EFFECTS OF TOBACCO USE ON ORAL HEALTH – AN OVERVIEW
K.H. Awan. Effects of tobacco use on oral health – an
overview. Annal Dent Univ Malaya 2011; 18: 18–23.
Dental Research & Training Unit,
Research Management Centre,
Faculty of Dentistry, University of Malaya,
50603, Kuala Lumpur, Malaysia.
Tel No (Office): +603 7967 6493
Corresponding author: Dr. Kamran Habib Awan
among young people in North America, and more than
15% of adolescent smokers use these tobacco
products. Pipe smoking is one of the oldest methods
of smoking and was brought to Europe by sailors from
America. Water pipes include special receptacles
through which smoke has to pass, ostensibly to reduce
its harmful effects. Hookah is an Indian water pipe. The
habit of reverse smoking by holding the glowing end
of cigarettes or cigars within the oral cavity is
described in parts of India, South America and the
Philippines. The habit is practiced extensively by older
women living in rural areas.
Many toxins are present in tobacco smoke.
Tobacco smoke is made up of “side-stream smoke”
from the burning tip of the cigarette and “main-stream
smoke” from the filter or mouth end. Tobacco smoke
contains thousands of different chemicals which are
released as particles and gases. The particulate phase
includes nicotine, “tar” (itself composed of many
chemicals), benzene and benzo(a)pyrene. The gas
phase includes carbon monoxide, ammonia,
dimethylnitrosamine, formaldehyde, hydrogen
cyanide and acrolein. Some of these have marked
irritant properties and some 60, including
benzo(a)pyrene and dimethylnitrosamine, have been
shown to cause cancer.
The tar yield of different brands of cigarettes
range from 0.5 mg to 26 mg (averaging 12.5 mg), with
the most popular brands containing 15-17 mg of tar.
In the European Union (EU) cigarettes have to contain
less than 12 mg of tar from 1998 (2). Nicotine yields
range from 0.05 mg to 1.7 mg, with the most popular
brands yielding 1.0 mg of nicotine. In developed
countries over 95% of manufactured cigarettes
consumed are filter-tipped.
About 10% consume tobacco as roll-your-own
cigarettes mostly among lower socioeconomic groups.
Tobacco use is linked with many serious illnesses, such
as cancer, cardiopulmonary diseases, as well as with
many health problems. Every year, the use of tobacco
products causes a heavy toll of deaths and severe
human disease worldwide. One of the many health
problems linked to tobacco use is its detrimental
impact on oral health. Tobacco causes a whole series
of oral health problems, ranging from life-threatening
(precancerous changes leading to oral cancer) and
serious (periodontal disease, teeth decay) to social (bad
breath). Tobacco is consumed through the mouth in a
variety of forms, varied from smoked tobacco to
smokeless tobacco chewing on itself or combined with
areca nut. All these forms of tobacco have damaging
effects on the oral health. The most significant
preventive measure to prevent the oral health problems
caused by tobacco use is to stop using tobacco
products. The risk of developing oral cancer drops
rapidly when a smoker ceases tobacco use. After ten
years of not using tobacco, an ex-smoker/user’s risk of
oral cancers is about the same as that for someone who
has never smoked. To stop using tobacco products is
not an easy task. Fortunately, there are a number of
therapies available to assist in quitting of tobacco. It
is important to remember that, while it will be difficult,
ceasing to use tobacco has immediate health benefits,
including increased life expectancy and reduced risk
of tobacco related diseases and conditions.
Key words: Tobacco, smoking, Oral cancer, betel quid,
Tobacco is the single greatest cause of preventable
death globally (1). Tobacco is consumed in a variety
of different ways, though smoking of manufactured
cigarettes is the most prevalent form of its use. The
emergence of widespread cigar use particularly among
adolescents of both sexes has been reported in the past
decade in the US. Cigars have higher total nicotine
content than cigarettes do and can deliver nicotine
both through smoke and through direct oral contact
with the tobacco wrapper. Cheroots are small cigars
made of heavy bodied tobacco. Bidi smoking is a
popular form of tobacco use in south Asia, accounting
for one-third of the tobacco produced in India for
smoking. Bidis and Kreteks are gaining popularity
Tobacco and oral health 19
Smokeless (chewing) tobacco (ST)
There are two main types of smokeless tobacco -
chewing tobacco and snuff. The most written about is
smokeless tobacco use among Asians taken with betel/
areca quid. Over 90 percent of Indians add tobacco to
the betel quid mixture. Commercially prepared betel
quid products that contain mostly areca nut and flakes
of tobacco are called Gutka. Other ST products which
carry signif icant mutagenicity are Toombak used in the
Sudan, Shamma in the Jizan province in Saudi Arabia,
powdered tobacco and alkali mixtures such as Nass/
Naswar used in northern and central Asia and in
Pakistan, Khaini (a mixture of ST and lime) used in
Bihar state of India and Nepal, and boiled/sweetened
ST called Zarda mostly used by people from
Bangladesh (3). All these forms of tobacco use are
associated with an increased risk of oral cancer.
Second-hand or environmental tobacco smoke (ETS)
ETS is carcinogenic to human beings. Meta-
analyses have shown a significant association between
lung cancer and smoke exposure from a spouse and
also between lung cancer and exposure at work. Risks
for other cancer types are inconclusive. There is at
present insufficient evidence that children exposed to
parental smoke have an altered risk of developing any
Tobacco which annually kills 4.9 million people
worldwide at present is estimated to take 10 million
lives every year by 2020. The more depressing part is
that half of them will die in their middle age. A global
estimate of smoking prevalence by each country is
given in a WHO data base for reference (4). These are
based on adult and youth smoking behaviours
collected from population-based, cross sectional
surveys at a given point of time. China is the largest
producer of tobacco in the world as well as the largest
consumer. A national prevalence survey in 1996
among adults (age 15+) found that 63% of males
smoked. In Malaysia, three National Health and
Morbidity surveys which have been conducted since
1986, the prevalence of smoking among adults age 18
and above were more than 20%; i.e. 21.5% in 1986,
24.8% in 1996 and 22.8% in 2006 (5, 6).
National surveys of persons aged 18 and older
from 1970 onwards report a decline in prevalence in
USA and most western European countries (7, 8). The
rate of decline among women is less than for men, and
the quit index for men is substantially higher than for
women. Both in UK and USA there are now twice as
many former cigarette smokers as current smokers. In
general, the prevalence of smoking in most population
groups is lowest among those with the highest
educational level. By race, smoking among adult
blacks is similar to whites in most countries. Denmark
has the highest rates of smoking in the EU.
Smoking-attributed diseases include cancer of
trachea, lung, bronchus, lip, mouth and pharynx,
ischemic heart disease, stroke, hypertension,
bronchitis, chronic obstructive pulmonary disease,
emphysema and asthma. Due to substantial decrease
in smoking in countries such as the UK, male lung
cancer rates have decreased rapidly in the last decade
(9). On current trends, the annual number of smoking-
attributable deaths among women should exceed that
for men shortly after the year 2000.
Effects of tobacco on teeth and oral health
The damaging and harmful effects of tobacco
usage on oral health are now well recognized, in
particular a higher prevalence and severity of
periodontal diseases among smokers and the
association of tobacco use with candidosis (10, 11),
and with oral malignancies (12, 13). Several recent
documents have reviewed the scientific evidence
relating to the oral disease burden attributable to
tobacco use (14) and have highlighted the role and the
need for the dental profession to get involved with
tobacco intervention (15).
Smoking cause’s discolouration of teeth and some
argue that tobacco in fact might increase dental decay
as it lowers salivary pH and the buffering power.
Smoking is likely to cause halitosis and may affect
smell and taste. Smokers may present with generalised
melanosis of the oral mucosa that often necessitate
investigations to exclude other systemic disorders.
Wound healing is impaired in tobacco smokers
possibly due to local vasoconstriction and poor
neutrophil function. There is fair evidence that tobacco
use is a major factor in the progression of periodontal
disease (16-20). Smokers have an increased prevalence
of periodontitis, and their disease severity is higher
with greater alveolar bone loss resulting in deeper
pockets compared with non-smokers (11). Acute
necrotising ulcerative gingivitis (ANUG) has been
shown to be associated with heavy smoking.
Periodontal therapy often fails among smokers and it
is difficult to halt attachment loss. Possibly for similar
reasons dental implant failure is more common in
smoking subjects compared with non-smokers.
Over 80 percent of oral cancers are associated with
tobacco use (21). Oral squamous cell carcinoma
presents in a variety of ways such as white and red
patches, non-healing ulcers or exophytic growths.
Most early lesions are asymptomatic. Persistent
ulceration with rolled margins and fixation to
underlying tissues are pathognomonic signs of oral
malignancy. In late stages, disease spreads to adjacent
structures notably involving regional lymph nodes, and
20 Annals of Dentistry, University of Malaya, Vol. 18 2011
can cause mobile teeth and loss of teeth or even
pathological mandibular fractures. These stages may
be associated with pain, numbness or paraesthesia.
The clinical features of oral cancer are described
elsewhere. Currently diagnosing oral cancer relies on
pathological examination by biopsy and use of
imaging techniques to estimate the spread of the
disease. In addition, a number of adjunctive tools are
available which may facilitate the diagnosis of oral
cancer in the early stages (22-24).
Oral leukoplakia is the most common potentially
malignant lesion defined as a predominantly white
lesion of oral mucosa that cannot be characterised as
any other definable lesion (25). The appearance of
leukoplakia varies from uniformly white homogeneous
lesions to non-homogeneous speckled lesions with
red and/or nodular features. Leukoplakia is often
associated with tobacco use though idiopathic forms
of leukoplakia are recognised. The site of the oral
cavity affected by leukoplakia is often said to be
associated with the type of tobacco habit practiced;
lateral tongue and floor of mouth in cigarette smokers,
palate in pipe smokers and reverse smokers,
commissures in bidi smokers, buccal groves in tobacco
chewers where they park the quid and lower or upper
labial mucosa in snuff dippers. In a recent study in the
Netherlands, 64% of men and 60% of women with oral
leukoplakia were smokers (26). Tobacco use in men
was significantly associated with leukoplakia of
buccal mucosa and with all leukoplakia of floor of
mouth in both sexes. Oral leukoplakia in smokers
needs to be investigated by biopsy to assess any
dysplasia. Moderate to severe oral epithelial dysplasia
when present necessitate surgical intervention.
Intervention studies have demonstrated that
leukoplakia present in smokers might be reversible
when smoking habit was reduced or given up.
Erythroplakia is defined as ‘A f iery red patch that
cannot be characterized clinically or pathologically as
any other definable disease’ (27). Tobacco may
underlie some cases of erythroplakia.
Smoker’s palate (Leukokeratosis nicotina palati)
A greyish white discolouration of the palate with
multiple red elevated dots (inflamed minor salivary
gland openings) is often encountered in chronic
smokers. This is considered as a benign lesion as
cancer is not known to arise from this benign keratosis.
Reverse smoker’s keratosis
This is serious potentially malignant lesion
encountered in people who place the glowing end of
the cigar or cigarette inside the mouth. The clinical
appearance is often a mixture of red and white
plaques. Excrescences are found within the lesion
corresponding to inflamed minor salivary glands.
Whereas aforementioned smoker’s palate is not
considered as a precancerous lesion, palatal changes
in reverse smokers are a high risk lesion that is
associated with cancer development (28).
Tobacco smoking (i.e., cigarette, pipe or cigar
smoking) particularly when combined with heavy
alcohol consumption has been identified as the
primary risk factor for approximately 80% of oral
malignancies (29). The risk of oral and pharyngeal
cancers is similar for cigarette and cigar smokers, with
an overall risk seven to ten times higher than for never
smokers. This is not surprising as the oral cavity is
exposed to the carcinogens in smoke whether the
smoke is inhaled or not. When the frequency of daily
tobacco use is computed, there is strong dose response
relationship between smoking rates and risk of mouth
cancer. Addition of ST to the areca quid raises the
relative risk of the product by nearly 15 times.
There are 55 carcinogens (Table 1) in cigarette
smoke that have been evaluated by the International
Agency for Research on Cancer (IARC) and for which
there is “sufficient evidence for carcinogenicity” in
either laboratory animals or humans (30). Other
carcinogens not evaluated by the IARC may also be
Table 1. Summary of carcinogens in tobacco*
Type No. of
Polycyclic aromatic hydrocarbons (PAH) 10
Aromatic amines 3
Heterocyclic aromatic amines 8
Miscellaneous organic compounds 15
Inorganic compounds 7
*According to the International Agency For Research on Cancer (IARC),
Case-control studies from Europe have reported
adjusted odds ratios (ORs) of 11.1 for oral cavity and
12.9 for pharyngeal cancer (31). In particular, smoking
frequency and duration, and age at start have
significant associations. After giving up tobacco for a
decade or so, the risk of oral cancer of a past smoker
drops significantly to levels almost comparable to
Smoking patients show reduction of inflammatory
clinical signs that might be associated with local
vasoconstriction from nicotine, influence on
vasculature and cellular metabolism. This may
suppress symptoms of gingival inflammation.
Pathogenesis of periodontitis in smokers could be
linked to defects in neutrophil function, impaired
Tobacco and oral health 21
serum antibody responses to periodontal pathogens
and potentially diminished gingival fibroblast
function suggesting altered host response and
susceptibility (32). It is claimed that among smokers,
more patients remain culture positive for periodontal
pathogens after therapy. This may contribute to the
often observed unfavourable treatment results among
Detection of tobacco consumption is mostly based
on taking a social history. This should include
questions on type of tobacco habit, daily frequency
and duration of use. Age of commencement is also an
important risk factor for many disorders and should be
recorded. Current smokers could be regular or
occasional smokers, regular being daily smokers. Some
have the habit of binge smoking when consuming
alcohol only but are unlikely to be addicted to
Tobacco handling can usually be seen on heavily
smoking patients’ fingers and the tobacco stains on
the oral mucosa and teeth. Dorsal tongue is often
stained in many smokers. A bad breath can also
highlight a smoker.
Validation of smoking can be done using the
carbon monoxide breath test (piCO, Bedfont) or by
measuring salivary, urine or serum cotinine which is a
metabolite of nicotine. Cut off concentration of
salivary cotinine is taken as 14 ng/ml to detect a
Level of dependence to tobacco can be assessed
using the Fagerström test.
Treatment and interventions
Tobacco dependence shows many features of a
chronic disease. Regular smokers are addicted to the
habit as tobacco use results in true drug dependence.
A minority is able to quit in one attempt but the
majority may need some assistance to cease tobacco
use. Numerous effective treatments are now available,
and the dentists, oral physicians and their team
members should become actively involved in efforts
to reduce smoking.
Smoking cessation advices delivered by dentists
have shown to be effective. Brief advice given by a
clinician lasting about 3 minutes can yield a cessation
rate up to 5% (33, 34). With additional support such
as recommended use of nicotine replacement therapy
the quit rates achieved could be doubled. In treating
a smoker (willing to quit) the 5A’s (35), designed as a
brief counselling intervention, is helpful (Table 2).
As with other chronic diseases, the most effective
treatment of smoking requires multiple approaches in
addition to clinician’s advice. Pharmacotherapy is
proven to be effective, and several products are
available; nicotine patches, nicotine gum, nicotine
lozenge, nicotine inhaler and nicotine nasal spray.
Non-nicotine medication approved for smoking
cessation is bupropion (Zyban) therapy starting one
week before the quit date and continued up to 12
weeks after quitting. There are several medical contra-
indications particularly those with a predisposition to
seizures and/or a history of epilepsy. Pregnant and
breast-feeding mothers should not be prescribed this
drug. Bupropion therapy increases the chances of
quitting considerably up to 30%.
Prevention of tobacco use is a key element in
public health. As tobacco use and experimentation
starts in early life preventive approaches should be
appropriately targeted to young people. Paedodontists,
orthodontists, school dentists and family practitioners
can take steps to initiate advice to young children
never to start smoking. Banning tobacco smoking in
public places, legislation on tobacco advertising and
taxation are known to effect tobacco sales. Primary
prevention, the helping of people not to use tobacco
in the first place and assisting current smokers to quit,
is an effective way to reduce morbidity and mortality
from oral cancer.
The oral health ill-effects of tobacco in whole or in
part are well known, and there is weighty evidence that
tobacco use has considerable influence on oral health.
But tobacco use is a modifiable risk factor for oral
diseases, and an obvious professional interest in
tobacco intervention can make a big difference in the
health of an individual or the outcome of a given
disease. Dentists have probably the greatest access to
‘healthy’ tobacco users in the healthcare system, and
even in the absence of tobacco-related diseases in the
mouth, the dentist will easily recognize these patients.
Therefore, dentists should pursue more formal training
in tobacco cessation counselling, which should be as
much a part of their job as plaque control and dietary
Table 2. The 5 A’s of tobacco cessation*
1. Ask about tobacco use - every patient/every visit
2. Assess willingness to make a quit attempt
3. Advice (those willing) to quit tobacco use. Those unwilling
will need motivation to return to the topic at a later time
4. Assist in quit attempt – set a quit date, emphasize
total abstinence, prompt support seeking, provide
supplementary material and recommend pharmaco-
therapy (see below)
5. Arrange follow up and refer to a specialist clinic if the
quit attempt has failed
* Fiore MC. US public health service clinical practice guideline: treating
tobacco use and dependence. Respir Care. 2000; 45(10): 1200-62.
22 Annals of Dentistry, University of Malaya, Vol. 18 2011
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