Smoking and periodontal disease, smoking as a risk factor, incidence of smoking, effects of smoking on periodontium, smoking and gingivitis and smoking and periodontitis, effect of surgical and non surgical therapy on smokers

1. Smoking and Periodontal
Disease
Presented by:
Pallavi Prashar
MDS 2nd year

2. Introduction
• Smoking is associated with a wide spectrum of
disease 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.

3. Smoking Epidemic
United States
• In 1993 25.4% of population smoked
– 27% of men
– 24% of women
• In 2007, this decreased to 20.8%
– 23.9% of men
– 18% of women
• As per NHANES III
– During period 1988 to 1994
• 27.9% of adults were current smokers
• 23.3% of adults were former smokers
• Smoking was higher in younger age group (34 years) than in older age group
(55 years)

4. European Union
• An average of 29% of the adult population
smoke, ranging from 17.5% in Sweden to
45% in Greece.
• Most smokers start the habit as teenagers,
with the highest prevalence in the 20–24-
year-old age group.
• Socioeconomic differences also exist with
higher smoking in the lower socioeconomic
groups.

5. India

7. Different methods of tobacco smoking
Pipes

8. Classification of smokers
Heavy
smokers
20 / day
Light smokers
19 / day
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
Non Smoker
Who have not
smoked 100
cigarettes in their life
time and do not
currently smokes

9. • Many smokers are trying to quit and
therefore, simply asking how many cigarettes
they are smoking today may not give an
accurate assessment of their life time
exposure.
• To get around this problem Pack Years
should be calculated as follows:
Pack Years = (no. of packs smoked/day) X (no. of years
of smoking)

10. Constituent Of Tobacco Smoke
• Cigarette smoke is a very complex mixture of
substances with over 4000 known
constituents and comprises of:
Gasseous phase
Carbon monoxide
Ammonia
Formaldehyde
Hydrogen Cyanide
Acrolein
Benzopyrene
Dimethylnitrosamine
Solid (particulate) phase
Nicotine
Tar
Benzene
Benzopyrene

12. • Tar
– In its condensate form is sticky brown substance that stains fingers and
teeth yellow brown.
• Nicotine
– Alkaloid found within tobacco leave and evaporates when the cigarette is
lighted.
– It is quickly absorbed and reaches the brain within 10-19 secs.
– 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 (Benowitz 1988).
– Nicotine is absorbed rapidly in the lung where the smoke is well buffered.
– It is highly addictive and causes rise in BP, Increased heart rate and
respiratory rate, and peripheral vasoconstriction.
Tar and nicotine yields reduced due to use of filters
Dose of tobacco intake – depends on the way an individual smokes
(Benowitz 1989)

13. Assessment of smoking status
• The patient’s exposure to tobacco smoke can be
measured in a number of ways, including
interviewing the subject using simple questions or
more sophisticated questionnaires and biochemical
analyses (Scott et al. 2001).
• Biochemical analyses:
– 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

14. • 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 (Jarvis et al.
1988).
• The mean plasma and salivary cotinine
concentrations of
– regular smokers are approximately 300 ng/ml and
urine concentrations are about 1500 ng/ml.
– Non-smokers typically have plasma/saliva
concentrations under 2 ng/ml, but this may be raised
slightly due to environmental exposure (passive
smoking).

15. Tobacco
smoking
Plaque and
oral flora
Periodontal
tissues
Homeostasis
and healing
potential
Periodontal
therapy
Immune
response

16. EFFECTS OF SMOKING ON PREVALENCE AND SEVERITY OF
PERIODONTAL DISEASE
Effect of smoking on gingiva
 Changes in the epithelium - hyperkeratotic,
hyperplastic
 Greyish discoloration of the gingiva
 Increased amounts of IL-1, IL-6 and PGE2
(Johnson et al 1996)

17. Smoking – predisposing factor for ANUG
  use of tobacco   frequency of ANUG
(Rowland 1999)
 Reason:
Tar in the smoke  irritating effect on gingiva
Nicotine  vasoconstriction of capillaries
(Lindeboom 2005)

19. SMOKING
influence the tissue response to irritation.
activates the release of epinephrine
promotes contraction of peripheral vessels
reducing blood flow to the gingiva
loss of vitality to the gingival epithelium
onset of ANUG .{Karadachi et al}

20. Effect of smoking on gingival blood flow
Transient decrease
(Clarke et al 1981)
the infusion of nicotine
resulted in a transient
decrease in gingival
blood flow in a rabbit
model.
Transient increase
(Baab & Oberg 1987)
using laser Doppler flowmetry
to monitor relative gingival flow
in 12 young smokers,
observed an immediate but
transient increase in relative
gingival blood flow during
smoking, compared to the
presmoking or resting
measurements.

21. • The authors hypothesized that the steep rise in
heart rate and blood pressure due to smoking
could lead to an increase in the gingival
circulation during smoking.
• These results were confirmed by Meekin et al.
(2000) who showed that subjects who smoked
only very occasionally experienced an increase
in blood flow to the head, whereas regular
smokers showed no change in blood flow,
demonstrating tolerance in the regular smoker.
• Morozumi et al. (2004) showed that the gingival
blood flow significantly increased at 3 days
following quitting

22. Gingival inflammation and bleeding
 Smokers experienced less gingival bleeding
(Bergstrom & Floderus- Myrhed 1983)
 NHANES III : Dose–response effect (Dietrich et al
2004)
 Quit-smoking program – improvement in
parameters
(Nair et al 2003)
Rapid recovery of the
inflammatory response

23. Periodontitis
• Pindborg (1947) was one of the first investigators to study
the relationship between smoking and periodontal disease.
• Increased prevalence and severity of periodontal
destruction.
– On average, smokers are 4 times likely to have periodontal disease
as compared to person who had never smoked.
– Former smoker were 1.7 times more likely to have periodontitis than
person who had never smoked
– Older adults are approximatelty 3 times more likely to have severe
periodontal disease and number of pack years of tobacco use is
significant factor in tooth loss, coronal root caries and periodontal
disease.
– Cigarette smoking is associated with increased severity of
generalized aggressive periodontitis I young adults.
– Smokers between the age of 19-30 years are 3.8 times more likely to
have periodontitis than non smoker.

24. • Deeper probing depths and a larger number of deep
pockets (Feldman et al. 1983; Bergstrom & Eliassson
1987a; Bergstrom et al. 2000a)
• More attachment loss including more gingival
recession (Grossi et al. 1994; Linden & Mullally 1994;
Haffajee & Socransky 2001a)
– Smokers are more than 6 times as likely as non smokers to
demonstrate continued attachment loss.
– The prevalence of moderate and severe periodontitis and
percentage of teeth with 5mm is more severe in current
cigarette smoker.
– Cigar and pipe smoker showed a severity of disease
intermediate b/w the current cigarette smokeer and non
smoker.

25. • More alveolar bone loss (Bergstrom & Floderus
Myhred 1983; Bergstrom & Eliasson 1987b;
Feldman et al. 1987; Bergstrom et al. 1991, 2000b;
Grossi et al. 1995)
– Over a 10 year period bone loss has been reported to be
twice as rapid in smokers as in non smokers.
– Proceeds more rapidly even in presence of excellent
plaque control.
• More tooth loss (Osterberg & Mellstrom 1986; Krall
et al. 1997)
– Young individuals smoking more than 155 cigarettes/day
shows highest rate of tooth loss (Holm G,1994)
– Tooth loss is increase in cigar and pipe smoker as
compared to non smoker.

26. • Increased prevalence of periodontal disease with
increased number of cigarettes smoked/day.
• Decreased prevelance and severity with smoking
cesation
– Risk of periodontitis decreases with the increasing
number of years since quitting smoking
– Negative effects of smoking on host are reversible with
smoking cesation and therefore, smoking ceastion
should be integral part of periodontal education and
therapy.

27. Effects of Smoking on Etiology and Pathogenesis
of Periodontal Disease
• The increased prevalence and severity of periodontal
destruction associated with smoking suggests that the host-
bacterial interactions normally seen in chronic periodontitis
are altered, resulting in more aggressive periodontal
breakdown.
• This imbalance between bacterial challenge and host
response may be caused by
– changes in the composition of the subgingival plaque,
– with increases in the numbers and virulence of pathogenic
organisms,
– changes in the host response to the bacterial challenge,
– or a combination of both.

28. Microbiology
• Smokers may have higher levels of plaque than nonsmokers, which may
be accounted for by poorer levels of oral hygiene rather than higher rates
of supragingival plaque growth (Bergstrom 1981; Bergstrom & Preber
1986).
• Several studies have shown that smokers harbor more microbial species
which are associated with periodontitis than non-smokers, including
– P. gingivalis,
– A. actinomycetemcomitans,
– Tanerella forsythia (Bacteroides forsythus) (Zambon et al. 1996),
• Smokers are 2.3 times more likely to harbour T. Forsythia than non smokers and former
smokers
– P. intermedia,
– Peptostreptococcus micros,
– Fusobacterium nucleatum, Campylobacter rectus (van Winkelhoff et al.
2001),
– Staphylococcus aureus,
– Eschericia coli, and
– Candida albicans (Kamma et al. 1999).

29. • Increased colonization of shallow periodontal pockets by
periodontal pathogens.
• 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 2001a,b).
• In contrast several studies have failed to show differences in
the bacterial species between smokers and non-smokers
(Preber et al 1992; Darby et al. 2000; Bostrom et al. 2001;
van der Velden et al. 2003).

30. Immune-inflammatory response
Effects on PMN function
• 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 inhibition of neutrophil
and monocyte–macrophage defensive functions by high
concentrations of nicotine that may be achieved in patients
using smokeless tobacco (Pabst et al. 1995).
• MacFarlane and co-workers (1992) demonstrated abnormal
PMN phagocytosis associated with a high level of cigarette
smoking.

31. • Neutrophil defects have been associated with an increased
susceptibility to periodontitis, including cyclic neutropenia
where there is a reduction in the number of neutrophils, and
conditions such as leukocyte adhesion deficiency (LAD 1
and LAD 2), which may be responsible for cases of
generalized prepubertal periodontitis as described by Page
et al. (1983).
• Neutrophils obtained from the peripheral blood, oral cavity,
or saliva of smokers or exposed in vitro to whole tobacco
smoke or nicotine have been shown to demonstrate
functional alterations in
– chemotaxis,
– phagocytosis, and
– the oxidative burst

32. Smoking and lymphocytes function
• The leukocytosis observed in smokers results in
increased numbers of circulating T and B
lymphocytes.
 Chronic exposure to nicotine
Impairment of antigen-mediated T cell signalling
Inhibits antibody-forming cell responses
Immunosuppression
(Sopori et al 1998)

33.  sIgG levels are reduced in smokers – IgG2
(Fredriksson 1999)
 Effects of cigarette smoking on serum IgA
and IgM classes – controversial
 Smoking decreases salivary IgA
 IgE is greatly elevated in smokers
 Reduced antibody levels to periopathogens

34. Cytokines
• Elevated levels of tumor necrosis factor alpha (TNF-
α) have been demonstrated in the gingival
crevicular fluid (GCF) of smokers,
• Elevated levels of prostaglandin E2 (PGE2),
neutrophil elastase, and matrix metalloproteinase-8
(MMP-8).
• In vitro studies also have shown that exposure to
nicotine increases the secretion of PGE2 by
monocytes in response to lipopolysaccharide (LPS).

35.  Higher levels of IL-8, lower levels of IL-4
(Giannopoulou et al 2003)
 IL-1 levels half of that found in non-smokers
(Petropoulos et al 2004)
 IL-6, IL-1 - no significant differences (Bostrom
et al 2000)

36. Other Factors
 Elastase, 2-macroglobulin and 1-anti-trypsin levels
 Lower concentrations in heavy smokers (Persson 2001)
• Tobacco smoking has a chronic effect on the elevated
levels of soluble ICAM (sICAM) and there is evidence that
the subject may return to more normal levels after quitting
smoking (Scott et al. 2000b; Palmer et al. 2002).
• GCF the levels of sICAM are much lower in smokers
despite very much higher serum levels than non-smokers
(Fraser et al. 2001).

37. Physiology
• ↓Gingival blood vessels with ↑inflammation
• ↓GCF flow and bleeding on probing with ↑
inflammation
• ↓Subgingival temperature
• ↑Time needed to recover from local anesthesia
• Oxygen concentration in healthy gingival tissue
appears to be less in smokers than non smokers,
although this condition is reversed in presence of
moderate inflammation.

38. Gingival Crevicular Fluid
 GCF nicotine concentrations - 300 times that of
plasma (20ng/ml)
 Lower resting GCF flow rate (Persson et al 1999)
 Reduced GCF flow
 Defense mechanism hampered
 Less flushing – removal of microbes and waste
products
 Episode of smoking  transient increase in GCF
flow rate (McLaughlin et al 1993)
 Quit-smoking programme – flow rate greater at 5
days postquitting (Morozumi et al 2004)

39.  gingival
redness
Fewer
gingival
vessels
 GCF
Less
bleeding
sites
Suppression of the
normal inflammatory
response
(Bergstrom 1986)

40. EFFECTS OF SMOKING ON RESPONSE TO
PERIODONTAL THERAPY
Non surgical periodontal therapy
• ↓Clinical response to scaling and root planing
– Numerous studies have indicated that current smokers do not
respond as well to periodontal therapy as non-smokers or former
smokers.
• ↓Reduction in pocket depth
– pocket depth reduction is more effective in nonsmokers than in
smokers after nonsurgical periodontal therapy (Phase I therapy),
including oral hygiene instruction, scaling, and root planing
– Average pocket reductions of 2.5 mm for nonsmokers and 1.9 mm for
smokers were observed in pockets that averaged 7 mm before
treatment, even though plaque scores were less than favorable.
(Bergstorm ,1988)

41. • ↓Gain in clinical attachment levels
– The poorer reductions in probing depths and gains in attachment
level amount to a mean of approximately 0.5 mm.
– Much of this may be due to less recession of the marginal tissues in
smokers as there is less edema and more fibrosis in the gingiva.
(Lindhe 5th edition)
• ↓Negative impact of smoking with ↑level of plaque control.
• When pockets persist in smokers and nonsmokers after
therapy, adjunctive topical antimicrobial therapy can be
used to try to resolve the remaining pocket depths.
• When scaling and root planing are used in combination with
topical subgingivally placed tetracycline fibers, subgingival
minocycline gel, or subgingival metronidazole gel, smokers
continue to show less pocket reduction than nonsmokers.
• Response to non-surgical treatment may be seen merely as
resolution of infl ammation and improvement of the epithelial
attachment together with some formation of collagen.

42. Surgical therapy and Implants
• ↓Pocket depth reduction after surgery
– In a longitudinal comparative study of the effects of four different
treatment modalities, including coronal scaling, root planing, modified
Widman flap surgery, and osseous resection surgery, smokers
consistently showed less pocket reduction and less gain in clinical
attachment levels than nonsmokers or former smokers. (Kaldahl
WB,1996)
• ↑Deterioration of furcations after surgery
• ↓Gain in clinical attachment levels, ↓ bone fill, ↓ pocket depth
reduction after bone graft procedure ↑ recession, and ↑
membrane exposure after GTR
• ↓Pocket depth reduction after DFDBA
• Conflicting data on the impact of smoking on implant
success. Implant failure is 2.5 times greater (Wilson 1999)
• Smoking cessation should be recommended before
implants.

43. Maintainence therapy
• The detrimental effects of smoking on treatment outcomes
appears to be long-lasting and independent of the frequency
of maintenance therapy.
• ↑Pocket depth during maintenance therapy
• ↓Gain in clinical attachment levels
• ↑Recurrent/refractory disease in smokers
• ↑Need for re-treatment in smokers
• ↑Need for antibiotics in smokers to control the negative
effects of periodontal infection on surgical outcomes
• ↑Tooth loss in smokers after surgical therapy

44. Effect of smoking cessation on periodontal
disease outcome
• The periodontal status of former smoker is intermediate to
that of current smokers or non smoker and appears to be
usually closer to that of non-smokers.
• One who quits smoking had better response to periodontal
treatment as compared to non quitters and failed quitters.
• The benefits of smoking cessation on periodontium is likely
to be mediated through various pathways such as:
– Shift towards a less pathogenic microflora
– Recovery of gingival micro-circulation
– Improvement in aspects of the immune inflammatory responss

45. Smoking cessation
• Guidelines for health care provider when giving cessation
advice includes ‘five A’s’ which are:
Brief
Intervention
Program
ASK
ADVISE
ASSESSASSIST
ARRANGE

46. • Ask
– Ask the patient about their smoking status
– This should be part of medical history
• Advice
– Advice smokers of the association between oral disease and smoking
– Be informative, honest and helpful but not judgemental
– The patients response to information will reveal their interest in quitting
• 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 assessment, every time you see the
patient.
• Assist
– Assist the patient in their quit attempt
• Arrange
– Arrange follow up or referral to professional smoking cessation service

47. Pharmacotherapy
• Nicotine withdrawal agents:
– Nicotine containing
– Non-nicotine containing
Nicotine containing agents
• These contains nicotine and deliver measured amount of
nicotine so that gradually nicotine intake can be reduced
• It does not contain any toxic product such as tar and CO in
cigarette smoke.
• These are available in following forms:
– Patches: available in different doses and worn for 16-24 hrs/day
– Lozenges and gums: available in different flavours, should be
chewed slowly to allow the nicotine to be absorbed through the
mouth
– Nasal spray
– Inhalator: plastic mouth piece with a supply of nicotine cartridge that
fits to one end, nicotine is absorbed in mouth by drawing on it like
cigarette

48. Non-nicotine containing agents
• Bupropion
– Success rate at 12 months is 20-30%
– Used as an antidepressant at higher doses but is
effective for smoking cessation at low doses.
– It is usually prescr ibed starting 1-2 weeks before the quit
date
– Initially at 150 mg OD for 6 days, then 150 mg BD for &-9
weeks
– Contra-indicated in patients with epilepsy, anorexia
nervosa, bulimia, bipolar disorder or severe liver disease.
– The most common side effects are insomnia (up to 30%),
dry mouth (10-15%), headache (10%), nausea (10%),
constipation (10%), and agitation (5-10%)

49. • Other methods
– Intensive counselling
– Motivational interviewing
– Cognitive behavorial therapy
– Hypnosis
– Acupuncture

50. Conclusion
As an environmental factor, smoking interacts with the
host and the bacterial challenge, resulting in an increased
susceptibility to periodontitis and poorer response to
treatment.
Recent guidance suggest that dental practices
should assess the smoking status of patients and motivate
smokers towards quitting.