Smoking has significant negative effects on the periodontium and increases the risk and severity of periodontal disease in several ways: 1) Smoking alters the subgingival microbiota in favor of pathogenic species and impairs the host immune response, making the tissues more susceptible to bacterial infection. 2) Components of smoke such as nicotine, carbon monoxide, and tar are toxic to periodontal tissues and cells, impairing wound healing and reducing blood flow and oxygen levels in the gingiva. 3) Smokers have higher rates of periodontitis, greater attachment and bone loss, and their periodontal disease is less responsive to treatment compared to non-smokers. Quitting smoking can reduce disease

1. Smoking and its effects
on the
Periodontium and
Periodontal therapy

2. CONTENTS
• Introduction
• Epidemiological evidence
• Toxic subtances in tobacco
• Mechanism for negative effects of smoking on periodontium
• Effect of smoking on gingival & periodontal tissues
• Smoking and periodontitis in adults
• Smoking and ANUG
• Smoking and systemic health
• Smoking and oral health
• Effect on periodontal therapy
• Cessation of smoking
• Conclusion

3. Periodontal disease is defined as
inflammatory destruction of periodontal
tissue and alveolar bone supporting the
teeth.
Progression and severity of the disease
depends on complex interactions between
several risk factors such as microbial,
immunological, environmental and genetic
factors, as well as age, sex, and race.
.
INTRODUCTION

4. Tobacco smoking is a significant risk factor for
periodontal disease
Specific
pathogenic
bacteria
Host
immune
inflam-
matory
response
Connective
tissue &
bone
metabolism
Clinical
expression
of disease,
initiation
progression
Environmental &acquired risk factors
[SMOKING]
Genetic risk factors
Ag
LPS
Ab
PMNs
Cytokines,PGE2
MMPs

5. EPIDEMIOLOGICAL EVIDENCE
• Cross-sectional and case-control studies
demonstrate a moderate to strong association
between smoking and periodontitis[Hill’s criteria].
• 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. (MacFarlane et al, 1992)

6. RISK ASSESSMENT -
ATTACHMENT LOSS
Variable Estimated odds ratio
Age 1.72 - 9.01
Smoking 2.05 - 4.75
Diabetes 2.32
P gingivalis 1.59
Education 0.65
(Grossi et al, 1994)

7. healthy low moderate high severe
40
30
20
10
0
Pack
years
ATTACHMENT LOSS AND SMOKING
(Grossi et al, 1994)

8. 10 year prospective study of
smoking and
periodontitis
[Bergstrom et al 2000]
Smokers lost significantly
more periodontal
bone compared to non-
smokers (p<0.001)

9. AGE, SEX, AND CIGARETTE SMOKING
Carranza stated women from ages 20 to 39
and men from ages 30 to 59 who smoke
cigarettes have twice the chance of having
periodontal disease or becoming
edentulous as do non-smokers
The effects of smoking on
periodontal status
to be more pronounced in
younger women.
[Goultschin et al.10]

10. PREVALENCE OF MODERATE AND
SEVERE PERIODONTITIS
• Current smokers - 25.7%
• Former heavy smokers - 20.2%
• Cigar/pipe smokers - 17.6%
• Non-smokers - 13.1%
[ Albandar et al 2000]

11. Stopping smoking (for 10 years)
reduces risk of
periodontitis to that of non-smokers
0-2 years -> OR=3.2
>10 years -> OR=1.2
The more you smoke the worse the
periodontitis
(dose response)
Smoking <10 cigs/day OR = 2.8
Smoking >30 cigs/day OR = 6.9
[Tomar and Asma 2000]

12. Tobacco contains over 4,000chemicals, many of
which are harmful. These include:
Benzene
- solvent used in fuel manufacture
Formaldehyde
- highly poisonous, colourless liquid used to preserve dead
bodies
Ammonia
- chemical found in cleaning fluids. Used in cigarettes to
increase the delivery of nicotine
Hydrogen cyanide
-poisonous gas used in the manufacture of plastics, dyes,
and pesticides.
- Often used as a fumigant to kill rats
Cadmium
- extremely poisonous metal found in batteries
Acetone
- solvent found in nail polish remover

13. COMPONENTS OF INHALED SMOKE
•Nicotine
•Carbon monoxide
•Tar
all of which can cause disease
POTENT CARCINOGENS
• Nitrosamines
• Polycyclic aromatic hydrocarbons
• Radiation-emitting polonium

14. Nicotine action
• Accelerates release of
neurotransmitter
dopamine in the
brain’s NA*
& increases
metabolism in NA
*NA = nucleus accumbens

15. •Nicotine retards growth of gingival
fibroblasts reduces fibronectin &
collagen increases collagen breakdown
Other actions are:
•raise blood pressure
•stimulants
•vasoconstriction
•psychological - social dependency
•physical dependancy - craving

16. CARBON MONOXIDE-ACTIONS
•Carbon monoxide is a poisonous gas found in
car fumes, which reduces the amount of
oxygen carried in the blood.
•Oxygen is vital for the body’s organs to
function efficiently.
• The reduction in oxygen changes the
consistency of the blood, making it thicker
and putting the heart under increased strain
as it pumps blood around the body

17. TAR-actions
•Tar contains many substances proven to
cause cancer.
•Irritants found in tar damage the lungs
causing narrowing of the tubes(bronchioles)
and damaging the small hairs (cilia) that
protect the lungs from dirt and infection

19. Effect of Smoking on
Plaque

20. PERIODONTAL PATHOGENS
The proportions of subjects positive for
A. actinomycetemcommitans,
P. gingivalis, and T. forsythesis were higher
among smokers.
{Zambon et al.(1996),using a fluorescence
technique in a Cross sectional study from
Erie County Study population}
Furthermore, increased counts of
exogenous flora (Escheria coli and Candida
albicans) have been reported in smokers

21. SMOKING AND HOST RESPONSE
• Smoking decreases salivary IgA and
serum IgG,and specifically reduces
IgG2 levels against A.a.commitans
(Bennet & Read, 82; Barbour et al.,97).
• The ability of tobacco products to
decrease the proliferating capacity
of T and B lymphocytes might
contribute to this diminished
production of protective
antibodies.

22. • Smoking can exert deleterious effects on
polymorphonuclear leukocytes (PMN) and other
neutrophil functions such as chemotaxis &
phagocytosis so that they cannot efficiently deal
with the bacterial infection
(Kenney et al., 1977; Eichel & Shahrik, 1969; Selby et al., 1992).
• Impaired phagocytosis function of neutrophils among smokers
with refractory periodontitis. (MacFarlane et al., 1992).

23. In addition, tobacco smoking may modify
the production of pro-inflammatory
cytokines IL-1 and TNF-ᾳ which are
considered key regulators of the host
response to microbial challenge.
( Kornman et al. ,1997)

24. Genetic Polymorphism and Smoking
Investigators have looked at genetic variability,
its relationship with periodontal disease, and its
interaction with smoking.
Tooth loss reported a positive genotype of IL-1
increases the risk for tooth loss by 2.7 times,
while smoking increases the risk by 2.9 times.
When both were combined, the risk increased to
7.7 times.[JCDP’08]

25. EFFECT OF SMOKING ON GINGIVA

26. Cigarette Smoking and Gingival
Bleeding
 Smokers expressed less gingival bleeding than
non-smokers
 This is also proved to be dose dependant
 This may be due to vasoconstrictive effect of
nicotine.Clarke et al 1984

27. Effect of Smoking on Gingival Blood
Flow
• In smokers,
gingival blood flow was significantly increased
by cigarette smoking.
• However, intravenous
administration of nicotine reduces the marginal
temperature of gingival sites suggesting a
decrease in gingival blood flow which lead to
the hypothesis this phenomenon is caused by
vasoconstriction induced by nicotine and stress.

28. Oxygen Tension in the Gingival Tissues
• Smoking Decreases Tissue Oxygen
• Tissue oxygen decreases: 65 ± 7 to 44 ± 3
mmHg [Jensen, et al. Arch Surg, 1991]
• Tissue oxygen 40-50 mmHg —> infection
Effects on the Gingival Vasculature
researchers found a high proportion
of small vessels compared with large vessels in
smokers than non-smokers but no difference in
the vasculature density.
[journal CDP nov08]

29. Evidence From Studies on (GCF)
 Smoking may result in lower resting GCF flow rate.
 The increase in GCF during an experimental gingivitis may be less
in smokers.
 Studies have shown higher levels of TNF-α and decreased levels of
IL-1α and IL-1β ,enzyme elastase in GCF when compared between
smokers and nonsmokers.
 This research has demonstrated there are lower levels of
cytokines, enzymes, and possibly polymorphonuclear leukocytes
(PMNs).
 This correlates with the lower levels of inflammation observed
clinically and within the tissues.
Kinane and Radvar 1997

30. Smoking and Fibroblast Function
Gingival Fibroblasts
In vitro studies have shown reduction in the
production of Type 1 collagen and fibronectin
and an increase in the collagenase activity.
Cellular changes like disruption
of cell orientation, changes in cytoskeleton,
presence of large vacuoles, and significant
reduction in cell viability have been noticed.

31. Smoking and gingival inflammation
Smokers may present with lower
levels of gingival inflammation than nonsmokers.
Furthermore,
development of gingival inflammation in
response to experimental plaque accumulation
(experimental gingivitis) was less pronounced
in smokers than in non-smokers.
[Albander et al 99, Lie et al 98]

32. Periodontal fibroblast
 PDL fibroblast growth, attachment and
integrin expression was inhibited by
nicotine at high concentrations (≥1 mg/ml)
 Nicotine at high concentrations (100 ng/ml
to 25μg/ml) to be cytotoxic by inhibiting
the vacuolation and proliferation of
fibroblasts. [Giannopovlou et al.27]
 PDL cell proliferation and protein synthesis
were also inhibited in a dose dependent
manner.
 Cell attachment was significantly less on
root surfaces obtained from heavy smokers
compared with nonsmokers.

33. Smoking and periodontitis in young adults
(≤35 years)
Several studies have shown young adult smokers
aged 19-30 years had a higher prevalence and
severity of periodontitis compared to non-smokers
despite similar or lower plaque levels.
The prevalence of periodontitis,
defined as having a site with attachment loss
of ≥2 mm and probing depths of ≥4 mm, was
three to four times higher in young smokers
compared to non-smokers.
[Haber et al]

34. Smoking and Periodontitis in Adults
Current smokers have deeper probing
depths, greater attachment loss, more bone
loss, and fewer teeth.
Smokers also exhibit
more supragingival calculus deposits.
Smokers were four times more likely to have
periodontitis as compared to non-smokers.

35. Among 20-49 year-olds, the adjusted
odds ratio for a mean attachment loss
of 1 to 1.99 mm among current smokers
was 2.29, whereas the odds ratio for
attachment loss ≥3 mm was over 18.43.
This suggests smoking is particularly
important in the etiology of severe
periodontal attachment loss.
{NHANES}

36. There is a strong dose-response relationship
between the amount smoked and the severity of
periodontal destruction which further supports the
role of smoking as a risk factor for periodontitis.
The most marked difference between smokers
and non-smokers in probing depths or attachment
loss occurs in the maxillary lingual area and
mandibular anterior area, suggesting a local
effect of smoking.

37. Effects of Smokeless Tobacco on
Periodontal Tissues
 It involves chewing a quid that includes betel
leaf,lime, areca nut, and tobacco.
 Tobacco use may significantly increase bleeding
on probing and periodontal attachment loss.
 Other studies have also shown the negative
effect of the areca nut on host immunity by
affecting PMNs.
 Arecanut extracts have also been shown to
inhibit the growth, attachment, and matrix
protein synthesis of cultured human gingival
fibroblasts.

38. Smoking and Acute Necrotizing Ulcerative
Gingivitis (ANUG)
An association between necrotizing forms
of periodontal disease and tobacco smoking
was reported as early as 1947
Preexisting gingivitis, emotional/psychic stress,
and smoking forms a triad of interrelated
predisposing factors in the etiology of the disease.
.

39. 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}

40. SMOKING AND SYSTEMIC HEALTH

41. Smoking and cardiovascular system
•Smoking causes coronary heart disease,
atherosclerosis, arteriosclerosis, heart attack the
leading cause of death
•Cigarette smoking causes reduced circulation by
narrowing the blood vessels (arteries) and puts
smokers at risk of developing peripheral vascular
disease
•Smoking causes abdominal aortic aneurysm
(i.e., a swelling or weakening of the main artery
of the body—the aorta—where it runs through
the abdomen).

42. Smoking and Respiratory Disease
Smoking causes lung cancer.
Smoking causes lung diseases (e.g.,
emphysema, bronchitis, chronic airway
obstruction) by damaging the airways and
alveoli (i.e., small air sacs) of the lungs.
Smoking and brain
Can cause stroke which may be fatal or
cause mental and physical disability

43. Smoking and Cancer
Smoking causes the following cancers:1
*Acute myeloid leukemia
*Bladder cancer
*Cancer of the cervix
*Cancer of the esophagus
*Kidney cancer
*Cancer of the larynx (voice box)
*Lung cancer
*Cancer of the oral cavity (mouth)
*Pancreatic cancer
*Cancer of the pharynx (throat)
*Stomach cancer

44. Smoking and Other Health Effects
Smoking has many adverse reproductive and
early childhood effects, including increased
risk for—
infertility,
preterm delivery,
stillbirth,
low birth weight, and
sudden infant death syndrome (SIDS).
Smoking is associated with the following
adverse health effects:
Postmenopausal women who smoke have lower bone
density than women who never smoked.

45. SMOKING – MORBIDITY
(miller et al 1999)
50% of total cancer deaths
84% of lung cancer deaths
30% of heart disease deaths
23% of respiratory deaths
80% of bronchitis and
emphysema deaths

46. Interaction between smoking and systemic
Health status and periodontitis
The combination of smoking with other systemic
factors further enhances the risk of periodontal
destruction.
.

47. •Studies say that the combination of diabetes and
heavy smoking in an individual over the age of 45
years who harbored P. gingivalis or T. forsythesis
resulted in an odds ratio of attachment loss 30
times that of a person lacking these risk
factors.(JCDP nov,2008)
•Smoking also increases the risk of attachment
and/or bone loss in AIDS and HIV serotype
patients.
•Periodontitis also may worsen the systemic
status of an individual

48. SMOKING AND ORAL HEALTH

49. Tobacco use in all forms, especially cigarette smoking, is
the number one risk factor for oral cancer.
Possible mechanisms are
•Irritants and toxic substances in tobacco
•Change in Ph
•Change in immune response
•Dryness due to heat produced while smoking
The most common form of cancer is Squamous
cell carcinoma.
•The most common sites of the oral cancer is the tongue and the
floor of the mouth.
• The other common sites are buccal vestibule, buccal mucosa,
gingiva and rarely hard and soft palate.
• Cancer of bucco-pharyngeal mucosa is common in smokers.

50. Abnormal Changes at Cancerization site
• Clinically:
– Leukoplakia
– Erythroplasia
– Dysplasia
– Carcinoma in situ

51. OTHER LESIONS:
SMOKER’S PALATE
• Palate becomes white with tiny red spots-raised
duct opening of salivary glands [dried mud
appearance]
SMOKER’S MELANOSIS
• Brown spots on oral mucosa
HAIRY TONGUE
• Overgrowth of papilla on the surface of tongue
COATED TONGUE
• Tongue coated with food particles, bacteria and
debris from epithelium

52. DENTAL CARIES AND EROSION
• Smoking stimulates saliva flow immediately, does not
affect saliva in long term
• Decrease Ph and buffering action
Dental caries Erosion
GINGIVAL RECESSION

53. • STAINING OF TEETH
• HALITOSIS
• DELAYED WOUND HEALING
• DRY SOCKET
• SMOKER’S FACE

54. Effects Of Smoking On
Periodontal Therapy

55. CIGARETTE SMOKING AND ORAL HYGIENE
Several studies demonstrated higher levels of
oral debris in smokers than in non-smokers.
Increased levels of debris observed in smokers
have been tentatively attributed to personality
traits leading to decreased oral hygiene habits,
increased rates of plaque formation, or a
combination of the above.
[JCDP’08]

56. Toothbrushing efficiency of smokers was
much less and
the calcium concentration in the dental
plaque of smokers was found to be
significantly higher than in nonsmokers.
[Medicine and Biology Vol.14, No 2, 2007, pp. 53 – 59]

57. EFFECT OF SMOKING IN WOUND
HEALING
Smoking has
been shown to impair revascularization
during soft and hard tissue wound
healing,
which is critical for periodontal plastic,
regenerative, and implant procedures.
(Nolan et al.,85; Preber &
Bergström, 85a; 86; 90).

58. Non-surgical and Surgical Therapy
Numerous studies have shown smoking
compromises probing depth and/or attachment
gain outcomes following non-surgical or surgical
therapy.
The numerical differences between
smokers and non-smokers become more
pronounced in probing depths ≥5 mm, where
smokers demonstrated 0.4 mm to 0.6 mm
less improvement in clinical attachment levels
following scaling and root planning.
Following flap debridement surgery, smokers experienced
upto 1 mm less improvement in clinical attachment
levels in probing depths that were initially ≥7mm.

59. Antimicrobial Therapy in Smokers
• Because of the diminished treatment response
insmokers, clinicians may recommend adjunctive
antimicrobial therapy for smokers.
• Because subgingival pathogens are more difficult to
eliminate in smokers following SRP.
• Systemic amoxicillin and metronidazole or locally
delivered minocycline microspheres enhanced the
results of mechanical therapy.
• A recent study reported a positive response to sub-
antimicrobial doxycycline (anticollagenase) therapy in
combination with SRP in a group of severe periodontitis
patients that included smokers.

60. Soft and Hard Tissue Grafting
• In guided tissue regeneration procedures
smokers had significantly less root
coverage(57%) compared to nonsmokers
(78%)
• Smoking is detrimental to regenerative
therapy in interproximal and furcation
defects, whether treatment includes the use
of osseous graft, bioabsorbable membrane,
or a combination.
• The results have shown less than 50% as
much improvement in clinical attachment
levels in smokers, which amounted to
differences ranging from 0.35 mm to 2.9 mm.

61. Implant Therapy
• In the studies reviewed, 0% to 17% of
implants placed in smokers were
reported as failures as compared to 2%
to 7% in non-smokers.
• The 3-year data demonstrated 8.9% of
implants placed in smokers failed as
compared to 6% in individuals who had
never smoked or had quit smoking.
• The majority of implant failures in
smoking occurred prior to prosthesis
delivery.

62. Maintenance phase
• ↑pocket depth
• ↓gain in clinical attachment level
• Deeper and more residual pockets after flap
surgery
Refractory disease
• ↑recurrence and ↑need for
re treatment and antibiotic therapy
• ↑tooth loss after surgical therapy

63. TOBACCO CESSATION

64. 64

65. The “5 A’s” To Intervention
• ASK about tobacco use.
• ADVISE to quit.
• ASSESS willingness to make a
quit attempt.
• ASSIST in quit attempt.
• ARRANGE for followup.

66. Nicotine withdrawal: the 4 ‘D’s
Delay acting on the urge to smoke
Drink water slowly
Deep breathe.
Do something else (eg exercise)

67. PHARMACOTHERAPY
Pharmacotherapy + behavioural counselling improves long-term quit rates
Smokers of 10 or more cigarettes a day
who are ready to stop should be encouraged to use pharmacologial support as a cessation aid
Nicotine replacement
• Begin NRT on the quit date, (apply patches the night before)
• Use a dose that controls the withdrawal symptoms
• NRT provides levels of nicotine well below smoking
• Prescribe in blocks of two weeks
• Arrange follow up to provide support
• Use a full dose for 6 to 8 weeks then stop

68. NRT: Nicotine nasal sp
• Nasal sprays more closely mimic nicotine from cigarettes
• Common side effects with nasal sprays include nasal and throat
irritation, coughing and oral burning
NRT: Nicotine gum
• Instruct the patient to ‘chew and park’
• Absorption may be impaired by coffee and some acidic drinks
• Common side effects with gum include gastrointestinal
disturbances and jaw pain
• Dentures may be a problem!
• Patches provide a slow, consistent release of nicotine
throughout the day
• Available in various shapes and sizes,
• Common side effects with patches include skin sensitivity and
irritation
NRT: Nicotine patches

69. • Begin bupropion a week before the quit date
• Normal dose 150mg bd, (reduce in elderly, liver/renal disease)
• 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%)
• Interaction with antidepressants, antipsychotics and anti-
arrhythmics
• Nicotine replacement and buproprion should always be used
in conjunction with behavior modification
Bupropion
Nicotine Tabs
• Nicotine tablets deliver 2-mg or 4-mg dosages of nicotine over
30-minutes
• Common side effects with gum include burning sensations in
the mouth, sore throat, coughing, dry lips, and mouth ulcers

70. Nortryptiline
• Tri-cyclic antidepressant
• Not licensed for smoking cessation
• Low cost
• Side-effects include sedation, dry mouth, light-headedness, cardiac
arrhythmia
• Contra-indicated after recent myocardial infarction
Varenicline
• Begin varenicline a week before the quit date, increasing dose
gradually.
• Alleviates withdrawal symptoms, reduces urge to smoke
• Common side effects include: nausea (30%), insomnia, (14%),
abnormal dreams (13%), headache (13%), constipation (9%), gas (6%)
and vomiting (5%).
• Contra-indicated in pregnancy

71. Pre-
contemplation
Contemplation
Determination
Action
Maintenance
Relapse
Cycle of
change
Smokers may move
backwards or
forwards, to and fro
across the cycle many
times before finally
quitting

72. Impact of Smoking Cessation on Periodontal
Status and Treatment Outcomes
•While smoking cessation does not reverse
the past effects of smoking, the rate of bone and
attachment loss slows after patients quit smoking
and the severity of their disease is intermediate
compared to current and non-smokers.
•It is encouraging to note former smokers respond
to non-surgical and surgical therapy in a manner
similar to nonsmokers.
•Similarly, implant success rates for past smokers
were similar to nonsmokers.(JCDP’08)

73. CONCLUSION
It is clear that smokers
• Present with periodontitis at an early age
• Difficult to treat them with conventional therapy
• Continue to have progressive or recurrence of periodontitis
leading to tooth loss
The opportunity for dentists to become more active in
evaluation of tobacco use by patients and more aggressive in
offering counseling and cessation services can positively
impact both the oral and general health of dental patients.

74. Referances
• Carranza’s clinical periodontology, tenth
edition
• Journal of contemporary dental
practice2008
• www.digital.library.edu.au
• www.slideworld.org
• www.tobaccoinduceddiseases.com

75. Thank you