TOBACCO SMOKING & ORAL CANCER

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.

TYPES OF TOBACCO

Cigarrettes

Bidis

Pipe smoking

Kretek

Smokeless tobacco

Electric cigarrettes

Hookah

ORAL MANIFESTATION OF TOBACCO USE

Dental Condition

• Tooth discoloration

• Dental Caries

• Tooth Abrasion ( due to smokeless tobacco / Pipe smoking)

Gingival condition

• Acute Necrotizing Ulcerative Gingivitis

• Halitosis

• Gingivitis and periodontitis

• Smoker’s melanosis

Mucosal Condition• Burns and keratotic patches

• Hairy tongue

• Nicotinic stomatitis

• Smokeless tobacco keratosis

• Leukoplakia

• Erythroplakia

VARIOUS MUCOSAL

LESIONS CAUSED BY TOBACCO

LEUKOPLAKIA

HOMOGENOUS

raised plaque formation, varying in size with

irregular edges.

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.

Homogenous leukoplakia- bright, white and sharply defined border.

Extensive proliferative verrucous leukoplakia of the mandibular gingiva.

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.

ERYTHROPLAKIA

HOMOGENOUSSPECKLED

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

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

Keratosis – diffuse whitening of the entire palatal mucosa

elevated nodules often with central red dots

Nicotine Palatinus of reverse smoker

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.

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.

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.

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.

The increased malignant potential is due to generalized epithelial atrophy.

MECHANISM OF TOBACCO CARCINOGENESIS

Tobacco consumption is correlated withaccumulation of DNA damageexposure 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

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

CONCEPTUAL MODEL FOR UNDERSTANDING MECHANISMS OF TOBACCO CARCINOGENESIS

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.

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.

TOBACCO SMOKING & ORAL CANCER

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 lininggingiva or palate

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

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

Cigarette smokingSmoking > 40 sticks day – significantly increased risk

of oral cancerNo specific oral lesion relatedHeavy smokers – patchy mucosal pigmentation

Pipe smokingLikely 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 dysplasiaSnuff dipping can causes extensive hyperkeratotic

plaques-> verucous carcinoma/SCC

SQUAMOUS CELL CARCINOMA

Most common malignant neoplasm of the oral cavity. Also called epidermoid carcinoma. Site of occurrence

Lower lipTongueFloor of the mouth GingivaPalate – soft and hardTonsilUpper lipBuccal mucosaUvula

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)

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

Tumors grow slowly,

exhibit an exophytic

papillary (warty)

pattern and tend to

be diffusely

distributed

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

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

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

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

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