See

discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/215945280

Snuff dippers lesion: A case report

Article January 2011

CITATIONS

READS

939

6 authors, including:
Neeraj Grover

Suchitra Gupta

D.J. College of Dental Sciences & Research

D.J. College of Dental Sciences & Research

22 PUBLICATIONS 38 CITATIONS

11 PUBLICATIONS 14 CITATIONS

SEE PROFILE

SEE PROFILE

Kunal Sah
Saraswati Dental College and Hospital
43 PUBLICATIONS 88 CITATIONS
SEE PROFILE

All in-text references underlined in blue are linked to publications on ResearchGate,

letting you access and read them immediately.

Available from: Suchitra Gupta

Retrieved on: 20 September 2016

Snuff Dippers Lesion: A Case Report

Neeraj Grover*, Navin Mittal#, Suchitra Gupta**, Kunal Sah***, Sunitha JD+,
Meeta Mahal+

Abstract
Smokeless tobacco products (STP) have been in existence for thousands of years among populations in South
America and Southeast Asia. Over time, these products have gained popularity throughout the world.
Smokeless tobacco is consumed without burning the product, and can be used orally or nasally. Oral smokeless
tobacco products are placed in the mouth, cheek or lip and sucked (dipped) or chewed. These products can
give rise to precancerous and cancerous lesions, like leukoplakia, submucous fibrosis, snuff dippers lesion,
squamous cell carcinoma. Here we report a case which had all the typical features of snuff dippers lesion
and a short review on the STP and their usage in India.
Key Words : Snuff dippers lesion, Tobacco, Precancerous, Smokeless, Keratosis.

INTRODUCTION

wo specific tobacco-related lesions of the oral

mucosa, nicotine stomatitis and snuff dippers lesion
(more commonly called the tobacco pouch keratosis),
have often been included under the broad umbrella of
leukoplakia. However, since these lesions have a specific
known cause and prognosis, its better to classify them
separately from leukoplakia.1
The degree of clinical alteration depends on the type
and quantity of tobacco, the duration of tobacco usage,
and host susceptibility.1,2 The most common areas of
involvement are the anterior mandibular vestibule and
buccal sulcus. The lesion is a thin grayish white
translucent plaque that is soft on palpation. Stretching
of the mucosa often reveals a distinct pouch caused
by flaccidity in chronically stretched tissues in the area
of tobacco placement. Biopsy reveals parakeratin
chevrons, acanthosis and intracellular edema of the
superficial cells of the epithelium.3-5 It is considered a
precancerous lesion.2,4,6 However, habit cessation results
in normal mucosal appearance within 2 weeks in 98%
of the lesions.2,4

CASE REPORT
A 35 year old male patient reported with the chief
complaint of a whitish area in the left buccal vestibule
region since one year. Past medical history was noncontributory. Past dental history revealed habit of
cigarette smoking 3-4 per day, since 7 years and pan
masala placement in left buccal vestibule 4-5 times per
day since 5 years. On clinical examination, a white
*Professor and Head, **Sr. Lecturer, ***Reader, +Sr. Lecturer,
Department of Oral and Maxilofacial Pathology; #Professor
and Head, Dept. of Pedodontics; Teerthankar Mahaveeer
Dental College and Research Centre, Moradabad, UP.
JIDA, Vol. 5, No. 1, January 2011

plaque like lesion was found in the lower vestibular

region extending onto the labial mucosa, present in
relation to the lower incisors and showing a
hyperkeratotic, wrinkled appearance (Fig. 1).
A provisional diagnosis of spit tobacco keratosis or
leukoplakia was made. An incisional biopsy was done
and on microscopic examination, H & E stained section
showed hyperplastic stratified squamous epithelium
with acanthosis and prominent granular cell layer,
covered at the surface with hyperkeratosis, exhibiting
chevron formation. Also there was intracellular edema
of the superficial cells. Underlying connective tissue
showed dilated and engorged capillaries with few
scattered inflammatory cells (Figs. 2,3). A histopathological diagnosis of tobacco pouch keratosis was given.

DISCUSSION
Snuff pouch can occur at any age, even in children
and adolescents. Overall, it is estimated that 15 percent
of chewing tobacco users and 60 percent of snuff users
will develop clinical lesions, if mild examples are
included. Microscopically, smokeless tobacco keratoses
show hyperkeratosis and acanthosis of the mucosal
epithelium. True epithelial dysplasia is uncommon;
when dysplasia is found, it is usually mild in degree.1,7
Most tobacco pouch keratoses are readily reversible
within two to six weeks after cessation of the tobacco
habit. If the lesion does not resolve after the habit is
stopped, then an incisional biopsy of the area should be
performed and the patient managed accordingly.1,2
All smokeless tobacco products (STP) contain
nicotine, a potent addictive substance. The major group
of carcinogens in STP includes non-volatile tobaccospecific nitrosamines (TSNA) and N-nitroamino acids.
[8,9]
STP are used by many cultures in many parts of the
world, including the West, Middle East and the Indian
139

Fig. 1 : A white plaque like lesion having

a wrinkled appearance.

Fig. 2 : Low power photomicrograph showing

with chevron formation, prominent granular
cell layer.(H&E, 10X)

subcontinent. However, STP in these countries are

considerably different from those used in India.
Traditional American products undergo fermentation,
which imparts characteristic flavors but often also
results in higher concentrations of unwanted bacterially
mediated by-products, especially TSNA and nitrite. In
Sweden, moist snuff is exposed during manufacturing
to a heat treatment akin to pasteurization, giving a
virtually sterile product. In India, however, STP
processing is performed by individual farmers and small
companies with little control over fermentation and
curing, which increases the production of TSNA. Here
STP are not homogeneous, since tobacco is often
combined with betel leaf (Piper betle), sliced areca nut
(Areca catechu), and/or powdered slaked lime, additives
that enhance the toxicity as well as the psychotropic
effect of tobacco. In addition, here the STP users often
smoke concurrently, thus confounding the effects of STP
use.[7] TSNAs may also form in the mouth of smokeless
tobacco users through the enzymatic action of saliva on
tobacco constituents. Indian smokeless tobacco products
(khaini, zarda, etc.) tend to contain more nicotine (13.8
65.0 mg/g) than American smokeless tobacco (chewing
tobacco, dry snuff and moist snuff, 3.439.7 mg/g).
Smokeless tobacco use delivers as much or more nicotine
to the body as does cigarette smoking. Most smokeless
tobacco products in India contain alkalinizing agents
like calcium hydroxide. These can irritate the mucosa of
the mouth and esophagus and more importantly,
promote nicotine absorption by the oral mucosa into the
bloodstream, since their pH raising action dramatically
increases the proportion of unprotonated nicotine, the
most easily absorbed form.10
The most commonly used STP in India include
Gutkha, Khaini, Pan Masala, Betel quid, Zarda, Gul,
Qiwam, Mawa, Mishri, Naswar, creamy and dry snuff,
Snus (snuff) and Red tooth powder. These products are
manufactured by different techniques but their mode of
usage is similar; they are placed in the mouth, labial or
buccal vestibule and sucked (dipped) or chewed.11
According to the Global Adult Tobacco Survey in
India 2010, current tobacco use in any form: 34.6% of
140

Fig. 3 : High power photomicrograph

showing hyperparakeratosis, intracellular
edema of superficial cells. (H&E, 40X)

adults; 47.9% of males and 20.3% of females; Current

tobacco smokers: 14.0% of adults: 24.3% of males and
2.9% of females; Current users of smokeless tobacco:
25.9% of adults: 32.9% of males and 18.4% of females.12

CONCLUSION
In conclusion, tobacco use in any form, smoking or
smokeless continue to be practised by a large percentage
of the population in India. Smokeless tobacco use is about
twice as high as smoking. It has been recognized
internationally that smokeless tobacco use is associated
with early death, cancer and adverse reproductive
outcomes. Hence more awareness among the masses and
stricter rules and regulations are needed to reduce this
menace.

REFERENCES
1.

Neville BW, Day TA. Oral Cancer and Precancerous Lesions.

CA Cancer J Clin 2002; 52(4) : 195-215.
2. Neville BW, Damm DD, Allen CM, Bouguot JE. Oral and
Maxillofacial Pathology, 2nd ed. Pennysylvania: WB Saunders
Company Ltd. 2004; 635-37.
3. Bsoul SA, Huber MA, Terezhalmy GT. Squamous Cell
Carcinoma of the Oral Tissues: A Comprehensive Review for
Oral Healthcare Providers. Crest Oral-B at dentalcare.com,
Continuing Education Course, Revised August 6, 2008.
4. Jayanthi P, Ranganathan K. Differential Diagnosis of White
Lesions of Oral Mucosa. J Orofac Sci 2010; 2(2) : 58-63.
5. Sham ASK, Cheung LK, Jin IJ, Corbet EF. The effects of
tobacco use on oral health. Hong Kong Med J 2003; 9 : 271-7.
6. Nikitakis NG. Oral soft tissue lesions: A guide to differential
diagnosis Part I: Introduction and changes in color. Braz J
Oral Sci 2003; 2(6) : 291-99.
7. Rodu B, Jansson C. Smokeless Tobacco and Oral Cancer: A
Review of the Risks and Determinants. Crit Rev Oral Biol Med
2004; 15(5) : 252-63.
8. http://ec.europa.eu/health/archive/ph_risk/committees/
04_scenihr/docs/scenihr_o_013.pdf
9. http://www.healthline.com/sw/cpa-smokeless-tobaccoand-cancer-questions-and-answers
10. Ray CS, Gupta PC. Bidis and smokeless tobacco. Current
science 2009; 96(10) : 1324-34.
11. Smokeless Tobacco Fact Sheets [Internet]. Stockholm,
Sweden: 3rd International Conference on Smokeless Tobacco,
c2002; Available from: http://cancercontrol.cancer.gov/
tcrb/stfact_sheet_combined10-23-02.pdf
12. http://netindian.in/news/2010/10/19/0008356/azadreleases-report-global-adult-tobacco-survey-india-2010.
JIDA, Vol. 5, No. 1, January 2011