2. • Smoking is harmful to every organ in the body, and it is associated
with multiple diseases include lung cancer, heart disease, stroke,
emphysema, bronchitis, and cancers of the oral cavity, bladder, kidney,
stomach, liver, and cervix.
• Smoking: It is the major risk factors for increasing prevalence and
severity of periodontal disease.
• Risk factors can be divided into 2 types:
1. Intrinsic factor.
2. Extrinsic factor.
3. Tobacco smoke contains over 4,000 of chemicals, many of which are harmful.
These include:
1. Benzene: solvent used in fuel manufacture.
2. Formaldehyde: highly poisonous, colorless liquid used to preserve dead
bodies.
3. Ammonia: the delivery of nicotine. chemical found in cleaning fluids. Used in
cigarettes to increasethe delivery of nicotine.
4. Hydrogen cyanide: poisonous gas used in the manufacture of plastics, dyes,
pesticides and often used as a fumigant to kill rats.
5. Cadmium: extremely poisonous metal found in batteries.
6. Acetone: solvent found in nail polish remover.
4. Potent carcinogens:
A. Nitrosamines.
B. Polycyclic aromatic hydrocarbon.
C. Radiation-emitting polonium.
Components of inhaled smoke:
1. Carbon monoxide: is a poisonous gas found in car
fumes, which reduces the amount of oxygen carried
in the blood.
2. Tar: is the sticky brown substance proven to cause
cancer and stains fingers and teeth to the yellow and
brown colours.
3. Nicotine: which is an alkaloid, is found within the
tobacco leaf and evaporates when the cigarette is
lighted. It is quickly absorbed in the lungs, and it
reaches the brain within 10 to 19 seconds. Nicotine is
highly addictive.
5. Nicotine action
Nicotine can be causes:
Retards growth of gingival fibroblasts.
Reduces fibronectin & collagen.
Increases breakdown collagen.
A rise in blood pressure.
Increased heart and respiratory rates.
Peripheral vasoconstriction.
6. • Cross-sectional and case control studies demonstrate a
moderate to strong association between smoking and PD.
• Smokers are four times as likely to develop periodontitis
as non-smokers.
• Smoking may be responsible for more than half of the PD
among adults.
• up to 90% of refractory periodontitis patients are smokers.
Epidemiological evidence
8. 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.
Effect of Smoking on the plaque
9. 1) Reduction of the gingival inflammations.
2) Reduction of bleeding on probing due to
vasoconstrictive (effect of nicotine).
The effect of smoking on gingivitis is:
10. A. Increase the prevalence and severity of periodontal destruction.
B. Increase pocket depth, attachment loss, bone loss.
C. Increase the prevalence of sever periodontitis and tooth loss with
increase the number of cigarettes smoked per day.
D. Decrease prevalence and severity with smoking cessation.
The effect of smoking on periodontitis:
11. The microbiological effect of smoking an periodontal
disease are the followings:
Increase the levels of periodontal pathogens in the deep
periodontal pockets.
Increase the colonization of the shallow periodontal pockets by the
periodontal pathogens.
12. The immunological effect of smoking of the periodontal
disease are:
Impairment of chemotaxis and phagocytosis activities of
neutrophils.
Reduction in the production of the antibodies essential for killing
the bacteria, especially (IgG2).
Increase in the production of the TNF-α ,PGE2 and neutrophil
collagenase and elastase in the GCF.
13. ↓ Gingival blood vessels and bleeding on probing with ↑
inflammation (vasoconstriction).
↓ Gingival crevicular fluid flow with ↑ inflammation.
↓ Subgingival temperature.
↑ Time needed to recover from local anesthesia.
The physiological effect of the smoking on the periodontal
diseases are:
14. The effects of smoking on periodontal therapy are:
Non-surgical Therapy
↓ Clinical response to root surface debridement..
↓ Pocket depth reduction.
↓ Gain in clinical attachment levels.
↓ Negative impact of smoking with
↑ level of plaque control.
15. ↓ Pocket depth reduction and ↓ gain in clinical attachment levels
after access flap surgery.
↑ Deterioration of furcations after surgery.
↓ Gain in clinical attachment levels, ↓ bone fill,↑ recession, and ↑
membrane exposure after guided tissue regeneration.
↓ Root coverage after grafting procedures for localized gingival
recession.
↓ Pocket depth reduction after bone graft procedures.
↑ Risk for implant failure and periimplantitis.
Surgical Therapy
16. Maintenance phase :
↑ Pocket depth and attachment loss.
↑ Disease recurrence in smokers.
↑ Need for retreatment in smokers.
↑ Tooth loss in smokers after surgical therapy.
17. TOBACCO CESSATION
• The “5 A’s” To Intervention
1.ASK about tobacco use.
2.ADVISE to quit.
3.ASSESS willingness to make a quit attempt.
4.ASSIST in quit attempt.
5.ARRANGE for follow-up.
• Nicotine withdrawal: the 4 ‘D’s
1. Drink water slowly
2. Deep breathe
3. Do something else (eg exercise)
4. Delay acting on the urge to smoke
18. pharmacotherapy
• Nicotine replacement (2-mg or 4-mg over 30-min.)
1. NRT: Nicotine patches: Common side effects skin
sensitivity and irritation
2. NRT: Nicotine nasal spray: Common side effects
nasal and throat irritation, coughing and oral burning
3. NRT: Nicotine gum: Common side effects
gastrointestinal disturbances and jaw pain
4. Nicotine Tabs: Common side effects burning
sensations in the mouth, sore throat, coughing, dry lips,
and mouth ulcers
• Bupropion(150mg bd)
• The most common side effects are insomnia, dry mouth, headache
, nausea, constipation , and agitation.