SMOKING

AND
ORAL HEALTH
By
Tan Xiao Yun
Nisa Nasuha
Contents
01 Introduction to Tobacco Use

02 Oral Effects of Tobacco Use

03 Systemic Effects of Tobacco Use

04 Strategies of Smoking Cessation

Introduction to Tobacco Use
Prevalence of smoking is the percentage of men and women ages 15 and over
who currently smoke any tobacco product on a daily or non-daily basis. It
excludes smokeless tobacco use. The rates are age-standardized.
● Malaysia smoking rate for 2020 was 22.50%, a 0.3% decline from 2019.
● Malaysia smoking rate for 2019 was 22.80%, a 0% increase from 2018.
● Malaysia smoking rate for 2018 was 22.80%, a 1.1% decline from 2015.
● Malaysia smoking rate for 2015 was 23.90%, a 1.7% decline from 2010.
Prevalence of current smokers was significantly higher in males (43.0%)
compared to females (1.4%)
Adults aged 25-44 years old reported the highest prevalence of smoking
(28.3%), but those with tertiary educational attainment, those with an income
level at the lowest or highest quintile had significantly lower prevalence of
smokers
Cigarette was the main
tobacco product used by
current smokers (87.9%),
followed by smokeless
tobacco (47.1%). Only a
small portion of smokers
used pipe and cigar
Chemical Compounds in Cigarette Smoke
HEALTH CONSEQUENCES
ON SMOKING
 Oral Effects of Tobacco Use
● Effect of Tobacco on Teeth
● Effect of Tobacco on Gingiva and Periodontium
● Effect of Tobacco on Oral Mucosa
● Effect of Tobacco on Microbiology & Local
Physiology
 Effects of Tobacco on Teeth
1. Teeth Staining
● Tobacco stain, a brown/black extrinsic stain is
typically found on the enamel surfaces of smokers
● Pronounced in cervical areas and lingual aspects of
mandibular incisors
● Caused by:
a) Retention of components of tar and nicotine on the
teeth
b) Reaction of furfural and acetaldehyde present in
tobacco smoke with amino groups of pellicle
glycoprotein
● Extent of staining depends on duration and frequency
of the habit as well as oral hygiene of the individual
2. Dental Caries
● Tobacco smoking is associated with increased caries rate
● Mechanism:
a) Reduced salivation and hence reduced buffering effect of the saliva
b) Higher number of Lactobacilli and S. mutans
c) Lower salivary cystatin activity (Cystatin can contribute to maintaining oral
health by inhibiting certain proteolytic enzymes)
● It has also been suggested that smokers have poor oral hygiene, fewer dental
visit and lesser overall health standards, leading to increased caries risk,
especially at the cervical, interproximal and root surface.

3. Tooth Abrasion
● Holding a pipe in to same location while smoking may result in notching of
incisal edge and cusp tips
 Effects of Tobacco on The Mucosa
A) Staining of Mucosa

1. Smoker’s Melanosis
● Smoking is capable of stimulating oral mucosa melanocytes to produce
excessive melanin
● Results in brown pigmentation of gingival or buccal mucosa in 5%-22% of
heavy smokers
● Intensity of smoker’s melanosis is dose-dependent
● It is not premalignant and pigmentation may be reversed upon cessation
of smoking
2) Nicotine Palatinus
● Asymptomatic lesion associated
with heavy pipe and cigar smoking
● Usually appears as white keratotic
change in the hard palate,
combined with multiple small
elevated nodule at the centre
● Does not reveal premalignant
potential
● Resolve after smoking cessation
3. Oral Candidiasis
● Studies have shown that great majority (83%) of oral candidiasis
patients are moderate to heavy smokers and they have a higher rate
of oral Candida carriage
● Median rhomboid glossitis, a Candida-induced tongue change is
most frequently seen in smokers and markedly improved upon
smoking cessation
● Tobacco smoking causes Candidiasis as nicotine promotes C.
albicans growth rate and adhesion

Median rhomboid glossitis

 B) Oral Precancerous Lesions

1. Leukoplakia and Erythroplakia

● White (leukoplakia) or red plaque (erythroplakia) of the oral mucosa that cannot be
characterised clinically or pathologically as other definable lesion
● Occurs as a response to chronic irritant factor
● Premalignant lesion associated with development of oral cancer

Leukoplakia Erythroplakia Erythro-leukoplakia

● Smokers have a 6-fold increase in the risk of developing leukoplakia
compared to non-smoker
● In a study, it was found that majority of smokers with leukoplakia (74%)
smoked > 20 cigarettes per day compared to 34.5% of those without
leukoplakia
● Leukoplakia of the floor of mouth appeared to be more significantly
more often present in smokers than in non-smokers
● Smokers with leukoplakia and erythroplakia have annual cancer
transformation rate of about 5%
● Speckled leukoplakia has a cancer potential of at least 25% - 41%
2. Smokeless Tobacco Keratosis
● A white keratotic plaque
● More wrinkled, has a semi-translucent appearance
with tobacco encrustations over the surface
● Located in areas of direct contact with snuff or
chewing tobacco
● A precancerous entity but malignant potential is less
than true leukoplakia
3. Oral Cancer
● Over 80% of oral cancers are associated with tobacco use
● Oral squamous cell carcinoma (OSCC) can present in white and red patches,
non-healing ulcer or exophytic growth
● Persistent ulceration with rolled margin and fixation to the underlying
tissues are pathognomonic signs of oral malignancy
● In the later stages, disease spreads to adjacent structures notably involving
regional lymph nodes
● Can lead to tooth mobility, tooth loss, pain and paresthesia

Invasive OSCC of the

right buccal mucosa
 Effects of Tobacco Use on Gingiva
and Periodontium
Periodontal Disease
● Many epidemiological studies showed that smoking is a significant risk factor
for the development of periodontal diseases
● Smokers accumulate markedly more calculus than non-smokers and the
quantity of calculus is correlated with the frequency of smoking
● Smokers have 2.5 - 3.5 times greater risk of severe periodontal attachment
loss
● Periodontitis in smokers also presents differently when compared with
non-smokers
● Smokers have deeper probing depths, more gingival recession, attachment
loss and alveolar bone loss
 Pathogenesis of Smoking on Periodontal Disease

A. Alteration of Oral Flora

● Tobacco smoke contains CO which lowers the oxygen saturation of haemoglobin in
the healthy gingiva
● Reduced oxygen tension within pockets favour growth of anaerobic bacteria, even
in shallower pockets
● Smoking extends a favourable habitat for periodontal pathogens such as
Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans and
Prevotella intermedia in pockets of less than 5mm
B. Reduced vascularity
● Less gingival redness and bleeding on probing (BOP) found in smokers
with experimental gingivitis compared with non-smokers due to
vasoconstrictive property of nicotine
● Smoking also exerts a chronic effect by impairing the vasculature of
periodontal tissues hence, impairing revascularization
C. Alteration of Immune-Inflammatory Response
● Alters host immune response to microbial challenges on periodontal tissues
by impairing the mechanisms to combat infection, enhancing destruction of
the surrounding healthy periodontal tissues and impairing wound healing
a) Increases number of neutrophils in the systemic circulation but there is a
decrease in number that reaches the gingival sulcus
b) Impairs phagocytosis and chemotaxis of neutrophils
c) Affects humoral and cell-mediated immunity by reducing IgA, IgG, IgE and
CD4 T cells
d) Neutrophil-derived proteolytic enzymes eg) MMPs and elastase also
increases significantly in tobacco smokers
● Alters the level of inflammatory cytokines by increasing TNF-α, IL-1, IL-6,
IL-8 and COX-2 in the gingival crevicular fluid
● Reduces proliferation, migration, matrix production, and attachment to
surfaces of fibroblasts
● Accelerates alveolar bone height reduction rate
 Effects of Tobacco on
Microbiology and Physiology
● Alteration in Oral Flora
● Alteration in Host Immune-Inflammatory Response
● Altered Taste Sensation
● Impaired Wound Healing
● Halitosis
Altered Taste Sensation
● Smokers exhibited significantly lower taste sensitivity than non-smokers
● The higher the nicotine dependence, the lower the taste sensitivity
● Several hypotheses concerning the mechanism of taste sensitivity
decrease
a) Significant changes in shape, size and vascularization of the fungiform
papillae
b) Decrease in number of taste cells
c) Indirect result of tobacco substances impacting salivary gland
d) Reduced zinc, vitamin B, E and folic acid
e) Nicotine acts as a central level and modulates the taste signal
Impaired Wound Healing
● Smoking has an adverse effect on the wound healing in the mouth
after periodontal scaling, periodontal surgery and extraction.
● It has been reported that increased frequency of smoking and
smoking on the day of surgery significantly increased incidence of
alveolar osteitis
● Pathogenesis: Increased plasma level of adrenaline and
noradrenaline after smoking, leading to peripheral vasoconstriction
and impaired neutrophil functions
Halitosis
● Both smoking and chewable tobacco forms
produce unpleasant breath odours
● Halitosis is produced predominantly by the
retention and subsequent exhalation of
inhaled smoke in the lungs
● Pipe and cigar tobacco contain more sulfur
than cigarettes hence users tend to have more
offensive halitosis than cigarette smokers
Systemic Effects of Tobacco Use
● Respiratory disease
● Cardiovascular disease
● Cerebrovascular Accident /
Stroke
● Type 2 Diabetes Mellitus
● Autoimmune Diseases
● Other cancers
 Respiratory Diseases
Mechanism of Tobacco Smoke in Inducing Respiratory Diseases

A) Induction of Inflammation
● Tobacco smoke exerts toxic effects on the airway epithelium, causing cell
damage or death as well as local inflammation
● Ciliotoxicity impairs normal clearance function of the epithelium
● Goblet cell hyperplasia causes increased mucus production + reduced
clearance induces mucous retention in the respiratory tract, causing
bacterial colonization and infection, ultimately inflammation
● Reactive oxygen radicals present in the tobacco smoke or produced by it
within lungs result in alteration or destruction of cells of the lungs
B) Mutation / carcinogenic effect
● Induce alterations of cell proliferation, chromosomal damage and
activation of oncogenes that can lead to carcinogenesis
1. Chronic Obstructive Pulmonary Disease
(COPD)
● Obstructive respiratory condition most closely
associated with cigarette consumption, namely
chronic bronchitis and emphysema
● Chronic bronchitis: Inflammation of the lining of
bronchial tubes
● Emphysema: Irreversible enlargement of alveoli,
accompanied by destruction of their walls, most
often without obvious fibrosis
● Signs and symptoms: SOB, chest tightness,
wheezing, productive cough
● Pathogenesis of smoking-related COPD includes protease/antiprotease
and oxidant/antioxidant hypothesis and abnormal repair processes.
● Proteolytic products from inflammatory cells if not adequately
counterbalanced by protective antiprotease systems, lead to bronchial
injury and alveolar architecture destruction
● Neutrophil elastase damages respiratory epithelium, enhances mucous
production by goblet cells
● Alveolar macrophages and its enzyme elastase contribute to loss of
elasticity of alveoli
2. Lung Cancer
● Since the beginning of the 20th century, lung cancer has become the most common
type of lethal cancer throughout the world
● It is estimated to be the 10th most common cause of death accounting for ~ 1 million
deaths around the world annually
● Smoking is linked to small cell carcinoma, squamous cell carcinoma and
adenocarcinoma
● Critical risk factors are early start of smoking during teenage years and early adulthood,
duration of smoking, number of cigarettes smoked daily and inhalation process
● Toxic injury or death of cells creates an environment of constant generation of
inflammatory and growth signals, including oxidants that result in hyperplasia,
metaplasia, mutagenic and carcinogenic of resident cells
● Signs and symptoms: Persistent cough, haemoptysis, SOB, wheezing, chest pain,
fatigue and unexplained weight loss
3) Cardiovascular disease
● Cigarette smoking is a major cause of CVD
● Has been responsible for approximately
140,000 premature deaths annually from CVD
● Influences other cardiovascular risk factors
such as glucose intolerance and low serum
level of HDL
● Pathogenesis: development of
atherosclerotic changes, narrowing of the
vascular lumen, induction of hypercoagulable
state, leading to atherosclerotic plaque and MI
● Smoking also causes peripheral artery
disease, aortic aneurysm
4) Cerebrovascular Accident / Stroke
● Happens when there is loss of blood flow to part
of your brain
● Stroke is a leading cause of death and disability
worldwide, but most strokes can be prevented
by addressing a small number of key risk factors
● Someone who smokes 20 cigarettes a day is six
times more likely to have a stroke compared to a
non-smoker.
● Smoking promotes atherosclerotic plaque
formation on the wall of cerebral artery wall,
leading to cerebral ischemia
5) Type 2 Diabetes Mellitus
● Chronic metabolic disorder characterized by persistent hyperglycemia. It
may be due to impaired insulin secretion, resistance to peripheral actions of
insulin, or both
● Smoking increases the risk of developing T2DM by 30%-40% in smokers
● Risk of developing diabetes increases as the number of cigarettes smoked
grows
● Smokers diagnosed with diabetes are at higher risk for kidney disease,
blindness and circulatory complication leading to amputation
● Results have indicated nicotine exposure could induce a reduction of insulin
release, and negatively affect insulin action, suggesting nicotine could be a
cause for development of insulin resistance
6) Autoimmune Diseases
● An autoimmune disease is a condition that
results from an anomalous response of the
immune system, wherein it mistakenly targets
and attacks healthy, functioning parts of the
body as if they were foreign organisms.
● Cigarette smoke compromises immune
homeostasis and that altered immunity is
associated with an increased risk for several
disorders with and underlying immune
diasthesis
● Smoking increases the risk of rheumatoid
arthritis and may lead to SLE and IBD
7) Other Cancers
STRATEGIES OF
SMOKING
CESSATION
2 types of clinical intervention
depending on the intensity of
intervention and level of service
provided
● i. Brief clinical intervention
● ii. Intensive clinical intervention
Brief Intervention
The five major steps (5 A’s) for intervention are described below and
summarised

01 Ask about tobacco smoking

● All patients should be asked about their smoking status
and the findings should be documented in the patient’s
notes
● For people who smoke or have recently stopped smoking,
the smoking status should be checked and updated at
every visit to prevent relapse
● Systems should be in place in all health care settings to
ensure that smoking status is accurately documented at
every visit
Brief Intervention
The five major steps (5 A’s) for intervention are described below and
summarised

02 Advice to quit
● Advice to quit should be given clearly to all patients found
to be smoking
● Every tobacco user should be offered at least a brief
intervention which consists of brief cessation advice from
the health care providers because studies have shown that
advise by health care providers (medical, dental,
pharmacist, nurses etc.) increases rates of abstinence
Brief Intervention
The five major steps (5 A’s) for intervention are described below and
summarised

02 Advice to quit
● Advice should be:
● Clear—"I think it is important for you to quit smoking now and I can
help you." "Cutting down while you are ill is not enough."
● Strong—"As your clinician, I need you to know that quitting
smoking is the most important thing you can do to protect your
health now and in the future. The clinic staff and I will help you."
-relate

● Personalised—Tie tobacco use to current health/illness, and/or its

social and economic costs, motivation level/readiness to quit,
and/or the impact of tobacco use on children and others in the
household.
Brief Intervention
The five major steps (5 A’s) for intervention are described below and
summarised

03 Assess willingness to make a quit attempt

● Is the tobacco user willing to make a quit attempt at this time?
● If the patient is willing to make a quit attempt at this time,
provide assistance
● If the patient will participate in an intensive treatment, deliver
such a treatment or refer to an intensive intervention
● If the patient clearly states he or she is unwilling to make a quit
attempt at this time, provide a motivational intervention built
around the “5 R’s”: relevance, risks, rewards, roadblocks, and
repetition
Brief Intervention
The five major steps (5 A’s) for intervention are described below and
summarised

04 Assist in quit attempt

● For the patient willing to make a quit attempt, use counselling
with pharmacotherapy (when indicated) to help him or her quit
● Preparations for quitting: (STAR)
● Set a quit date
● Tell family, friends, and co-workers about quitting and request
understanding and support
● Anticipate challenges to planned quit attempt, particularly
during the critical first few weeks
● Remove tobacco products from his or her environment
Brief Intervention
The five major steps (5 A’s) for intervention are described below and
summarised

05 Arrange follow up
● Follow-up soon after the quit date, preferably during the first week.
Subsequent follow-ups are recommended weekly within the first
month, and then every two weeks for the 2nd and 3rd month, and
monthly after that up to 6 months
● For those who successfully quit, schedule follow-up, either in
person or via telephone. Actions during follow-up:
o Congratulate success
o If tobacco use has occurred, review circumstances and elicit
commitment to total abstinence
o Assess pharmacotherapy use and problems. Consider using more
intensive treatment, if not available, referral is indicated
Intensive Clinical Interventions
More effective than brief treatment. Achieved by increasing the length of
individual treatment sessions, the number of treatment sessions and
specialized behavioural therapies.
Components of an intensive tobacco dependence intervention:-
Assessment
01 ● Assessments should determine whether tobacco users are willing to
make a quit attempt using an intensive treatment programme

02 Programme clinicians
● One counselling strategy would be to have a medical/health care
clinician deliver a strong message to quit and information about health
risks and benefits, and recommend and prescribe medications
recommended
● Nonmedical clinicians could then deliver additional counselling
interventions
Intensive Clinical Interventions
Programme intensity
03
● When possible, the intensity of the programme should be:
- Session length – longer than 10 minutes
- Number of sessions – 4 or more

04 Programme format
● Either individual or group counselling may be used
- Telephone counselling also is effective and can supplement
treatments provided in the clinical setting
- Use of self-help materials and cessation Web sites is optional
- Follow up interventions should be scheduled
Intensive Clinical Interventions
05 Type of counselling and behavioural therapies
● Counselling should include practical counselling (problem
solving/skills training) and intra-treatment social support

06 Medication
● The clinician should explain how medications increase
smoking cessation success and reduce withdrawal symptoms
● Certain combinations of cessation medications also are
effective
● Combining counselling and medication increases abstinence
rates
 Stage-of-change model in
smoking cessation
Precontemplation Current smokers who are NOT planning on quitting within the next 6 months

Contemplation Current smokers who are considering quitting within the next 6 months and
have not made an attempt in the last year

Preparation Current smokers who have made quit attempts in the last year and are
planning to quit within the next 30 days

Action Individuals who are not currently smoking and stopped within the past 6
months (recently quit)

Maintenance Individuals who are not currently smoking and stopped smoking for longer
than 6 months but less than 5 years (former smokers)
Management of smokers according
to the stage-of-change
● Management of smokers according to the readiness to stop smoking (state of
change)

Precontemplation ● Assist by enhancing willingness or motivation and ability or

confidence through these measures
● Provide a pamphlet and let the patient know you are there to
help when the patient is ready to quit
● Explore the individuals’ perceived pros and cons of smoking
and quitting
● Use 5R’s; the importance of quitting
Management of smokers according
to the stage-of-change
● Management of smokers according to the readiness to stop smoking (state of
change)

Contemplation The cessation measures are as follows:

● Give pamphlet, briefly review pharmacotherapy option, provide
information about state quit lines
● Offer future assistance when patient is ready
● Relate any evidence of tobacco-related disease during patient
care
Management of smokers according
to the stage-of-change
● Management of smokers according to the readiness to stop smoking (state of
change)

Preparation ● Assist by helping him/her develop a personalized quit plan with

a quit date
● Set a quit date. Ideally, it should be within 2 weeks. Reduce the
number of cigarettes gradually before the set date
Management of smokers according
to the stage-of-change
● Management of smokers according to the readiness to stop smoking (state of
change)

Action ● Discussing any challenges to staying quit and methods to

prevent relapse
The cessation measures are as follows:
● Provide emotional support, and affirm benefits of not using
tobacco stated by patient
● Review pharmaceuticals, if any, being used; support proper use
● Refer patient to a tobacco quitline/online support
● Encourage use of a support system (family, friends)
● Note quit date and patient’s progress in chart
● Provide words of encouragement to continue (takes
approximately 2 to 3 minutes)
Management of smokers according
to the stage-of-change
● Management of smokers according to the readiness to stop smoking (state of
change)

Maintenance ● Discussing any challenges to staying quit and methods to

prevent relapse
● The measures are as follows:
● Provide verbal support ; point out any positive oral-health
effects
● Help patient develop strategies to prevent relapse (take
● approximately 1 minute)
 For patients who are
unwilling to quit
Such patients may respond to a motivational intervention built around the “5R’s”:
Motivational interviewing strategies
Enhancing motivation to quit tobacco
-the 5 R’s
-used for patient who is not ready to quit but has entered into some level of discussion
Pharmacological intervention
choice of specific first line pharmacotherapy should be guided by:- efficacy,
safety, suitability and cost

Nicotine based Non nicotine based

nicotine replacement therapy - gum, patch, varenicline, sustained release (SR) bupropion,
lozenges and inhaler and
nortriptyline.
Pharmacological intervention
Pharmacological intervention
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THANK YOU!