This presentation describes the smoking as a risk factor for periodontal disease.

1. SMOKING AND
PERIoDONTIUM
DR MANISHA SINHA
I STYEAR PG
RAJARAJESWARI DENTAL COLLEGE AND HOSPITAL

2. CONTENTS
 Introduction
 Epidemiological evidence
 Various forms of tobacco
 Constituents of tobacco
smoke
 Classification of smoking
status
 Smoking and systemic health
 Smoking as a risk factor for
periodontal disease
 Impact of smoking on
periodontal disease
 Effects of smoking on the
etiology and pathogenesis of
periodontal disease
 Effect on periodontal therapy
 Cessation of smoking
 Conclusion
 References

3. INTRODUCTION
 A direct causal relationship between smoking exposure and the prevalence
and the severity of periodontal disease has been firmly established
(American Academy of Periodontology 1996, Grossi et al. 1994)
(Johnson2004)
 According to the National Health and Nutrition Examination Survey III,
smokers were four times as likely to have periodontitis as persons who had
never smoked after adjusting for age, gender, race/ethnicity, education, and
income/poverty ratio.
 The use of tobacco products, in general, and smoking products, in particular,
is the major preventable risk factor for the initiation and progression of
periodontal diseases.

4.  Cross-sectional and case-control studies demonstrate a
moderate to strong association between smoking and
periodontitis.
 Smokers are 4x as likely to develop periodontitis as
non-smokers.
 Smoking may be responsible for more than half of the
periodontal disease among adults.
 Up to 90% of refractory periodontitis patients are
smokers.
EPIDEMIOLOGICAL EVIDENCE

5. It has been estimated there are 1.1 billion smokers worldwide
and 182 million (16.6%) of them live in India.
Tobacco is used in smoking and smokeless forms in India.
Among tobacco users, 34% smoke Bidis, 31% are regular
cigarette smokers, and 35% use smokeless tobacco. Bidis are
chocolate, mint, or fruit flavored tobacco cigarettes hand-rolled
in tendu or temburni leaf and are common throughout India and
southeast Asia and are especially appealing to young smokers.
The prevalence of smoking among 13-15 year old school going
students in India ranges from 19.7-34.5%, even the lowest was
considerably higher than the global median of current cigarette
smoking (13.9%).

6. VARIOUS FORMS OF TOBACCO
SMOKED
1. Beedi
2. Cigarette
3. Cigar
4. Pipe
5. Chillum
6. Hookah
7. Hookli
8. Naswar
9. Dhumli
SMOKELESS
1. Snuff
2. Chewable
tobacco
3. Gutka
4. Mawa
5. Khaini
6. Mishri
7. Zarda
Can be either:

7. CONSTITUENTS OF TOBACCO SMOKE
• Gas phase
 Carbon monoxide
 Nitrosamines
 Hydrazine
 Vinyl chloride
 Oxides of nitrogen
 Hydrogen cyanide
 Acetaldehyde
 Acrolein
 Ammonia
 Formaldehyde
 Particulate Phase
Tar
benzene
Nicotine
Phenol
Cresol
Naphthylamine
N - Nitro Sonornicotine
Benzopyrene
Trace metals (eg: Nickel,
arsenic, polonium 210)
Indole
Carbazole
Catechol
More than 4000 chemicals have been found to be
present in tobacco smoke.

8. Tar yield Benzene Formaldehyde Ammonia
Hydrogen
cyanide
Cadmium Acetone

9. Among the substances
found in tobacco smoke
is the alkaloid nicotine,
which appears to be
responsible for the
dependence that
characterizes the
smoking habit.
During smoking,
nicotine is rapidly
absorbed into the
bloodstream, where 30%
remains in its free form.
It is highly lipid soluble
and readily penetrates
cell membranes
Nicotine is considered the most
pharmacologically active
compound in tobacco smoke.
Most is absorbed through the
lung alveoli, but nicotine can
also be absorbed more slowly
through the oral mucosa in
sufficient quantities to have a
pharmacological effect.

10. NICOTINE
 Nicotine has pronounced effects on the cardiovascular system. During smoking it
increases the heart rate, cardiac output, and blood pressure by autonomic
stimulation, which also effects peripheral vasoconstriction.
 There is also evidence that nicotine acts directly on blood vessels and capillaries
to produce vasoconstriction.

11. Absorption
 When tobacco is chewed or smoked the nicotine is released as the free
base and absorbed into the blood stream from where it is distributed to
the brain.
 As it enters the body, it is distributed quickly through the blood
stream and can cross the blood brain barrier.
 Takes about 7 s to reach the brain when inhaled, which is faster than
the iv infusion.
 Nicotine in tobacco smoke from most cigarettes is not well absorbed
from oral mucosa because nicotine is in an ionized form
.

12. Fate and excretion
Approx. 80 to 90% of nicotine is altered in the body, mainly in the liver.
Cotinine is the major metabolite.
Half life of nicotine– 2 hrs.
The rate of urinary excretion - dependent upon the pH of the urine.
Nicotine is also excreted in the milk of lactating women who smoke.

13. MEASURE OF
PATIENT’S
EXPOSURE
TO TOBACCO
Exhaled carbon monoxide in the
breath
Cotinine , a metabolite of nicotine
is measured in the saliva,plasma
/serum and urine.
Cotinine measurements are more reliable than
nicotine since it has higher half life 14-20 hours
compared to 2-3 hrs of nicotine (Jarvis et al 1988)
The mean plasma and salivary
cotinine concentrations of regular
smokers are approximately 300
ng/ml.
Non smokers the cotinine
concentration are about 2 ng/ml
,but this may be slightly raised due
to environmental exposure(passive
smoking)

14. CLASSIFICATIONOFSMOKERS
CURRENT SMOKER
Who have smoked ≥100 cigarettes in their
life time and currently smokes.
FORMER SMOKER
Who have smoked ≥100 cigarettes in their life
time and do not currently smokes

15. GLOSSARY
Mainstream smoke –
• refers to
the smoke that is
inhaled by a smoker
and then exhaled
into the
environment.
Side stream smoke –.
• refers to the smoke
that wafts off the
end of a burning
cigg, cigar or pipe
Amount smoked: .
• The average
number of
cigarettes smoked
per day, on days
when cigarettes
were smoked
Environmental
Tobacco Smoke
(ETS): .
• Also called second-
hand smoke.
Inhaling ETS is
called passive
smoking. Usually
refers to cigarette
smoke in the
environment of a
nonsmoker
Every day smoker:
• An adult who has
smoked at least 100
cigarettes in his or
her lifetime, and
who now smokes
every day.
Previously called a
“regular smoker”.

16. Someday Smoker
• Consistently as
having ever
smoked 100
cigarettes during
smoker’s lifetime
and currently
smoking on some
days
Intermittent
smoking
• Not smoking on a
daily basis
Social Smoker
• Smoking <5
cigarettes per day
in last 2 years

17.  LIGHT SMOKERS
Smoking less than 1 pack/day, less than 15 cig/day, less than 10 cig/day,
and smoking 1–39 cig/week( Okeyumi et al 2002,Husten 2009)
1. Low- rate daily smoking- fewer than 5 cig/ day
2.Very light smoking- fewer than 6 cig /day
3. chippers- consistently smoke no more than 5 cig/ day on the days when they do smoke.
HEAVY SMOKERS
Smoke greater than/equal to 25/more cigarettes a day.
(Wilson D 1992)

18. SMOKING AND SYSTEMIC
INVOLVEMENT
Nicotine when inhaled is retained and rapidly absorbed into the blood
stream affecting every organ of the body.

19. EFFECTS ON NUTRITION
 There is increasing evidence
that smokers require twice as
much as vitamin c as non
smokers since smokers
metabolize the vitamin more
rapidly.
 Smoking influences both
hunger and body weight
tending to postpone feelings of
hunger and to reduce body
weight
EFFECT OF PERIPHERAL
VASCULATURE
 Due to stimulation of
adrenalin there is
vasoconstriction of peripheral
blood vessels, which also
elevates blood pressure.

20. .
EFFECTS ON GI TRACT
 There is increased predilection
for Esophageal carcinoma and
Peptic ulceration
EFFECTS ON CNS
 Mimics the action of acetyl
choline of autonomic ganglia,
initially stimulating and
subsequently depressing
synaptic transmission.
 Responsible for dependence,
that characterizes the smoking
habit. Elevates the mood and
the person feels a sense of
pleasure and excitement.

21. EFFECT ON CVS
 Increases heart rate,cardiac
output ,blood pressure
 These are all due to
autonomic stimulation.
 Malignant hyper tension
and coronary artery
disease are the most
common diseases with
smoking.
EFFECT ON IMMUNE
SYSTEM
 Has an
immunosuppressive
effects on the host
 Impaired PMNL motility,
chemotaxis, phagocytosis
 Decreased antibody
production especially
IgG2 ( IgG2 important for
opsonization)

22. EFFECTS ON
RESPIRATORY SYSTEM
 Most of the nicotine enter
the lungs and absorbed
through the alveoli causing
chronic bronchitis,
emphysema and all types
of lung cancer.
EFFECTS ON ORAL
CAVITY
Each puff of a cigarette contains
about 18 mg is solid particulate
matter and rest consists of
carbon dioxide and carbon
mono-oxide mixed with oxygen
and nitrogen from air.
Risk of oral cancer is six times
with cigarette or or cigar
smoking & 16 times with the
usage of pipe smoking.

23. Saliva
 Increased flow rate of saliva.
This is a reflex phenomenon
produced by irritant
particulate matter in smoke.
The toxic material in a
cigarette can cause inhibition
of function of oral salivary
leucocytes.
Effects on Pregnancy
It causes negative influence of
smoke induced blockade of
the hemoglobin by carbon
monoxide. The fertility
rate of women is reduced and
risk of abortion, miscarriage,
preterm delivery is increased.
Smoking fathers also damage
the development of their
unborn child.
Lowbirth weight babies.
Smaller organs, sply lungs.

24. SMOKING
AND EFFECT
ON
PERIODONTIUM
EFFECTS ON GINGIVA
No striking gingival changes though it
has direct toxic effect on gingiva has
been reported.
Heavy smokers have grayish
discoloration and hyperkeratosis of
gingiva.
There is decreased inflammation and
edema

25. Effect on periodontal tissues
There is increased pocket depth, alveolar bone loss, attachment loss in smokers
than non smokers.
On alveolar bone
Smoking has been significantly associated with severity of bone loss. Increased
bone loss is directly related to increased amounts of smoking.
On Periodontal Ligament
Smoking has a role in altering periodontal host response. This is done by impairing
normal function of host response in neutralizing infections.

26. SMOKING AS A RISK
FACTOR FOR
PERIODONTAL DISEASE

27. smoking
Change in intra-oral temperature
Alters ph of saliva
Alters micro biota of oral cavity
Host defense
1. Decreased PMN function
2. inhibition of neutrophil
and monocyte–
macrophage
Decreased extracellular matrix
and alveolar bone
increased pro inflammatory cytokines
Compromise in wound healing
Connective tissue and
vascular destructions
Periodontal
disease
progression

28.  Disease progression slows in patients who quit smoking compared to those who continue to smoke
 Studies including NHANES III have shown that former smokers have lesser risk to periodontitis
and it is proportional to the number of years since quitting
 Over a period of ten years, smokers had 2 times greater bone loss than non-smokers despite
excellent plaque control
 Hence, effects of tobacco smoking are reversible and its a “modifiable” risk factor

29. EFFECTSON PLAQUE FORMATION
Smokers had poorer oral hygiene than non smokers.
Smokers had significantly more plaque than non-
smokers, and there was a trend towards increased
plaque deposits with increasing cigarette consumption.
Less plaque in smokers than in nonsmokers.
No difference in mean Pl index score (Bergstrom and
Eliasson 1987,Bergstorm and Preber 1986)

30. EFFECTSONCALCULUS FORMATION
Pipe smokers had supragingival calculus than cigarette smokers.This might be because the pH of
pipe smoke is higher than that of cigarette smoke, and because pipe smokers circulate the smoke
around the mouth, whereas cigarette smoke tends to be inhaled. (Albandar 2000)
There is an increased calcium concentration in fresh saliva in smokers following smoking (Khan 2005)
Nicotine affects the exocrine glands by an initial increase in salivary and bronchial secretions that are
followed by inhibition of the secretions.The calcium phosphates found in supragingival calculus are in
the main derived from the saliva.The organic components may also arise from this source, the
proteins and polypeptides constituting the major fraction (Erdemir 2006)

31. EFFECTSOF
SMOKINGON
PREVALENCE
ANDSEVERITY
OF
PERIODONTAL
DISEASE
For the last few decades, dentists and dental researches have
become more aware of the critical role of smoking on the incidence
and severity of periodontal disease and smoking is now considered
a risk factor in periodontal disease.
In 1983, Ismail et al. analysed smoking and periodontal disease and
found that after adjusting for potential confounding variables such
as age, oral hygiene, gender and socioeconomic status, smoking
remained a major risk indicator for periodontal diseases.

33. Smoking and
Gingivitis
 Reduced clinical signs of inflammation
 Reduced gingival bleeding on probing and oedema.
 Altered gingival crevicular fluid inflammatory cytokine profiles,
immune cell function and altered proteolylic regulation in
smokers.

34. Smoking and
Periodontitis
 Increased Prevalence and severity of periodontal destruction
 Presence of deeper probing depth and a larger number of deep
pockets
 More attachment loss including more gingival recession
 More teeth with furcation involvement
 Increased tooth loss and bone loss
 Increased Rate of periodontal destruction
 Increased Prevalence of severe periodontitis
 Increased Prevalence with increased number of cigarettes smoked
per day .
 Decreased Prevalence and severity with smoking cessation

35. Periodontal
Microbiology
in smokers  Several studies have explored the changes that may occur in
subgingival plaque as a result of smoking with conflicting
and inconclusive results.
 Smokers may have higher levels of plaque than non-smokers,
which may be accounted for by poorer levels of oral hygiene
rather than higher rates of supragingival plaque growth.

36.  Several studies have shown that
 smokers harbour more microbial
species which are associated
with periodontitis than non-
smokers, including
 P. gingivalis, A.
actinomycetemcomitans,
Tanerella forsythia
 P. intermedia,
Peptostreptococcus micros,
Fusobacterium nucleatum,
Campylobacter rectus.
Smokers may have a
higher proportion of sites
harboring these putative
periodontal pathogens, in
particular the palatal
aspects of the maxillary
teeth and the upper and
lower incisor regions.
(Haffajee & Socransky
2001)

37. Immunology Smoking exerts a major
effect on the protective
elements of the
immune response,
resulting in an increase
in the extent and
severity of periodontal
destruction.
The deleterious effects
of smoking appear to be
due in part to a down
regulation of the
immune response to
bacterial challenge.
Smokers have an
increased number of
leukocytes in the
systemic circulation
(Sorenson et al. 2004),
but fewer cells may
migrate into the
gingival crevice/pocket
(Eichel &Shahrik 1969).
Studies in vitro have
shown a direct defensive
functions by high
concentrations of
nicotine that may be
achieved in patients
using smokeless tobacco
(Pabst et al. 1995).

38.  Altered neutrophil chemotaxis, phagocytosis, and oxidative burst
 Increased tumor necrosis factor-cr and PGE in GCF
 Increased collagenase and elastase in GCF

39. Immunoglobu
lins
 It has been reported that serum IgG levels in smokers may be
reduced (Quinn et al. 1998) with depression of IgG2
 Levels of serum IgA and IgM classes are variable and IgE may be
elevated.

40. CONCL
USION
CONCLUSION

42. REFERENCES
 Clinical periodontology Carranza, 10th edition
 Clinical periodontology and implant dentistry Lindhe ,5th edition
 Smoking and periodontal disease, periodontology 2000.vol.32
 The effect of smoking on periodontal treatment response . J Clin
Periodontol 2006
 Systematic review of the effect of smoking on nonsurgical periodontal
therapy Periodontology 2000, Vol. 37
 The influence of smoking on host responses in periodontal infections
Periodontology 2000, Vol. 43

43.  Smoking and its Effect on Periodontium – Revisited. Gurparkash Singh
Chahal, Kamalpreet Chhina, Vipin Chhabra, Amna Chahal. Indian Journal
of Dental Sciences,Volume 9,Is.sue 1,January-March 2017.
 Smoking and periodontal disease,d.f. kinane,i.g. chestnutt. 11(3):356-365
(2000)
 Tobacco Use and Its Effects on the Periodontium and Periodontal Therapy
 Health Effects of Light and Intermittent Smoking: A Review,Rebecca et
al.2010 april 6: 121(13):1518-1524.
 Pharmacology of Nicotine: Addiction, Smoking-Induced Disease, and
Therapeutics ANNU Rev Pharmacol toxicl 2009:49:57-71.

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