TOBACCO-ASSOCIATED ORAL

LESIONS
A BRIEF PRESENTATION BY
SAMRIDHI SRIVASTAVA
2019-BDS-64
FOURTH YEAR
MRDC
ORAL LESIONS ASSOCIATED WITH
THE USE OF TOBACCO
 – Stomatitis Nicotina
 – Snuff Dipper Lesion

 – Cigarette Smoker’s Lip Lesion

STOMATITIS NICOTINA PALATINI
 AKA-
 Smoker’s palate,
 Stomatitis nicotina palati.

 DEF- It refers to a specific white lesion that develops on

the hard and soft palate in heavy cigarette, pipe and cigar
smokers.
 In many cultures, hand-rolled cigarettes and cigars are
smoked with the burning end held within the mouth.
This habit is called reverse smoking and the lesion
associated with it is called reverse smoker palate.
 The reason for occurrence of the lesion is due to heat
rather than an effect of tobacco.
STOMATITIS NICOTINA PALATINI
 Types (Clinical)
 Mild: Consisting of red,
dot like opening on
blanched area
 Moderate: Characterized
by well defined elevation
with central umbilication
 Severe: Marked by
papules of 5 mm or more
with umbilication of 2–3
mm.
STOMATITIS NICOTINA PALATINI
 Palatal Change in Reverse
Smoking
 Keratosis: Diffuse whitening of the
entire palatal mucosa
 Excrescences: 1–3 mm elevated
nodules, often with central red dots
corresponding to the opening of palatal
mucous glands
 Patches: Well-defined, elevated white
plaques, which could qualify for the
clinical term ‘leukoplakia’
 Red areas: Well-defined reddening of
the palatal mucosa
 Ulcerated area: Crater-like areas
covered by fibrin
 Non-pigmented area: Area of palatal
mucosa which is devoid of
pigmentation.
STOMATITIS NICOTINA PALATINI
 Clinical Features
 Age and sex distribution: It is usually seen in men who are
pipe smokers. It is common in middle-aged and elderly
people
 Site: Most commonly affected site is palate. The lesion is well
developed and prominent on keratinized hard palate. It is
restricted to the area which is exposed to heavy cigarette
smoke
 Onset: Initially there is redness and inflammation of the
palate
STOMATITIS NICOTINA PALATINI
 Clinical Features
 Appearance:
 In the early stages, mucosa is reddened.
 It subsequently becomes grayish white, thickened and fissured.

 Fissures and cracks may appear producing a wrinkled, irregular surface.

 In some cases, there may be papular or multinodular appearance.

 Papules do not coalesce and are separated from one another by

intervening normal appearing mucosa.

 Tonsillar pillars are usually erythematous

 Dried mud appearance: In some cases, palatal keratin becomes so

thickened that it imparts fissure or dried mud appearance.

 Salivary gland opening: Discoloration is homogenous with the exception

of numerous erythematous spots. It represents focal thickening

surrounding the orifice of the salivary gland which appears as white
umbilicated nodule with red center that may stain brown by deposition of
tar.
STOMATITIS NICOTINA PALATINI
 Diagnosis
 Clinical diagnosis: History of cigar or pipe smoking and
reverse smoking with generalized lesion of palate
 Laboratory diagnosis: In biopsy epithelium shows acanthosis
and hyperkeratosis. Epithelium lining of minor salivary gland
often shows squamous cell metaplasia and hyperplasia.
STOMATITIS NICOTINA PALATINI
 Differential Diagnosis
 Papillary hyperplasia: The lesion displays cobblestone
appearance and in stomatitis nicotina, there is red center
located on the palate of pipe or cigar smokers. The papules of
the papillary hyperplasia are focal
 Darier’s disease: They appear diffusely on palate in
cobblestone pattern
 Focal epithelial hyperplasia: It is not common on palate and
they are not erythematous
 Cowden syndrome: These are multiple papillary nodules
commonly seen on gingiva.
STOMATITIS NICOTINA PALATINI
 Management
 Stoppage of habit: It is completely reversible once the habit is
discontinued. The lesions usually resolve within 2 weeks of
cessation of smoking
 Biopsy: Biopsy of nicotine stomatitis is rarely indicated. But
biopsy should be performed on any white lesion of the palatal
mucosa that persists after 1 month of discontinuation of
smoking habit.
SNUFF DIPPER LESION
 AKA-
 Snuff pouch,
 Tobacco pouch keratosis,
 Spit tobacco keratosis,
 Smokeless tobacco keratosis.

 The habit of chewing tobacco is called as smokeless

tobacco or spit tobacco use.
 Etiopathogenesis
 Nicotine: The compound N-nitroso-nor-nicotine (NNN),
which is derived partly from bacterial action on nicotine
during the curing process, is contributed by the action of
salivary nitrites when tobacco is held in the mouth; occurs in
greater concentration in snuff tobacco.
SNUFF DIPPER LESION
 Clinical Features
 Location: It occurs in mucosal surface, where snuff is
habitually held
 Gingiva and periodontal tissue: There is painless loss of
gingival and periodontal tissue in the area of tobacco contact
 Teeth: There is extrinsic stain present on the teeth. There is
also cervical erosion of teeth with more prevalence of dental
caries
SMOKELESS TOBACCO KERATOSIS
 DEF- It is white plaque present in the mucosa where
chewing tobacco is kept.
 CLINICAL FEATURES
 Itis thin, gray or gray-white translucent lesion.
 Margin of the lesion blends gradually into the surrounding
mucosa.
 The appearance of lesion depends upon hours of daily use
and use of different tobacco leaves
 Snuff pouch, tobacco pouch: Mucosa is soft, velvety touch
feel on palpation and stretching of mucosa reveal distinct
‘pouch’. Stretched mucosa appears fissured and ripped in
sand on a beach after an ebbing tide
SMOKELESS TOBACCO KERATOSIS
 MALIGNANT TRANSFORMATION
 Verrucous carcinoma has been reported to occur from snuff
dipper lesion. This is also called as snuff dipper cancer.
 MANAGEMENT
 Stoppage of habit: Maximum lesion is regressed following the
cessation of habit
 Biopsy: Any lesion which remains after 6 months of quitting
the habit, should be sent for biopsy.
CIGARETTE SMOKER’S LIP LESION

 Seen commonly in smokers of unfiltered cigarettes.

 CLINICAL FEATURES
 They are generally flat or slightly elevated nodular white
lesions
 SITE- on one or both lips, corresponding to the site at which
the cigarette is held and apparently smoked down to an
extremely short length.
 There is increased redness and stippling of lip in localized
area.
 Margin has elliptical, circular or irregular borders.
 Color is pale to white and is slightly elevated with nodular
or papillary shape.
CIGARETTE SMOKER’S LIP LESION
DIFFERENTIAL DIAGNOSIS
 Leukoplakia,
 Lichen planus,

 Mechanical fiction,

 Chemical burn,

 Chronic lip biting,

 Candidiasis
TREATMENT
 Cessation or reduction of smoking.
LEUKOPLAKIA

 Leucos = white, plakia = patch

 Oral leukoplakia is the most common precancerous lesion of

the oral mucosa.

 The term leukoplakia coined by Schwimmer in 1877.

 Clinical diagnosis – no histological connotation.

 LEUKOPLAKIA: DEFINITIONS
WHO DEFINITION OF OL (1978) leukoplakia is a white
patch or plaque that cannot be characterized clinically or
pathologically as any other disease. The definition indicates that
the term leukoplakia does not carry a histologic connotation .

Axell et al(1984) A white patch or plaque that cannot be

characterized clinically or pathologically as any other disease
and is not associated with any physical or chemical causative
agent except use of tobacco.
ETIOLOGICAL FACTORS
Local factors
Tobacco – 80% cases
Alcohol
Chronic irritation
UV radiation
Chemical –Sanguinaria
Candidiasis
Virus: HPV 16

Systemic
Genetic
Nutritional deficiency

Idiopathic

(Bouquot JE, Whitaker SB. Quintessence Int 1994; 25: 133-140)

CLASSIFICATION
1. Bouquot JE & Whitaker SB
1. Phase1: Thin/Preleukoplakia
2. Phase 2: Homogenous / fissured/ thick leukoplakia
3. Phase 3: Granular/ nodular/ verruciform/ rough
leukoplakia
4. Phase 4: Erythroleukoplakia/ speckeled/
nonhomogenous leukoplakia

2. Axell 1996
1. Homogenous leukoplakia
2. Non homogenous
1. Erythroleukoplakia
2. Nodular
CLINICAL FEATURES
Age :
Middle age & older age, increases with age
>30 years
Peak incidence: >50 years

Prevalence in India is 0.2-4.9%

Sex :
•Male : Female 3:2 (India)
•Male : Female 1:1 (Worldwide)
 Phase 2 Thick/ Fissured
/Homogenous
PHASE 1 THIN OR
PRELEUKOPLAKIA
 HOMOGENEOUS LESIONS

• Relatively consistent pattern

throughout

 Papillomatous

 Wrinkled (like dry, cracked Cracked mud

mud)

 Pattern of fine line(cristae)

 Corrugated (like a beach at

ebbing tide).
Ebbing tide
PHASE 3 NODULAR PHASE 4 – SPECKELED /NON
/GRANULAR/ HOMOGENOUS,
VERRUCIFORM ERYTHROLEUKOPLAKIA
DIFFERENTIAL DIAGNOSIS
HOMOGENOUS LEUKOPLAKIA
 Leukoedema

 Cheek biting

 Electronic, galvanic or mercury contact allergy

 Smokeless tobacco lesion

 Hyperplastic candidiasis

 Plaque type lichen planus

 White sponge nevus

MIXED / NON- HOMOGENOUS LESIONS
 Erosivelichen planus
 Lupus erythematosus:Discoid

 Chemical burn/ injury

PROLIFERATIVE
VERRUCOUS LEUKOPLAKIA
(PVL)
Proliferative -Persistent , Progressive, Diffuse and Multifocal
Verrucous -Warty, Verrucal, Exophytic
Leukoplakia -Arise in Flat White Keratotic Patches

Age: 5th to 6th decades

Gender: Female : Male = 4:1
Site: Mandibular gingiva

Recurrence rate: high

DIAGNOSTIC WORK-UP
1.History and clinical examination

2.Chair side investigation

1.Conventional
2.Advanced

3.Laboratory investigations
1.Biopsy
CHAIR SIDE INVESTIGATIONS

Conventional
1.VITAL STAINING:

 1% Toluidine Blue Toluidine Blue

Sensitivity: 93.5% to 97.8%
Specificity: 73.3% to 92.9%

 Lugol’s Iodine
 Rose bengal staining
 Sensitivity: 93.9%
 Specificity: 73.7%
2. Exfoliative Cytology:
Class I (Normal): only normal cells observed

Class II (Atypical): presence of minor atypia, no evidence of malignant

changes

Class III (Intermediate): cells display wider atypia that may be suggestive
of cancer, but are not clear-cut, may represent precancerous lesions.
Biopsy is recommended

Class IV (Suggestive of cancer): few cells with malignant characteristic or

many cells with borderline characteristic. Biopsy is mandatory

Class V ( Positive for cancer): cells that are obviously malignant. Biopsy is
mandatory.
34
ADVANCED
ORAL BRUSH BIOPSY

35
 Chemiluminisence-
 Vizilite
system-Dysplastic cells appear acetowhite
 VELscope

36
LABORATORY INVESTIGATIONS
BIOPSY (Gold Standard)
1.Incisional

2.Excisional
3.Punch
 HISTOPATHOLOGICAL
FEATURES
Architecture changes
1. Loss of polarity of basal cells
2. The presence of more than one layer of cells having a basaloid
appearance
3. Drop-shaped rete ridges
4. Irregular epithelial stratification
5. Loss of intercellular adherence
6. Keratinization of single cells or cell groups in the prickle cell layer
7. The presence of mitotic figures in the superficial half of the epithelium
Cellular changes
8. Cellular and nuclear pleomorphism
9. Nuclear hyperchromatism
10. Enlarged nuclei
11. Mitotic figures that are abnormal in form
12. Increased number of mitotic figures
13. Increased nuclear- cytoplasmic ratio

Pindborg et al 1997
Classification and Staging System for Oral Leukoplakia
L -SIZE OF THE LEUKOPLAKIA
L1- Size of single or multiple leukoplakia together < 2 cm
L2-Size of single or multiple leukoplakia together 2±4 cm
L3- Size of single or multiple leukoplakia together >4 cm
Lx- Size not specified

P - PATHOLOGY
P0 - No epithelial dysplasia (no or perhaps mild epithelial dysplasia)
P1-Distinct epithelial dysplasia (“mild to moderate'' and moderate to possibly
severe epithelial dysplasia)
Px - Absence or presence of epithelial dysplasia not specified in the pathology
report

STAGING SYSTEM
Stage I - L1P0
Stage II - L2P0
Stage III - L3P0 or L1/L2P1
Stage IV - L3P1
(I. van der Waal, K.P. Schepman, E.H. van der Meij. Oral Oncology 2000; 36: 264-266)
40
TREATMENT
 Counseling of the patient for habit cessation
 Elimination of risk factors like alcohol and smoking , and advise
Nicotine substitutes.
 Medical management:
 Carotenoids
o Beta-carotene
o Lycopene
 Vitamins
o Vitamin C
o Vitamin E
o Vitamin A
 Polyphenols
 Bleomycin
 Photodynamic therapy

41
Surgical management
 Scalpel surgery
 Cryosurgery
 Laser ablation

Close Follow Up
4 months for the first 2 yrs
6 months until 5yrs
VITAMINS
 Vitamin C
 RDA 100-200mg/day
 Smokers 140mg/day

 Vitamin E
 800IU/day for 6-9months

 Vitamin A
BLEOMYCIN
 It is a cytotoxic antibiotic .
 Topical bleomycin in treatment of OL is used in dosages of 0.5
% /day for 12 to 15 days or 1% /day for 14 days.
 It shows a significant reduction of dysplasia and keratinization.
SURGICAL TREATMENT
 Conventional surgery
 Cryosurgery : cell death occurs at 20°C. cryoprobe
refrigerated by liquid nitrogen.
 Electrocautery : Tissue destruction by high voltage
current.
 LASER
MALIGNANT POTENTIAL

Homogenous: 1-7%
Granular/ verruciform: 4-15%
Erythroleukoplakia: 18-47% , 28%
Moderate dysplasia: 4-11%
Severe dysplasia: 20-35%
Floor of mouth: 16- 39%
Ventral surface of tongue: 47%

(Neville BW et al. Oral and maxillofacial pathology, 2nd edition, 2002,

p33-345)
REFERENCES
 BURKET’S ORAL MEDICINE 11th Edition
 Textbook of oral medicine, Anil Govindrao Ghom, 3rd
edition
 Mangai Yarkkarasi Follow Working at Student, J. (no
date) Oral lesions associated with the use of tobacco,
Share and Discover Knowledge on SlideShare. Available
at: https://www.slideshare.net/mangaiyarkkarasi/oral-
lesions-associated-with-the-use-of-tobacco-54767751
(Accessed: January 29, 2023).
 Ribeiro AS , Salles PR, Aparecida da Silva T, Mesquita RA.
A Review of the Nonsurgical Treatment of Oral
Leukoplakia International Journal of Dentistry 2010: 1-10
THANK YOU