Você está na página 1de 6

Vol 10, No 2, 2012 149

obacco has become a global epidemic and the
abuse of tobacco is a worldwide health problem.
The Indian situation as far as tobacco consumption
is concerned is far worse because of the preva-
lence of the tobacco chewing habit, which covers a
spectrum of socioeconomic and ethnic groups and
is spread over urbanised areas as well as remote
villages (Reddy and Ali, 2008).
There is suffcient evidence to infer a causal rela-
tionship between smoking and various systemic
diseases (Fielding, 1985; Benowitz, 1997; Yanbae-
va et al, 2007). Tobacco addiction is to be blamed
for approximately 5 million deaths each year or 1 in
10 adult deaths. Tobacco in its many forms is a risk
factor for oral cancer, oral mucosal lesions, peri-
odontal disease, gingival recession and coronal
and root caries.
Prevalence of Oral Mucosal Lesions Among
Tobacco Users
Poornima Chandra
/Poornima Govindraju
Purpose: To determine the prevalence of oral mucosal lesions associated with tobacco among patients visiting the
dental hospital.
Materials and Methods: A selection of 1525 patients visiting the Department of Oral Medicine and Radiology were in-
terviewed regarding tobacco habits. Examination of the oral cavity was performed by trained examiners under good illu-
mination using diagnostic instruments. Oral mucosal lesions were diagnosed based on the clinical features.
Results: The patients were divided into groups based on their tobacco habits. Out of 1525 patients, 359 patients
(23.5%) had the habit and 265 (73.8%) of them had oral mucosal lesions. Leukoedema was the most prevalent lesion.
Leukoplakia was found in 3.5% of the patients. Malignancy was found only among chewers.
Conclusion: Nearly three-quarters of the patients with the tobacco habit had oral mucosal lesions. This emphasises that
routine examination of oral mucosa is important and that the patients must be motivated to quit this harmful habit.
Key words: leukoplakia, malignancy, mucosal lesions, tobacco
Oral Health Prev Dent 2012; 10: 149-153 Submitted for publication: 03.06.11; accepted for publication: 10.11.11
Reader, Department of Oral Medicine and Radiology, Rajarajeswari
Dental College and Hospital, Bangalore, India.
Senior Lecturer, Department of Oral Medicine and Radiology, Raja-
rajeswari Dental College and Hospital, Bangalore, India.
Correspondence: Dr Poornima Chandra, Rajarajeswari Dental Col-
lege and Hospital, Ramohalli Cross, Kumbalgodu, Mysore Road, Ban-
galore-560060, Karnataka, India. Tel: +91-080-2843-7150, Fax: +91-
080-2843-7468. Email: drpoornichandra@yahoo.com
Understanding the distribution, aetiology, natural
history and epidemiology of oral mucosal patholo-
gies is essential to promote primary prevention,
early diagnosis, prompt treatment and the provi-
sion of appropriate health services (Furlanetto et
al, 2006). In this study, we aimed to determine the
prevalence of various oral mucosal lesions associ-
ated with the use of tobacco.
A selection of 1525 patients visiting the Depart-
ment of Oral Medicine and Radiology, Rajarajeswari
Dental College and Hospital, Bangalore, India were
interviewed regarding their overall health and tobac-
co use. Smokers were further enquired regarding
the type smoked, duration and frequency. Patients
history pertaining to the type, duration, frequency
and placement of the quid in the oral cavity was
elicited from the users of smokeless tobacco.
Examination of the oral cavity was performed by
trained examiners under good illumination using
diag nostic instruments. The WHO guidelines and
colour atlas were followed during examination
(Kramer et al, 1980). Oral mucosal lesions (OML)
Chandra et al
150 Oral Health & Preventive Dentistry
were diagnosed based on the clinical features.
When clinical diagnosis was inconclusive, histo-
pathological examination was done. The data thus
obtained were subjected to statistical analysis.
The study was approved by the ethics committee
of Rajarajeswari Dental College and Hospital. In-
formed consent was obtained from the patients se-
lected for the study. All patients with history of to-
bacco consumption were made aware of the harmful
effects of tobacco and were motivated to quit the
Out of 1525 patients interviewed, 359 patients
(23.5%) used some form of tobacco. Of these, 359
patients, 265 (73.8%) had oral mucosal lesions
ranging from tobacco-induced melanosis to malig-
nancy. Based on the form of tobacco used, the pa-
tients were divided into 3 groups: 1. smokers, 2.
chewers and 3. users of both forms (Table 1).
Prevalence of tobacco habit
The most prevalent tobacco habit among our pa-
tients was smoking and was most commonly found
in the age group of 21 to 35 years (Table 2). Smok-
ing tobacco was used in the form of cigarettes and
bidis while smokeless tobacco was used mostly in
the form of gutkha. The quid was mostly a mixture
of areca nut and tobacco.
Prevalence of oral mucosal lesions
The number and severity of OMLs was directly pro-
portional to the duration and frequency of tobacco
use, although there were a few exceptions. The
prevalence of OMLs was highest in group 2. Bidi
smokers manifested with a greater number of mu-
cosal lesions than those who smoked cigarettes.
Group 1: The most prevalent lesion among smok-
ers was leukoedema (7%), followed by smokers
palate (4.6%) and tobacco-induced melanosis (4%)
(Table 2). The majority of the oral lesions were
found in the age group of 36 to 65 years (Table 3).
Group 2: Oral submucous fbrosis (OSMF) and
chewers mucosa were the most prevalent lesions
(2%), followed by tobacco-pouch keratosis (1.4%)
(Table 3). The oral lesions were most prevalent in
the age group of 21 to 35 years.
Group 3: Tobacco-induced melanosis was the
most prevalent lesion (0.6%), followed by smokers
palate (0.5%) and chewers mucosa (0.5%). OMLs
were most prevalent in the age group of 21 to 35
Groups 1 and 3 consisted only of males. In our
study, homogeneous leukoplakia was more preva-
lent in group 1, and most of them were bidi smok-
ers. Speckled leukoplakia was more commonly
found in group 2. Both forms of leukoplakia were
more prevalent among female chewers than male
chewers. Malignancy was found only among chew-
ers, 0.3% in males and 0.06% in females.
The Global Adult Tobacco Survey, India conducted
by the International Institute of Population Scien-
ces, Mumbai, on behalf of the Ministry of Health
and Family Welfare carried out in 20092010 re-
ported that more than one-third of the adults in In-
dia use tobacco in some form. About 29% of adults
use tobacco on a daily basis, whereas a little more
than 5% use it occasionally. The prevalence of to-
bacco use among males is 48% as compared with
20% among females.
If tobacco were to be introduced today, it would
not be approved for human consumption anywhere
in the world. Thousands of compounds are found in
both forms of tobacco. Many of these compounds
are not only irritants and toxins, they are also car-
cinogens. The smoking form of tobacco contains
over 4000 different chemicals and at least 50 are
known carcinogens. Smokeless tobacco contains
28 carcinogens. Tobacco-specifc nitrosamines are
present in higher concentrations while nicotine con-
tent is lower in smokeless tobacco than in the
smoking form (Mehta and Hamner, 1993).
In 1912, Alder frst suggested that inhalation of
cigarette smoke might be a cause of lung cancer
(Lande, 2011). Since then, knowledge about the
adverse effects of tobacco has accumulated. The
US Surgeon Generals report 2004 states that
Table 1 Grouping of patients based on the tobacco habit
Group Tobacco habit Males Females
1 Smokers 182 0
2 Chewers 98 45
3 Users of both forms of tobacco 36 0
Chandra et al
Vol 10, No 2, 2012 151
smoking harms almost every organ of the body,
causing many diseases and reducing the health of
the smokers in general. Even now, as additional re-
search fndings become available, more and more
diseases are shown to be linked to tobacco (Lande,
Tobacco smoking affects multiple organ systems
resulting in numerous tobacco-related diseases.
The well-known health risks of tobacco smoking
pertain to diseases of the respiratory tract, such as
chronic obstructive pulmonary disease, and cancer,
particularly lung cancer and cancers of the larynx
and tongue (Yanbaeva et al, 2007). Both smoking
and chewing tobacco produce a number of OMLs
ranging from melanin pigmentation, wrinkling of the
oral mucosa to premalignant and malignant lesions.
Smoking induces increased melanin pigmenta-
tion in the oral mucosa. Smokers melanosis may
be due to the effects of nicotine on melanocytes
located along the basal cells of the lining epithe-
lium of the oral mucosa. Nicotine appears to di-
rectly stimulate melanocytes to produce more mel-
anosomes, which results in basilar melanosis with
varying amounts of melanin incontinence (Carpen-
ter, 2009). In our study, melanosis was more preva-
lent among smokers (4%). A study done on 500
Thai patients in Texas, USA showed similar results,
whereas other studies had either higher or lower
prevalences (Jainkittivong et al, 2002; Saraswathi
et al, 2006; Castellanos and Guzman, 2008).
Melan osis was also found in chewers (0.8%). It can
be hypothesised that the mechanical and chemical
irritation from smokeless tobacco may have in-
duced melanin pigmentation.
The pathogenesis of leukoedema is multifactor-
ial and smoking is one of the predisposing factors
or even a major cause (Jahanbani et al, 2009).
Other factors include betel nut chewing and chew-
ing of cocoa leaves (Wyk, 1985). In our study, leu-
koedema was more prevalent among smokers (7%)
Table 3 Tobacco-associated lesions among the study groups
Tobacco-associated lesions Group 1 Group 2 Group 3 Total
No. % No. % No. % No. %
Tobacco-associated melanosis 59 4 13 0.8 10 0.6 82 5.4
Leukoedema 108 7 6 0.3 5 0.3 119 7.8
Smokers palate 73 4.6 0 0 7 0.5 80 5.2
Oral submucous fbrosis 0 0 30 2 3 0.2 33 2.2
Lichenoid reaction 0 0 7 0.4 5 0.4 12 0.8
Tobacco pouch keratosis 0 0 21 1.4 1 0.06 22 1.4
Chewers mucosa 0 0 30 2 8 0.5 38 2.5
Homogenous leukoplakia 25 1.6 16 1 7 0.4 48 3.1
Speckled leukoplakia 1 0.06 4 0.3 2 0.1 7 0.4
Malignancy 0 0 2 0.1 0 0 2 0.1
No lesion 49 3.3 30 2 8 0.4 87 5.7
Table 2 Prevalence of tobacco habit among the study group
Age groups (years)
520 2135 3650 5165 6680
1 13 64 51 43 11 182
2 13 79 35 12 4 143
3 2 25 5 4 0 36
Chandra et al
152 Oral Health & Preventive Dentistry
in the age group of 36 to 50 years and 51 to 65
years. These fndings were similar to those of previ-
ous studies (Wyk, 1985; Zain and Razak, 1989;
Reichart et al, 1987; Mathew et al, 2008; Jahan-
bani et al, 2009; Castellanos and Guzman, 2008).
Whitish mucosa with red centres is a character-
istic fnding of the hard palate in smokers. The ae-
tiology is probably related more to the high tem-
perature rather than the chemical composition of
the smoke, although there is a synergistic effect of
the two (Axell et al, 1990). The prevalence of smok-
ers palate (4.6%) was similar to the previous stud-
ies done in Indian and Asian populations (Ikeda et
al, 1991; Mathew et al, 2008). Studies done in
Western populations showed that the prevalence of
smokers palate was much lower than in our study
(Bouquot and Gorlin, 1986; Corbet et al, 1994;
Jainkittivong et al, 2002; Neville et al, 2002; Espi-
noza et al, 2003; Pentenero et al, 2008). This could
be because pipe smoking is practised more fre-
quently in Western countries than in India.
OSMF is a high-risk pre-cancerous condition of
the oral mucosa seen in India and Southeast Asia,
which can be attributed to the betel chewing habit
among this population group (Axell et al, 1990). In
our study, the prevalence was 2% in group 2 and
0.2% in group 3. These results agree with previous
studies (Gupta et al, 1998; Saraswathi et al, 2006;
Mathew et al, 2008).
Oral lichenoid reactions (OLR) are considered
variants of oral lichen planus (Bhattacharya et al,
2003). They are associated with medications, den-
tal materials and tobacco. The term betel-quid
lichenoid reaction has been proposed by Zain et al
because of its association with the smokeless form
of tobacco (Zain et al, 1999). In our study, lichenoid
reaction was found with equal prevalence in groups
2 and 3 (0.4%). OLR was absent in group 1. These
results are similar to those of previous studies
(Daftary et at, 1980; Avon, 2004; Ismail et al,
Flaccidity in chronically stretched tissues in the
area of tobacco placement is known as tobacco-
pouch keratosis. The lesion is confned to areas in
direct contact with spit tobacco. It is typically a thin,
grey or grey-white, almost translucent plaque with
border that blends gradually into the surrounding
mucosa (Axell et al, 1990). In our study, the overall
prevalence was 1.4%. Other studies showed either
higher or lower prevalence rates than in our study
(Neville et al, 2002; Neville and Day, 2002).
Chewers mucosa is defned as a condition
caused either because of direct action of the quid
or due to traumatic effect of chewing or both. The
aetiology is trauma and possibly chemical. Its clin-
ical appearance is characterised by a brownish-red
discolouration of the oral mucosa with an irregular
epithelial surface that has a tendency to desqua-
mate or peel off. The buccal mucosa is most fre-
quently affected (Neville and Day, 2002). In our
study, the overall prevalence of chewers mucosa
was 2.5%. This is in accordance with an earlier
study (Mathew et al, 2008).
Leukoplakia, a pre-malignant lesion associated
with both forms of tobacco, had an overall preva-
lence of 3.5% and was more prevalent among men.
The reason for high prevalence in men could be
because men used both smoking and smokeless
forms of tobacco while women used only smoke-
less tobacco. Homogeneous leukoplakia was more
prevalent among smokers while the speckled form
was more common among chewers. These results
agreed with those of other authors (Axell, 1987;
Corbet et al, 1994; Kovac-Kavcic and Skaleric,
2000; Lin et al, 2001; Pentenero et al, 2008).
All the malignant lesions in our study were histo-
pathologically confrmed as squamous cell carcin-
oma. The prevalence of malignancy in our study
was 0.1% and all the lesions were reported in chew-
ers, with an equal prevalence among males and
females. These results are similar to those of stud-
ies done in Cambodian, Turkish and Italian popula-
tions (Ikeda et al, 1995; Campisi et al, 2001; Ce-
beci et al, 2009). Another study done on an Indian
population showed a prevalence of 1.7% (Mathew
et al, 2008), which is higher than in the present
This study presented epidemiological data on oral
mucosal leisons associated with the tobacco habit.
This might prove valuable in identifying high-risk
populations, planning future oral health studies
and implementing preventive programmes. In our
study, we found that the tobacco habit was most
prevalent in the age group of 21 to 35 years. Near-
ly three-fourths of the patients with a tobacco habit
had oral mucosal lesions. It was also observed that
the severity of the OMLs was proportional to the
duration of the habit. Hence, routine screening of
the oral mucosa is essential. The patients, espe-
cially the younger population, have to be counselled
on a regular basis in order to bring about long-term
results with regard to tobacco cessation.
Chandra et al
Vol 10, No 2, 2012 153
1. Avon SL. Oral lesions associated with the use of quid. J
Can Dent Assoc 2004;70:244248.
2. Axell T. Occurrence of leukoplakia and some other oral
white lesions among 20,333 adult Swedish people. Com-
munity Dent Oral Epidemiol 1987;15:4651.
3. Axell T, Zain RB, Siwamogstam P, Tantiniran D, Thampipit J.
Prevalence of oral soft tissue lesions in outpatients at two
Malaysian and Thai dental schools. Community Dent Oral
Epidemiol 1990;18:9599.
4. Benowitz NL. Systemic absorption and effects of nicotine
from smokeless tobacco. Adv Dent Res 1997;11:336
5. Bhattacharya I, Cohen DM, Silverman S. Red and white le-
sions of the oral mucosa. In: Greenberg MS, Glick M (eds).
Burkets Oral Medicine: Diagnosis and Treatment, ed 10.
Ontario: BC Decker, 2003:110.
6. Bouquot JE, Gorlin RJ. Leukoplakia, lichen planus, and oth-
er oral keratoses in 23,616 white Americans over the age
of 35 years. Oral Surg Oral Med Oral Pathol 1986;61:373
7. Campisi G, Margiotta V. Oral mucosal lesions and risk
habits among men in an Italian study population. J Oral
Pathol Med 2001;33:2228.
8. Carpenter WM. Smokers melanosis. http://emedicine.
medscape.com/article/1077501overview (Updated on
Oct 6, 2009, Accessed on Aug 17, 2011)
9. Castellanos JL, Guzman LD. Lesions of the oral mucosa: an
epidemiological study of 23785 Mexican patients. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 2008;105:79
10. Cebeci ARI, Gulsahi A, Kamburoglu K, Orhan BK, Oztas B.
Prevalence and distribution of oral mucosal lesions in an
adult Turkish population. Med Oral Patol Oral Cir Bucal
11. Corbet EF, Holmgren CJ, Philipsen HP. Oral mucosal lesions
in 6574 year old Hong Kong Chinese. Community Dent
Oral Epidemiol 1994;22:392395.
12. Daftary DK, Bhonsle RB, Murti RB, Pindborg JJ, Mehta FS.
An oral lichen planus- like lesion in Indian betel-tobacco
chewers. Scand J Dent Res 1980;88:2449.
13. Espinoza I, Rojas R, Aranda W, Gamonal J. Prevalence of
oral mucosal lesions in elderly people in Santiago, Chile. J
Oral Pathol Med 2003;32:571575.
14. Fielding JE. Smoking: Health effects and control. N Engl J
Med 1985;313:491498.
15. Furlanetto DLC, Crighton A, Topping GVA. Differences in
methodologies of measuring the prevalence of oral mu-
cosal lesions in children and adolescents. Int J Paed Dent
16. Gupta PC, Sinor PN, Bhonsle RB, Pandar VS, Mehta HC.
Oral submucous fbrosis in India A new epidemic? Natl
Med J Ind 1998;11:113116.
17. Ikeda N, Ishii T, Iida S, Kawai T. Epidemiological study of oral
leukoplakia based on mass screening for oral mucosal dis-
eases in a selected Japanese population. Community Dent
Oral Epidemiol 1991;19:160163.
18. Ikeda N, Handa Y, Khim SP, Durward C, Axell T, Mizuno T et
al. Prevalence study of oral mucosal lesions in a selected
Cambodian population. Community Dent Oral Epidemiol
19. Ismail SB, Kumar SKS, Zain RB. Oral lichen planus and li-
chenoid reactions: etiopathogenesis, diagnosis, manage-
ment and malignant transformation. J Oral Sci 2007;49:89
20. Jahanbani J, Sandvik L, Lyberg T, Ahlfors E. Evaluation of
oral mucosal lesions in 598 referred Iranian patients. The
Open Dentistry Journal 2009;3:4247.
21. Jainkittivong A, Aneksuk V, Langlais RP. Oral mucosal condi-
tions in elderly dental patients. Oral Dis 2002;8:218223.
22. Kovac-Kavcic M, Skaleric U. The prevalence of oral mucosal
lesions in a population in Ljubljana, Slovenia. J Oral Pathol
Med 2000;29:331335.
23. Kramer IR,Pindborg JJ,Bezroukov V,Infrri JS. Guide to epi-
demiology and diagnosis of oral mucosal diseases and
conditions. World Health Organization. Community Dent
Oral Epidemiol 1980;8:126.
24. Lande RG. Nicotine addiction. http://emedicine. med-
scape.com/ article/287555overview (Updated on July
27, 2011, Accessed on Aug 16, 2011)
25. Lin HC, Corbet EF, Lo ECM. Oral mucosal lesions in adult
Chinese. J Dent Res 2001;80:14861490.
26. Mathew AL, Pai KM, Sholapurkar AA, Vengal M. The preva-
lence of oral mucosal lesions in patients visiting a dental
school in Southern India. Ind J Dent Res 2008;19:99103.
27. Mehta FS, Hamner JE. Tobacco habits in India. In: Tobacco-
related oral mucosal lesions and conditions in India. Bom-
bay: Tata Institute of Fundamental Research, 1993.
28. Neville BW, Damm DD, Allen CM, Bouquot JE. Epithelial
pathology. In: Oral and maxillofacial pathology, ed 2. Phila-
delphia: Saunders, 2002:350.
29. Neville BW, Day TA. Oral cancer and precancerous lesions.
CA Cancer J Clin 2002;52:195215.
30. Pentenero M, Broccoletti R, Carbone M, Conrotto D, Gan-
dolfo S. The prevalence of oral mucosal lesions in adults
from the Turin area. Oral Dis 2008;14:356366.
31. Reddy SS, Ali KHSH. Estimation of nicotine content in popu-
lar brands of smoking and chewing tobacco products Ind J
Dent Res 2008;19:8891.
32. Reichart PA, Mohr U, Srisuwan S, Geerlings H, Theetranont
C, Kang Wan Pong T. Precancerous and other mucosal
lesions related to chewing, smoking and drinking habits in
Thailand. Community Dent Oral Epidemiol 1987;15:152
33. Saraswathi TR, Ranganathan K, Shanmugam S, Ramesh S,
Narasimhan PD, Gunaseelan R. Prevalence of oral lesions
in relation to habits: Cross-sectional study in South India.
Ind J Dent Res 2006;17:121125.
34. Wyk CWV. An investigation into the association between
leukoedema and smoking. J Oral Pathol 1985;14:491
35. Yanbaeva DG, Dentener MA, Creutzberg EC, Wesseling G,
Bouters EFM. Systemic effects of smoking. Chest
36. Zain RB, Razak IA. Association between cigarette smoking
and prevalence of oral mucosal lesions among Malaysian
army personnel. Community Dent Oral Epidemiol
37. Zain RB, Ikeda N, Gupta PC, Warnakulasuriya S, van Wyk
CW, Shrestha P, Axell T. Oral mucosal lesions associated
with betel quid, areca nut and tobacco chewing habits: con-
sensus from a workshop held in Kuala Lumpur, Malaysia,
November 2527, 1996. J Oral Pathol Med 1999;28:14.
Copyright of Oral Health & Preventive Dentistry is the property of Quintessence Publishing Company Inc. and
its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's
express written permission. However, users may print, download, or email articles for individual use.