phase may last for
several years.
•No metastasis
•Vertical.
•Neoplastic cells proliferate into
the dermis.
•Reflects increased virulence of
cells or decrease in host
immunity.
•Metastasis is common.
•Not all melanomas show
both phases.
•Some are in vertical growth
phase from the beginning

63.  Superficial spreading melanoma.
 Nodular melanoma.
 Lentigo maligna melanoma(Hutchinson
melanoma)
 Acral lentiginous melanoma.
 Mucosal lentiginous melanoma
 Amelanotic melanoma

64.  Most common type of cutaneous melanoma
in caucasians.(65%)
 It does not usually spread into connective
tissue. It shows radial growth phase.
 Also called melanoma in situ or premalignant
melanosis.
 If it infilterates into the connective tissue,
there is increase in size,colour,nodularity and
ulceration.
 The lesion presents as tan , brown , black or
admixed lesion on sun-exposed skin.

65.  It accounts for approximately 13% of
cutaneous melanomas.
 An aggressive infilterative form of lesion
 Colour may be pink-brown or black
 It shows vertical growth from the start
 Sometimes the cells are so poorly
differentiated that lesion becomes
depigmented and has same colour as normal
mucosa ( amelanotic melanoma)
 Predilection- back,head,neck skin of men

66.  10% of cutaneous melanomas
 Lentigo maligna is a precursor lesion for
melanoma. (Melanotic freckle of Hutchinson)
 It is melanoma in situ it consists of malignant cells
but does not show invasive growth.
 It can remain in this non-invasive form for years.
 The lesion occurs as a macular lesion on the malar
skin of middle aged and elderly caucasians.
 It occurs more often in women than men
 It shows radial growth phase

67.  When lentigo maligna develops into
melanoma, the resulting lesion is called
lentigo maligna melanoma.
 The transition to melanoma is marked by
the appearance of a bumpy surface.

68. SSMLM
 More aggressive
 Younger patients
 Trunk and lower limbs
 Quicker transition to vertical
growth phase
 Less aggressive
 Older patients
 Face
 Vertical growth happens later

69.  50% Commonest form of melanoma in Black
races and Asian skin
 The tumour is macular,lentiginous pigmented area
around a nodule
 Commonest form of oral melanoma
 It develops on non hair bearing surfaces of the
body which may or may not be exposed to
sunlight. ( palm, sole, nailbed)
 Aggressive form of disease.
 Initially it is a macular lesion ( radial growth), later
it becomes lobulated and exophytic ( vertical
growth)

71.  Atypical melanocytes are seen at epithelium-
connective tissue junction
 The cells spread horizontally and vertically
 Single or groups of abnormal cells are seen in
the epithelium
 The tumour cells contain melanin granules
 The intraepithelial component(radial growth
phase) of superficial spreading melanoma is
characterised by presence of large,epithelioid
melanocytes distributed in a so called “pagtoid”
manner.

76.  When vertical growth occurs, cords or sheets
of atypical melanocytes are seen in the deep
connective tissue
 Amelanotic tumour cells can be identified by
positive reaction to S-100 ( indicating neural
crest origin), HMB -45 ( indicating a
melanocytic tumour), Melano A ( Indicating
melanocytes)

77. A----Asymmetrical growth of lesion,one half
does not match the other half.
B----Border irregularity with blurred,notched or
ragged edges.
C----Colour variation from red to brown to black
to blue in the same lesion.
D----Diameter larger than 6 mm.
E----The lesion is raised or elevated above the
surface.

78.  The treatment of cutaneous malignant
melanoma is surgical excision
 Elective lymph node dissection is performed
if regional lymph nodes are palpable.
 Sentinel node biopsy is done if regional
lymph nodes are not palpable
 Chemotherapy,immunotherapy and radiation
therapy for cutaneous melanoma

80.  Oral melanomas have a very poor prognosis
than cutaneous melanoma.
 The site does not affect survival.
 Younger patients have better survival than
older patients.
 Acc. to pliskin, the 5-year survival rate(FYS)
for such tumours is approximately 7%.
 Invasion to depth more than 0.75mm is
indicative of very poor prognosis

81. Grading based on depth of invasion of the tumour-
CLARK SYSTEM
 Level 1: Tumour cells only in epidermis-100-98
 Level 2: Tumour cells in papillary dermis-96-72
 Level 3: Tumour cells in whole of papillary
dermis-90-46
 Level 4: Tumour cells in reticular dermis-67-31
 Level 5: Tumour cells invading subcutaneous fat-
48-12
 OTHER CLASSIFICATION-BRESLOW SYSTEM
classification for skin melanomas

82. Based on
T
N
M
Additional factors :
 Presence of ulceration
 Elevated serum lactic dehydrogenase
Tumour thickness
Regional node metastasis
Distant metastasis

83.  Stage I and II: No regional or distant
metastasis.
 Stage III: Regional node are involved.
 Stage IV : Distant metastasis present

84.  This is a low grade variant of oral squamous cell
carcinoma ( metastasis is extremely rare)
 First described by Ackerman in 1948
 It is associated with habit of chewing tobacco
(Smokeless tobacco or snuff tobacco)
 Ill filling dentures
 It represents 1-10% of all oral squamous cell
carcinomas
 Also reported in nonchewers; maybe associated
with HPV 16 and 18
 Similar tumors develop from nasal mucosa of snuff
users

86.  More common in men of older age group(60-
70years)
 Similar incidence in women who chew
tobacco (75%in males)
 The site of lesion corresponds to site where
the tobacco quid is placed
 Most common sites are mandibular
vestibule, gingiva, buccal mucosa, tongue
 Other sites are alveolar ridge, palate and
floor of mouth.

87.  Lesion appears as a well demarcated,
painless thick plaque with papillary or
verruciforn surface projections
 Lesions are usually white due to heavy
keratinization
 Some lesions appear red to pink if there is
less keratin and significant inflammatory
response
 As the lesion grows into the underlying
tissue, bone, cartilage, muscle and salivary
glands may be destroyed

88.  Enlarged regional nodes usually indicate a
reactive inflammatory response
 The neoplasm is cheifly exophytic,appears
as papillary in nature,covered by white
leukoplakic film
 Lesion commonly have rugae-like folds with
deep cleft between them
 Pain and difficulty in mastication are
common complaint

89. Lesions like leukoplakia and tobacco pouch keratosis
may be seen adjacent to the growth

90.  Benign appearance microscopically.
 The surface is papillary or verrucous form.
 Typically there are elongated, wide
reteridges that ‘push’ into the deeper
connective tissue
 Therefore, verrucous carcinoma is an
exophytic and endophytic growth.
 No significant cellular atypia is seen

91.  Surface is covered with thick layer of
parakeratin.
 Parakeratin also fills the spaces between the
surface projections.
 This is called ‘parakeratin plugging’-Hallmark
 Dense infiltration with chronic inflammatory
cells is seen in the subepithelial connective
tissue

92.  Diagnosis is based on histopathology.
 A large deep biopsy which includes a margin
of normal tissue is necessary for diagnosis.
 The entire tissue must be examined after
excision to detect presence of invasive SCC
in the same tumour

95.  This is a low grade malignancy
 Treatment of choice is surgical excision with a
wide margin but no radical neck dissection
 If SCC is present along with verrucous
carcinoma, it must be treated like a SCC
 Radiotherapy is used in inoperable cases
 Chemotherapy may be used as a adjunct.
 The prognosis is much better than SCC.

96.  Squamous cell carcinoma is a malignant
epithelial neoplasm exhibiting squamous
differentiation as characterized by
formation of keratin and presence of
intercellular bridges
 Most common malignant neoplasm of oral
cavity.
 Squamous cell carcinoma comprises 90-
95% of all oral malignancies
 Prevalence of oral cancer in India is
13.5/100,000 cases.(0.1%) (2005)

97.  The incidence of oral SCC of the oral cavity
differs widely in various parts of world and ranges
approximately 2 to 10 per 100,000 population per
year.
 High incidence countries those in south Asia such
as India, Pakistan , Bangladesh and countries
central and Eastern Europe ,Brazil.
 Incidence in oral carcinoma in blacks than in
whites
 M:F - 2:1, IN carcinoma of lower lip strong male
Predominence.
 ORAL SCC mainly found after the fourth decade.

98.  It forms 45% of all cancer in India.
 In India, the oral cavity(ICD-9,ICD141,ICD-143-145) is
one of the five leading sites of cancer in either gender.
 The age standardized incidence rates(ASR) very from 6.2
per100,000 in banglore to 16.1per 100,000 in bhopal
among urban males,and from 3.5per 100,000 in delhi
to7.8per 100,000in chennai among urban female.
 On the basis of the cancer registry data,it is estimated
that annually 75,000-80,000 new oral cancer develop in
India.
 In India,the majority of oral cancer associated with the
tobacco chewing habits,and usually preceded by
premalignant lesions.

99.  OF the areas of oral cavity, the mortality rate is
lowest for lip cancer(0.04per 100,000)and
highest for the tongue(0.7per 100,000) .
 More than 90% of oral cancers occurs in
patients at the age over 45 years.
 NCRP was initiated in India in1982.
 NCRP(NATIONAL CANCER REGISTRY
PROGRAMME) helped in highlighting the
magnitude and common sites of oral cancer in
India, was useful in planning NCCP (NATIONAL
CANCER CONTROL PROGRAMME)

100.  Males----Lungs and stomach.
 Females--------Breast and cervix.
 Head and neck cancers are 3rd most
common group of malignancy.
 Oral cancer most common group in head
and neck cancers,

101.  Ca tongue---- (25-50%)
 Ca lip----------21.5%
 Ca floor of the mouth-------(15%)
 Ca gingiva----- (10 to 12%)
 Ca buccal mucosa-------3%
 Ca palate-----------9%
In India : Buccal mucosa, mandibular alveolus
 No National Cancer registry for oral cancer
 Huge disease burden but no India data on
prevalence

102.  The cause of oral squamous cell carcinoma
is multifactorial.
 No single agent or factor is identified.
 But both extrinsic and intrinsic factors may
be involved in carcinogenesis.

103.  Extrinsic factors are external agents like
tobacco smoke, alcohol, syphilis and
sunlight.
 Intrinsic factors are systemic or generalized
states like malnutrition and iron deficiency
anemia, immunocompromised.
 Heredity is not a factor in oral carcinoma.
 Many cases are preceded by precancerous
lesion like leukoplakia.

104. 1. Tobacco: There is a very significant co-relation
between smoking habit and the incidence of
oral cancer.
 Risk of oral cancer is more with cigar and pipe
smoking, while the risk of lung cancer is more
with cigarette smoking.
 Smokeless tobacco or chewing tobacco also
shows strong correlation with development of
oral cancer.

105.  The risk of oral cancer in smokers is dose
dependent.
 The risk is also increased, the longer a
person smokes.
 The risk of palatal cancer is greatly
increased in persons who practice reverse
smoking.

106.  Paan or betel quid is a combination of areca
nuts, betel leaf, slaked lime, and sometimes
tobacco.
 The slaked lime (chuna) enhances absorption
of the other substances into the mucosa.
 Risk of oral cancer is increased by 8% in those
who chew paan.
 Areca ( supari) is a Type 1 carcinogen (
IARC)

107. 2. Alcohol : Synergistic effect with tobacco in
causation of oral cancer.
3. Syphilis: This is not relevant in present
times because syphilis is treated in early
stages with good antibiotics.
 Syphilis used to be treated with arsenic and
that may have been cause for high incidence
of cancer associated with syphilitic glossitis

108. 4. Sunlight or Actinic radiation
 This was significant only for basal cell carcinoma
of the lips
 The incidence is higher in males who are
generally more exposed to sunlight
 It is commoner in fair skinned persons
5. Orodental Factors
 Poor oral hygiene, faulty restorations, sharp
teeth, and ill-fitting dentures are co-factors
 These are synergistic factors with tobacco habit

109. 6. Diet and deficiency states
 Dietary deficiencies play a contributory role
in development of oral cancer
 Relationship between Sideropenic
Dysphagia and oro pharyngeal cancer is well
recognized
 Certain deficiency states like anemia,
Vitamin A deficiency make the epithelium
atrophic and thus more vulnerable to action
of carcinogen like tobacco.

110. Sideropenic Dysphagia: Plummer-Vinson
syndrome, Patterson - Kelly syndrome
 A precancerous condition.
 It is characterized by iron deficiency anemia,
generalized fatigue, difficulty in swallowing
due to formation of oesophageal webs,
angular chelosis, mucosal pallor, smooth
glossy tongue etc.

111.  It is associated wih an elevated risk of
squamous cell carcinoma of the esophagus,
oropharynx and posterior mouth.
 Malignancies develop at an earlier age in
persons with iron deficiency anemia.
 These persons have impaired cell mediated
immunity.

112.  Iron is essential for normal functioning of
epithelial cells.
 In deficiency states, there is high turnover of
epithelial cells.
 This results in atrophic or immature mucosa.

113. 7.Viruses:Role of Oncogenic viruses
 Viruses induce cancers by altering the DNA and
chromosomal structure of host cells and then
inducing the cells to proliferate in an
uncontrolled manner
 HPV is implicated in etiology of oral cancer
 HPV 16 and 18 are the high risk strains of HPV
 Viral proteins E6 and E7 are responsible for
carcinogenesis
 HPV related oral cancer has better prognosis

114. 8. Immunosuppression-
 Malignant cells may not be recognized and
destroyed at an early stage
 People with AIDS, those on
immunosuppressive therapy for organ
transplants, auto immune diseases are at
risk

115. 9. Genetic abnormalities-
 Normal proto oncogenes may be converted
into oncogenes by viruses, chemicals or
radiation
 These oncogenes stimulate cell division
 Thus oncogenes are involved in initiation
and progression of various neoplasm,
including oral squamous cell carcinoma
 Ras, myc, EGFR (c-erb B1) are commonly
mutated oncogenes

116. Genetic abnormalities
 Tumour suppressor genes may be
inactivated due to mutation
 Thus they permit genetically abnormal cells
to progress in the cell cycle
 Accumulation of these abnormal cells will
ultimately result in tumor formation
 P53, Rb, p16 are commonly mutated tumour
suppressor genes

117. A varied clinical presentation
1. Exophytic growth: fungating, papillary or
verrucous.
2. Endophytic: invasive, burrowing, ulcerated
lesion.
3. Leukoplakic patch.
4. Erythroplakic patch
5. Erythroleukoplakic patch.

118. 1. Leukoplakic patch.
2. Erythroplakic patch
3. Erythroleukoplakic patch.
 These are possibly early lesions, which will
further develop as either exophytic or
endophytic growths
 High index of suspicion necessary

119.  The exophytic lesion shows irregular,
fungiform, papillary or verruciform
projections above the surface
 It may appear red to white depending on
keratin and vascularity
 Surface may be ulcerated
 On palpation, the edges are hard and
indurated

120.  The endophytic lesion shows a depressed
area, which may be ulcerated in the centre
 The surrounding border has a rounded or
rolled appearance
 This is due to downward and lateral growth
of the tumour under the epithelium

121.  When the tumour spreads into bone, it
appears as a “moth eaten” radiolucent lesion
with ill defined margins
 On a radiograph…. D/D osteomyelitis or may
be rapidly growing bone destructive lesion
 Nerve invasion is characterized by
paresthesia and numbness

122.  OSCC arises from dysplastic surface epithelium
 Characterized by invasive islands and cords of
malignant squamous epithelial cells
 Invasion means extension of the dysplastic
epithelium through the basement membrane
into the connective tissue
 Dysplastic cells extend into adipose tissue,
muscle and bone.
 Cells also surround and destroy blood vessels
and lymphatics

123.  The dysplastic epithelium induces a immune
response in the connective tissue which is
seen as an inflammatory reaction
 Areas of necrosis may be seen
 Dysplastic epithelium induces formation of
blood vessels ( neo angiogenesis)
 It can also induce dense fibrosis in the
connective tissue ( Desmoplasia or scirrhous
change)

124.  Initially thought to restrict growth of tumour
cells.
 Shown that the fibrous tissue seen in
desmoplasia acts as a scaffold for migration
of tumour cells.
 So tumors with desmoplasia have poor
prognosis

125.  Histologically squamous cell carcinomas
are graded into well differentiated,
moderately differentiated and poorly
differentiated tumors. ( Broders grading
system)
 Differentiation refers to the extent to which
the tumor cell resembles the cell of origin,
both structurally and functionally.

126.  The resemblance of the tumor cell to
squamous epithelial cells and the amount of
keratin they produce helps to determine the
histological grade of the tumour.
 Epithelial atypia

127. 1. Most of the tumour cells are identifiable as
squamous epithelial cells
2. Large amounts of keratin is seen in the form of
keratin pearls of varying sizes
3. Malignant cells show dysplastic features like
cellular pleomorphism, nuclear
hyperchromatism, increased nuclear –
cytoplasmic ratio, individual cell keratinization,
abnormal mitoses

128. 1. The cells still resemble squamous epithelial
cells, but the similarity is less pronounced
2. The islands or clusters of cells are smaller in
size. Some cells are seen lying free in the
connective tissue
3. Amount of keratin formation is reduced

129. 1. Tumor cells show no similarity with
squamous epithelial cells. It is difficult to
even identify them as epithelial cells
2. Keratin formation is almost absent
3. The tumor cells showing all dysplastic
features are scattered throughout the
connective tissue.
4. The cells show an even greater lack of
cohesiveness

130.  In poorly differentiated squamous cell
carcinoma
 In metastatic tumours
Important epithelial markers
1. Cytokeratins
2. Keratin filament proteins ( KFP)
3. Keratin genes

131.  Cytokeratins are the basic structural proteins of
epithelial cells
 Cytokeratins are the leading biomarkers in
diagnostic pathology
 Cytokeratins demonstrate specific expression
pattern which is site specific and varies with the
level of differentiation.
 Cytokeratins are the ‘gold standard markers’ in
immunohistochemical diagnosis, classification
and sub typing of carcinomas and detection of
unclear metastasis.

132. Other histological parameters have been
considered in grading of SCC
 Pattern of invasion
 Tumor thickness
 Lymphocytic response
 Mitotic rate
However role of these parameters is still not
standardized

133.  Grading is a subjective process
 In case of SCC, grading does not corelate
with prognosis to the same extent as staging
 Clinical staging has a much better corelation
with microscopic grading

134.  Refers to clinical evaluation of the extent of
disease.
 Helps clinician to plan treatment.
 Helps to evaluate various treatment options.
 Helps in standardizing the disease for
communication between doctors.

135. T: Primary Tumor size
 TX: Primary tumour cannot be assessed
 T0: No evidence of primary tumor
 Tis: Carcinoma in situ
 T1: Primary tumor less than 2cms diameter.
 T2: Primary tumor 2-4 cms in diameter.
 T3: Primary tumor more than 4cms diameter.
 T4: Tumour invading adjacent structures eg:
cortical bone, tongue, skin of neck.

136. N: Regional lymph nodes
 NX: Regional lymph nodes can be assesed.
 N0: No palpable lymph nodes.
 N1: Ipsilateral palpable lymph nodes.
 N2: Contralateral or bilateral palpable nodes.
 N3: Fixed palpable nodes.

137. M: Distant metastases
 MX: Presence of distant metastasis can’t be
assessed
 M0: No distant metastases.
 M1: Clinical and radiographic evidence of
distant metastases.

138.  Stage 1: T1 No M0
 Stage 2: T2 N0 M0
 Stage 3: T3 N0 M0
T1 N1 M0
T2 N1 M0
T3 N1 M0
Stage 4: T1 N2 M0
T2 N2 M0
T3 N2 M0
T1 N3 M0
T2 N3 M0
T3 N3 M0
T4 N0M0
Any patient with M1

139.  EPC of lip occurs cheifly in elderly men.
 Etiology-
 Most common cause tobacco cheifly pipe
smoking
 Exposure to sunlight is an important
etiological factor for this site
 Chronic dental taruma
 Lower lip is affected more than the upper lip

140. 1. The early lesion is an ulcer with rolled
margins (exophytic growth) a small
indurated area or a leukoplakia patch
2. Slow Metastasis is to submental lymph
nodes on the same side(ipsilateral)
3. Lesions close to the midline may
metastasize to the opposite side due to
cross drainage of lymphatic vessels

141.  Comprises of 25 to 50% of all intraoral
carcinoma
 Causes are same
 Most common presenting sign of CA of
tongue painless exophytic mass with
indurated ulcer.
 Typical lesion develops on the lateral border
or ventral surface of tongue.
 The symptoms for these lesions include sore
throat and dysphasia.

142.  The side is important as lesions on the
posterior tongue have a higher grade of
malignancy ,metastasize early and thus have
a poorer prognosis.
 Treated by combination of surgery and X-
Ray
 The prognosis is not good

143. 1. The typical lesion is an indurated ulcer on one
side of the midline which may/may not be
painful.
2. More common in the anterior part of floor of
the mouth.
3. The lesion extends easily into the lingual
mucosa of the mandible, into the mandible
proper as well as into the tongue.
4. Metastasis in the sub maxillary lymph nodes
5. Prognosis is poor
6. 5- year survival low

144. 1. The lesion is usually a poorly defined ulcerative
painful lesion, which may cross the midline.
2. It extends rapidly to involve the lingual gingiva,
tonsils,uvula,underlying bone and nasal cavity
,while infiltrating in soft palate may extend into the
nasopharynx.
3. D/D from malignant lesions of minor salivary glands
4. The overlying mucosa is usually intact in case of
salivary gland tumor , while it is ulcerated in case of
squamous cell carcinoma.

145. 1. Important group because the early lesion is often
mistaken for common gingival infection.Thus
diagnosis is often delayed.
2. Mandibular gingiva is involved more than maxillary
gingiva.
3. It often develops in an edentulous area.
4. In dentulous areas,attached gingiva is affected more
than the free gingiva
5. Chronic irritation and inflammation are the cause
6. After tooth extraction
7. Usually manifested by ulceration and exophytic in
growth.

146. 5 There is early spread to the periosteum and
bone,due to proximity of these structures.
6 Metastasis is earlier from mandibular than
maxillary lesions.
7 Due to proximity of bone,surgery is the
preferred mode of treatment.The prognosis
is fair.

147. 1. This is the commonest site in the Indian
subcontinent. This may be related to the habit
of paan and tobacco chewing,in which the
quid is held at a particular site for prolonged
periods.(exophytic or verrucous)
2. Frequently preceded by leukoplakia.
3. Chronic trauma like jagged teeth,cheek
bitting, dental irritation.
4. The early lesion is a white, red and white
patch or an indurated ulcer or nodule.
5. The lesion develop along or inferior to a line
opposite to the plane of occlusion.

148. 1. Early signs and symptoms include swelling,
bulging of the maxillary alveolar ridge ,palate
or mucobuccal fold
2. Over eruption and loosening of the maxillary
premolars and molars
4 Nasal stuffiness and discharge may be the
only complaint.
5 In edentulous patients, discomfort related to
the dentures may be the initial complaint.
6 The complaints are related to extent of
involvement of various walls of the maxillary
antrum.

149. 7. Ulceration of the lesion into the oral cavity
or on skin occurs when the lesion is fairly
advanced.
8. Metastasis occurs late
9. But prognosis is poor as the lesion
frequently causes death by local infiltration
alone.

150.  If the lesion is totally in the soft tissue,
there is no radiological finding
 If the lesion has invaded into the bone, it
appears as a radiolucent area with ragged
borders, described as ‘moth-eaten’
appearance
 There is destruction of bone around the
teeth
 In advanced stage, the teeth appear to be
floating in empty space.
 Pathological fracture of bone may be seen

151.  Prognosis of oral squamous cell
carcinoma on all locations except
on the lower lip is poor
 Poor prognosis due to late
diagnosis and late initiation of
treatment
 Survival rate depends on clinical
stage of the disease and the
intraoral site which is involved

152.  Treatment modalities are surgery,
radiotherapy or a combination of both
 Chemotherapy is used as adjunct therapy
 Targeted therapy is the future of
management of OSCC

153.  Small tumors are treated surgically
 Larger tumors receive combined therapy
 If lymph nodes are palpable, elective neck
dissection is done along with neck irradiation
 Sentinel node biopsy is also done if occult
metastasis is suspected

154.  Prognosis is determined by 5 year survival
rate
 Varies from 68% for Stage 1 tumors to 27%
for Stage 4 disease
 In case of lower lip, survival ranges between
83% and 47%

155.  Persons with one oral or throat cancer are at
greater risk to develop second tumors
 This could happen simultaneously
(synchronous) or at a later date
(metachronous)
 Could be indicative of field cancerization,
due to exposure of entire mucosa to the
carcinogens

156. 