a presentation on smoking affecting the periodontium. All aspects covered. An important topic from dentist point of view.

1. Smoking and
Periodontal Disease

2. Introduction
• Tobacco smoking is an addictive habit first introduced
in Europe. Smoking is now recognized as the most
important cause of preventable death and disease.
• Currently, the most of adult population smoke cigarettes.
However, nowadays, the smokers are changing to
lower-tar brands.
• Consumption is rising in developing countries,
particularly where tobacco production brings great
economic benefits.

3. • Smoking is associated with a wide spectrum of
diseases including:-
Stroke, coronary artery disease, peripheral
artery disease, gastric ulcer and cancers of
the mouth, larynx, esophagus, pancreas,
bladder and uterine cervix.
It is also a major cause of chronic obstructive
pulmonary disease and a risk factor for low
birth weight babies.
Approximately 50% of regular smokers are
killed by their habit and smoking causes 30%
of cancer deaths.

4. • Cigarette smoke is a very complex mixture of
substances with over 4000 known constituents.
These include:-
carbon monoxide, hydrogen cyanide, reactive
oxidizing radicals, a high number of carcinogens,
and the main psychoactive and addictive molecule
– nicotine
• Many of these components could modify the host
response in periodontitis.

5. • Inter-subject smoking variation includes
frequency of inhalation, depth of inhalation,
length of the cigarette stub left, presence or
absence of a filter, and the brand of cigarette.
• The patient's exposure to tobacco smoke can be
measured in several ways including interviewing
the subject using simple questions or more
sophisticated questionnaires and biochemical
analyses.

6. • The tests include exhaled carbon monoxide in
the breath, which is commonly measured in
smoking cessation clinics, and cotinine (a
metabolite of nicotine) in saliva, plasma/serum,
or urine.
• Cotinine measurements are more reliable in
determining a subject's exposure to tobacco smoke
because the half-life is 14-20 hours compared with
the shorter half-life of nicotine which is 2-3
hours.

7. • The mean plasma and salivary cotinine
concentrations of regular smokers are
approximately 300ng/ml and urine
concentrations are about 1500 ng/ml.
• Nonsmokers typically have plasma/saliva
concentrations under 2ng/ml, but this
may be raised slightly due to environmental
exposure (passive smoking).

8. Nicotine Effect……….
• Inhalation of tobacco smoke allows very rapid
absorption of nicotine into the blood and transport to
the brain, which is faster than an intravenous infusion.
• Nicotine in tobacco smoke from most cigarettes is
not well absorbed through the oral mucosa because the
nicotine is in an ionized form as a result of the pH
(5.5).
• In contrast cigar and pipe smoke is more alkaline
(pH 8.5), which allows good absorption of un-ionized
nicotine through the buccal mucosa.

9. • Nicotine is absorbed rapidly in the lung where
the smoke is well buffered.
• The administration of nicotine causes :-
A rise in the blood pressure, an increase in
heart rate, an increase in respiratory rate and
decreased skin temperature due to peripheral
vasoconstriction.
• However, at other body sites, such as skeletal
muscle, nicotine produces vasodilatation.

10. Periodontal Disease In Smokers
• Pindborg (1947) was one of the first investigators to
study the relationship between smoking and
periodontal disease.
• He discovered a higher prevalence of acute
necrotizing ulcerative gingivitis
The typical appearance of
necrotizing ulcerative
gingivitis in a heavy
smoker with poor oral
hygiene.

11. Smokers with periodontitis, have:
1. Deeper probing depths and a larger number of deep
pockets
2. More attachment loss including more gingival
recession
3. More alveolar bone loss
4. More tooth loss
5. Less gingivitis and less bleeding on probing
6. More teeth with furcation involvement

12. Smoking and gingival inflammation
• A reduction in clinical signs of gingivitis has been
reported in smokers and this effect is independent of
plaque levels.
• Heavy smokers may have grayish discoloration and
hyperkeratosis of the gingiva:
An increased number of keratinized cells has been
found in the gingiva of smokers. Changes in the
epithelium were described as keratotic,
hyperkeratotic, and hyperplastic.

13. Smoking and gingival bleeding
• Smoking is known to produce peripheral
vasoconstriction, in some subjects, this is preceded
by vasodilatation.
• Degree of inhalation of tobacco smoke and the rate
of nicotine absorption.
Nicotine from cigarettes stimulates the sympathetic
ganglia to produce neurotransmitters including
catecholamines.

14. These affect the alpha-receptors in blood vessels
which in turn causes vasoconstriction.
The vasoconstriction of peripheral blood vessels
caused by smoking can also affect the periodontal
tissue as smokers have less overt signs of
gingivitis than nonsmokers and clinical signs of
gingival inflammation such as redness, bleeding,
and exudation are not evident in smokers.
The vasoconstrictive actions of nicotine may be
responsible for the decreased gingival blood flow.

15. Effects of Smoking on the Etiology and
Pathogenesis of Periodontal Disease

16. Smoking and oral
microorganisms
• Smoking has important effects on oral bacteria.
• Cigarette smoking could cause a lowering of the
oxidation-reduction potential, and this could cause
an increase in anaerobic plaque bacteria.
• There was a statistically significant shift in the
proportion of Gram-positive to Gram-negative
bacteria in 3-day-old plaque from smokers when
compared with non-smokers.

17. • Tobacco smoke contains phenols and cyanides,
which can account for antibacterial and toxic
properties.
• Smokers harbored significantly higher levels and
were at significantly greater risk of infection with
Tanarella forsythia than non-smokers.
• Adjusting for disease severity, Porphyromonas
gingivalis was also more likely to subgingivally
infect smokers than non-smokers

18. Effects on the host response
• Nicotine metabolites can concentrate in the
periodontium and their effects include the
promotion of vasoconstriction; and the
impairment of the functional activity of
polymorphs and macrophages.
• The numbers of neutrophils in peripheral blood
are also increased by tobacco use and their
migration through capillary walls.

19. Physiology
• Clinical signs of inflammation are less pronounced
in smokers than in nonsmokers.
• This may result from alterations in the
inflammatory response in smokers, as outlined
previously, or from alterations in the vascular
response of the gingival tissues.
• Although no significant differences in the
vascular density of healthy gingiva have been
observed between smokers and nonsmokers, the
response of the microcirculation to plaque
accumulation appears to be altered in smokers
compared with nonsmokers.

20. • With developing inflammation, a rise in GCF
flow, bleeding on probing, and gingival blood
vessels are less in smokers than nonsmokers. In
addition, the oxygen concentration in healthy
gingival tissues appears to be less in smokers than
nonsmokers, although this condition is reversed in
the presence of moderate inflammation.
• Subgingival temperatures are lower in smokers
than nonsmokers, and recovery from the
vasoconstriction caused by local anesthetic
administration takes longer in smokers.

21. • These cumulative data suggest that
significant alterations are present in the
gingival microvasculature of smokers
compared with nonsmokers and that these
changes lead to decreased blood flow and
decreased clinical signs of inflammation.
• This explains the long observed
phenomenon of a transient increase in
gingival bleeding when a smoker quits.

22. Effects of Smoking on Response to
Periodontal Therapy

23. • Following non-surgical therapy, healing in terms
of gingival bleeding reduction and pocket-depth
reduction was less favorable in smokers.
• The clinical results showed a statistically
significant reduction of pocket depth and number
of diseased sites in both smokers and non-smoker
patients.
• These findings are in agreement with recent long-
term results which suggest that tobacco smoking
interferes with the healing process following non-
surgical periodontal therapy.

24. • James and colleagues investigated the in vitro
effect of nicotine on fibroblast activity. They
found that it inhibited attachment and growth of
periodontal ligament fibroblasts.
• The results of these studies all indicate that
smoking has a deleterious effect on wound
healing and may help to explain why smokers
respond less favourably to periodontal therapy.

25. Maintenance Therapy
• The detrimental effect of smoking on treatment
outcomes appears to be long-lasting and
independent of the frequency of maintenance
therapy.
• After four different modalities of therapy,
including scaling and root planing, modified
Widman flap surgery, and osseous surgery,
maintenance therapy was performed by a hygienist
every 3 months for 7 years.
• Smokers consistently had deeper pockets than
nonsmokers and less gain in attachment when
evaluated each year for the 7-year period.

26. • Even with more intensive maintenance
therapy, Smokers possess deeper and more
residual pockets than nonsmokers, even
though no significant differences in plaque or
bleeding on probing scores were found.
• Smokers also tend to experience more
periodontal breakdown than nonsmokers after
therapy.

27. • In studies of patients who failed to respond to
conventional therapy, including different combinations
of oral hygiene instruction, scaling and root planing,
surgery, and antibiotics, approximately 90% of these
poorly responding patients were smokers.
• It is clear from these studies that smokers (1) may
present with periodontal disease at an early age, (2)
may be difficult to treat effectively with conventional
therapeutic strategies, and (3) may continue to have
progressive or recurrent periodontitis. For this
reason, smoking cessation counseling must be a
cornerstone of periodontal therapy in smokers.

28. Smoking Cessation
• Various methods for helping patients to quit
smoking in the dental environment have been
described.
• ASK: Ask the patient about their smoking
status.
• This should be part of the medical history.

29. • ADVISE: Advise smokers of the associations
between oral disease and smoking.
Be informative, honest, and helpful but not judgmental.
• ASSESS: Assess the patient's interest and readiness
to attempt smoking cessation.
Patients may not yet be in an action phase to quit
smoking, which is why it is always important to make
these assessments every time you see the patient.
• ASSIST: Assist the patient in their quit attempt.
If you are trained, many techniques can be used.
Alternatively, assist the patient in seeking the help they
need.

30. • ARRANGE: Arrange follow-up or referral to
professional smoking cessation services.
The most important aspect of this is to keep in
regular contact particularly around the quit date and
in the immediate period after.

31. Effects of Smoking Cessation on
Periodontal Treatment Outcomes
• Studies have demonstrated that smokers have
significantly worse periodontal status (deeper
probing depths, more attachment loss, and bone
loss) than either former smokers or nonsmokers
and usually have poorer treatment outcomes.

32. • There are very few intervention studies on the
effect of smoking cessation on periodontal
treatment outcomes (i.e., studies in which
smokers were helped to quit and the effect on
periodontal status was then assessed).
• Two short-term studies have indicated that
smoking has a negative impact on the gingival
vasculature and that these changes are reversible
upon quitting smoking.

33. • One intervention study has assessed the impact of
smoking cessation on outcomes after nonsurgical
periodontal treatment.
• This study employed dental hygienists who were
trained as smoking cessation advisors and
achieved a 20% quit rate at 12 months in a
population of smokers who also had periodontitis
using a variety of strategies, including
Counseling, Nicotine Replacement Therapy,
and Bupropion.

34. Nicotine Replacement Therapy
• Nicotine replacement therapy (NRT) gives
you nicotine – in the form of gum, patches,
sprays, inhalers, or lozenges – but not the
other harmful chemicals in tobacco.
• NRT can help relieve some of the physical
withdrawal symptoms so that you can focus
on the psychological (emotional) aspects of
quitting.

35. • To conclude, smoking is the major risk
factor for periodontitis, and smoking
cessation should be an integral part of
periodontal therapy in patients who smoke
and needs to be considered a priority for the
management of periodontitis in smokers.

36. References
• Carranza’s clinical Periodontology 11th Ed
• Jan Lindhe
• Ana Pejčić, Radmila Obradović, Ljiljana Kesić, Draginja
Kojović : SMOKING AND PERIODONTAL DISEASE A
REVIEW, Medicine and Biology Vol.14, No 2, 2007, pp. 53
– 59
• Bergstrom J, Eliasson S, Dock J. Exposure to tobacco
smoking and periodontal health. J Clin Perio 2000; 27: 61-
68.

37. THANK YOU