tobacco smoking and oral cancer

1. TOBACCO SMOKING &
ORAL CANCER

2.  Tobacco products are products made entirely or partly of leaf
tobacco as raw material, which are intended to be
smoked, sucked, chewed or snuffed.
 All contain the highly addictive psychoactive ingredient,
nicotine.
 Tobacco use is one of the main risk factors for a number of
chronic diseases, including cancer, lung diseases, and
cardiovascular diseases.

3. TYPES OF TOBACCO
Cigarrettes
Bidis

4. Pipe smoking
Kretek

5. Smokeless tobacco

6. Electric cigarrettes
Hookah

7. ORAL MANIFESTATION
OF TOBACCO USE

8.  Dental Condition
• Tooth discoloration
• Dental Caries
• Tooth Abrasion
( due to smokeless tobacco / Pipe smoking)

9.  Gingival condition
• Acute Necrotizing Ulcerative Gingivitis
• Halitosis
• Gingivitis and periodontitis
• Smoker’s melanosis

10.  Mucosal Condition
• Burns and keratotic patches
• Hairy tongue
• Nicotinic stomatitis
• Smokeless tobacco keratosis
• Leukoplakia
• Erythroplakia

11. VARIOUS MUCOSAL
LESIONS CAUSED BY
TOBACCO

12. LEUKOPLAKIA
HOMOGENOUS
raised plaque
formation, varying
in size with
irregular edges.
NON-
HOMOGENOUS
Nodular or
speckled
Verrucous
Ulcerated
white patches on an
erythomatous base
verrucous proliferation
raised above the
mucosal surface.
red area, with white
patches generally present
at the periphery. Give the
appearance of an
ulceration.

13. Homogenous leukoplakia-
bright, white and sharply
defined border.
Extensive proliferative verrucous
leukoplakia of the mandibular gingiva.

14. LEUKOPLAKIA
 A white patch that cannot be wiped off the mucosa.
 Usually affects men > women, 30 yrs and above.
 Most common site : buccal mucosa and commissures.

15. ERYTHROPLAKIA
HOMOGENOUS SPECKLED FORM
 usually it was red lesion,
however it often exhibits
interspersed with white
plaque.
• It affect buccal mucosa,
soft palate
• Appears bright red, soft,
velvety lesion
Erythroplakia

16.  A red patch
 Asymptomatic lesion.
 Common sites: floor of the mouth,
lateral surface of the tongue, and
buccal mucosa.
 The surface is frequently velvety in
texture

17. Keratosis – diffuse whitening
of the entire palatal mucosa
elevated nodules often
with central red dots
Nicotine Palatinus of reverse smoker

18. Characterized into:
1. Keratosis – diffuse whitening of the entire palatal mucosa
2. Excrescences – 1-3mm elevated nodules often with
central red dots corresponding to the opening of palatal
mucous glands.
3. Patches – well-defined elevate white plaques which could
qualify for the clinical term of leucoplakia.
4. Red areas – well-defined reddening of the palatal mucosa.
5. Ulcerated areas – crater-like areas covered by fibrin.
6. Non-pigmented areas – areas of palatal mucosa which are
devoid of pigmentation.

19. Smokeless tobacco keratosis
oSnuff pouch or smokeless
tobacco keratosis is a white
keratotic lesion.
o It has a translucent
appearance rather than an
opaque whiteness.

20.  The microscopic appearance of tissue from a lesion
does not reveal excessive keratinisation, which is
characteristic of leukoplakia.
 This lesion is located only in areas of direct contact
with snuff or chewed tobacco and is reversible
when the affected patients stop the habit.

21. Oral submucous fibrosis
 is a premalignant condition characterized by slowly
progressive chronic fibrotic disease of the oral
cavity and oropharynx, in which the oral mucosa
loses its elasticity and develops fibrous bands,
which ultimately lead to difficulty in opening the
mouth.
 Several aetiological factors are suggested but it is
now accepted that OSMF is clearly caused by
areca nut chewing.

22.  The increased malignant potential is due to
generalized epithelial atrophy.

23. MECHANISM OF TOBACCO CARCINOGENESIS
 Tobacco consumption is correlated with
 accumulation of DNA damage
 exposure to tobacco-related chemical carcinogens
 Can provide direct damaging effects on the cellular DNA
in the human oral cavity.
 There are >60 carcinogens in cigarette smoke & at least
16 in unburned tobacco have been evaluated by IARC
* IARC – International Agency for Research on Cancer

24. Strong carcinogens
(1-200ng per cigarette)
Weak carcinogens
(nearly 1mg per cigarette)
Tobacco-specific nitrosamines (TSNAs)
 N-nitrosonornicotine (NNN)
 4-[methylnitrosoamino]-1-[3-
pyridyl]-1-butanone (NNK)
Polyclyclic aromatic hydrocarbons (PAHs)
 Benzo(a)pyrene (B(a)P)
Aromatic amines
 4-aminobiphenyl
 Acetyldehyde
 Catechol
 Isoprene
• The total amount of carcinogens in cigarette smoke
adds up to 1–3 mg per cigarette
• PAHs, TSNAs are likely carcinogen involvement in oral
cancer
Table 1: Example of carcinogens in tobacco-smoke

25. CONCEPTUAL MODEL FOR UNDERSTANDING
MECHANISMS OF TOBACCO CARCINOGENESIS

26. CARCINOGEN BIOMARKERS
 Provide objective measures of carcinogen uptake,
metabolic activation and detoxification in people who
use, or are otherwise exposed to tobacco products
 Among carcinogen biomarkers:
 DNA adducts potentially provide the most direct link to cancer
 Protein adducts are useful alternatives to DNA adducts
 Urinary metabolites are probably the most practical biomarkers
and provide important information about carcinogen dose and
metabolism.
 Important in establishing carcinogen dose in people who
are exposed to tobacco products and in understanding
mechanisms of carcinogenesis, and might ultimately be
useful in predicting cancer risk.

27.  Damaged genomic DNA has been detected as DNA-
adducts in various tissues of cigarette smokers .
 These findings strongly suggested a causal role of
tobacco use in oral carcinogenesis.
 However, continued intraoral placement of smokeless
tobacco failed to evoke malignant conversion of oral
mucosal cells of animals in vivo, indicating that tobacco
use alone may not suffice development of oral cancer .
 Hence, other environmental factors including alcohol
consumption, nutritional deficiencies, and DNA tumor
viruses have also been implicated in oral carcinogenesis.

28. TOBACCO SMOKING &
ORAL CANCER

29. INTRODUCTION
 Oral cancer is any cancerous tissue growth located in the
mouth.
 May be primary or secondary lesion.
 Usually occurs in older past 5th decade.
 Common in men than female
 Commonly involves
 the tissue of the lips
 the tongue
 the floor of the mouth
 cheek lining
 gingiva or palate

30. ETIOLOGY
 Possible carcinogens
 Tobacco
 Alcohol
 Betel quid habit
 Sunlight (lip only)
 Infections
 Syphilis
 Candidosis
 viruses
 Mucosal diseases
 Oral epithelial dysplasia
 Linchen planus
 Oral submucous fibrosis
 Genetic disorders (rare)
 Dyskeratosis congenita
 Fanconi’s anaemia

31. TOBACCO USE
 Effect of tobacco on the mouth depend on the way
it is used and this varies in different country
 Westernized & Malaysia – cigarettes> pipe smoking
 India, southern USA – tobacco chewing/ snuff
dipping

32.  Cigarette smoking
 Smoking > 40 sticks day – significantly increased risk
of oral cancer
 No specific oral lesion related
 Heavy smokers – patchy mucosal pigmentation
 Pipe smoking
 Likely to develop stomatitis nicotina of palate, a white
patch with no malignant potential
 Smokeless tobacco & betel quid
 Carcinoma tends to arise at the site in the mouth
where the tobacco is habitually held
 Often preceded by red/ white lesions or dysplasia
 Snuff dipping can causes extensive hyperkeratotic
plaques-> verucous carcinoma/SCC

33. SQUAMOUS CELL CARCINOMA
 Most common malignant neoplasm of the oral cavity.
 Also called epidermoid carcinoma.
 Site of occurrence
 Lower lip
 Tongue
 Floor of the mouth
 Gingiva
 Palate – soft and hard
 Tonsil
 Upper lip
 Buccal mucosa
 Uvula

34. CLINICAL FEATURES
 Deep seated ulcerated mass (extending into the adjacent tissue)
 Fungating ulcerated mass (extending away from the adjacent
tissues)
 Ulcer margins commonly elevated
 Adjacent tissues commonly firm to palpation (indurated)
 May be residual leukoplakia and/or erythroplakia
 Continuous enlargement
 More common in adult males
 Positive cervical lymphadenopathy may be present
 Local pain, referred pain (often to the ear) and paresthesia
(often of the lower lip)

35. VERRUCOUS CARCINOMA
 A diffuse largely exophytic superficial spreading, highly
keratinized, warty form of well differentiated SCC that is
unlikely to metastasize.
 Mostly involved- gingiva, alveolar mucosa, buccal mucosa
 Can also involved-hard palate, floor of mouth

36.  Tumors grow slowly,
exhibit an exophytic
papillary (warty)
pattern and tend to
be diffusely
distributed

37. SPINDLE CELL CARCINOMA
 Biphasic or monophasic neoplasm composed of SCC and
malignant spindle cell population
 Occurs primarily in males
 Often affects lower lip, lateral posterior of tongue or alveolar
ridge
 Less aggressive than other forms of poorly differentiated
carcinoma

38.  Typically appear as polypoid mass
 It may resemble other forms of
squamous cell carcinoma
presenting as a fungating nodular
mass or an endophytic ulceration
 Patient may complain hoarseness,
pain, burning sensation, dsypnea,
dysphagia, loose teeth, swelling or a
non-healing ulcer

39. BASAL CELL CARCINOMA
 Has tendency to originate within the base of the tongue, floor
of mouth, buccal mucosa, retromolar pad and gingiva
 Most BCC solitary but often multiple in those occurring in
Gorlin-Goltz syndrome

40.  Usually starts as a slightly
elevated papule that slowly
enlarges and eventually
develops a central, crusted
ulcer with an elevated
smooth rolled border
 If untreated the tumor
enlarges and invades
adjacent tissues and
structures by direct
extension but rarely
metastasize

41. REFERENCES
 Stephen SH. Tobacco carcinogens, their biomarkers and
tobacco induced cancer 2003
 http://monographs.iarc.fr/ENG/Classification/
 Cawson RA, Odell EW. Cawson’s Essentials of oral
pathology and oral medicine. 8th ed. Edinburgh:
Churchill Livingstone 2008
 Neville BW, Damm DD, White DK. Colour atlas of clinical
oral pathology. Lewiston, New York: B.C. Decker 2001