This document discusses the effects of smoking on periodontal health. It covers epidemiological evidence that smoking increases the risk of periodontitis 2-5 times and is a major risk factor. The toxic chemicals in tobacco such as nicotine, carbon monoxide, and tar are discussed. These chemicals can impair the immune response and increase periodontal pathogens, leading to inflammation and tissue destruction. Clinical signs of periodontitis are made worse in smokers, such as increased attachment and bone loss. Smoking is also a major risk factor for oral cancer. The document examines the effects of smoking on gingival blood flow, wound healing, and the complications it can cause for periodontal therapy.

1. SMOKING AND
PERIODONTIUM
DR. ANTARLEENA SENGUPTA
I MDS, DEPTT OF PERIODONTOLOGY,
MCODS MANGALORE
2019.

2. CONTENTS
1. INTRODUCTION
2. EPIDEMIOLOGICAL EVIDENCE
3. TOXIC PRODUCTS INTOBACCO
4. EFFECT OF SMOKING ON ORAL HEALTH
5. EFFECT OF SMOKING ON GINGIVA
6. SMOKINGAND PERIODONTITIS IN
ADULTS
7. SMOKINGAND SYSTEMIC HEALTH
8. EFFECT ON PERIODONTALTHERAPY
9. CESSATIONOF SMOKING
10. CONCLUSION
11. REFERENCES
2

3. INTRODUCTION
» TOBACCO USE: a dependence to nicotine and a chronic relapsing medical disorder (International Classification of
Diseases, 10th Revision [ICD-10 F17])
» Smoking increases the risk of periodontitis by 2‐ to 5‐folds
» Important modifying factor of periodontitis
» Direct causal relationship between smoking exposure and the prevalence and the severity of periodontal disease was
firmly established by American Academy of Periodontology, 1996.
» According to the new classification of periodontitis, the current level of tobacco use influences the grading of
periodontitis.
» Tobacco smoke contains over 3800 chemicals, including carbon monoxide, hydrogen cyanide, and reactive oxidizing
radicals, and 60 of these chemicals are known or suspected to be carcinogens
3

4. PATHOGENESISOFSMOKING-RELATEDPERIODONTITIS
5
SMOKING
MICROBIAL CHALLENGE
Host immune-inflammatory
response
Clinical signs of disease initiation
& progression
Connective tissue & bone
metabolism
Environmental & acquired risk factors+ genetic risk factors
Antigens
Virulence
factors
Antibody
PMNs
MMPs
Cytokines &
prostanoids

5. CLASSIFICATION
» SMOKINGTOBACCO
• BEEDI
• CONVENTIONALCIGARETTE
• REVERSE SMOKING
• E-CIGARETTE
» SMOKELESSTOBACCO
• GUTKA
• SNUFF
6

6. E-CIGARETTESANDPERIODONTALDISEASE
7
1. Participants who used electronic nicotine
products also had an increased odds of
reporting bone loss around teeth which
is indicative of advanced periodontal
disease.
2. E-cigarette vapor has been shown to
promote cell apoptosis, necrosis and
persistent DNA damage in gingival
epithelium.
3. Perceived as less harmful than
conventional cigarette smoking and
reported by some as a safer alternative
to cigarette smoking

7. REVERSESMOKING
» Reverse smoking is a peculiar form of smoking in which the smoker puts the lit end of
a chutta into his/her mouth during smoking and then inhales the smoke from the lit end.
» A chutta is a coarsely prepared cheroot varying in length from 5 to 9 cm which could be
either hand rolled or factory produced.
» Typically, the reverse smoker smokes up to two chuttas a day because in this form of
smoking a chutta lasts longer.
» The highest intraoral temperatures of the chutta can reach up to 760°C, and the intraoral air
can be heated to 120°C.
» Air is supplied to the zone of combustion through the non-heated extreme of the cigarette,
at the same time, the smoke is being expelled from the mouth and ashes are thrown out or
swallowed.The lips keep the chutta wet, which increases its time of consumption from 2 to
18 minutes.
» F>m
» Specific and peculiar custom in groups with low economical resources.
» Prevalent in Andhra Pradesh
8

8. EPIDEMIOLOGICALEVIDENCE
» 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)
» 10 year prospective study of smoking and periodontitis (p<0.001) :- Smokers lost significantly more periodontal bone
compared to nonsmokers [Bergstrom et al., 2000]
9
25.7
20.2
17.6
13.1
0
5
10
15
20
25
30
Prevalenceofperiodontitis
Current smokers
Former heavy smokers
Cigar/pipe smokers
Non-smokers
[Albandar et al., 2000]

9. ATTACHMENTLOSSANDSMOKING
5
10
20
30
40
TYPE OF SMOKER
NO.OFPACKYEARS
HEALTHY LOW MODERATE HIGH SEVERE
10(Grossi et al, 1994)

10. PACKYEARSANDCOTININELEVELS
11
(Ebersole et al., 2015)

11. TOXIC
PRODUCTS IN
TOBACCO
12

12. TOBACCO
BENZENE
FORMALDEHYDE
AMMONIA
HCN
CADMIUM
ACETONE
13
Tobacco contains over 3800 chemicals, many of which are harmful. These include:
Solvent used in fuel manufacture
Highly poisonous, colorless
liquid used to preserve dead
bodies
chemical found in cleaning fluids.
Used in cigarettes to increase the
delivery of nicotine
poisonous gas used in the manufacture of
plastics, dyes, and pesticides.
- Often used as a fumigant to kill rats
extremely poisonous metal
found in batteries
solvent found in nail polish remover

13. COMPONENTSOFINHALEDSMOKE
14

14. NICOTINE–MECHANISMOFACTION
15

15. 16
- Binds to receptors on
neurons in ventral
tegmental area.
- Impulse travels down axon
- Dopamine– at axon
terminals in nucleus
accumbens & prefrontal
cortex
- Binds to dopamine
receptors on other neurons
- Rewarding effects of
smoking– relaxation/
increased ability to focus.
- retards growth of gingival
fibroblasts
- reduces fibronectin &
collagen
- increases collagen breakdown
Other actions are:
•raise blood pressure
•stimulants
•vasoconstriction
•psychosocial dependency
•physical dependency - craving

16. CARBONMONOXIDE
» reduces the amount of oxygen carried in the blood.
» Changes consistency of blood (more viscous) increased
cardiac strain to pump
» Low energy
» Shortness of breath (respiratory insufficiency)
» Fatigue
» Precipitates atherosclerosis.
17

17. » A brown, sticky substance that consists of tiny particles and is formed when tobacco smoke condenses. It
is deposited in the lungs and coats the surface of the alveoli.
18
1. Inflammation of the mucous
membranes (the epithelium
and connective tissue
containing the mucous glands)
lining the trachea, bronchi and
bronchioles, causing them to
release more mucus.
2. Paralyzes the cilia on the
surface, thus the mucus, filled
with dust and microorganisms
accumulates in the lungs.
TAR--EFFECTSONTHEGASEXCHANGESYSTEM

18. 19
1. Build-up mucus on the walls of the airways
reduces it’s diameter, hence reduces the
rate where air can reach the alveoli
2. Leads to cough-- response from the body
to try to remove the build-up mucus
3. Coughing builds up scar tissues which
reduces air movement and rate of diffusion
4. As cilia no longer removes mucus and
pathogens, infections arise as bacteria can
replicate, increase their population and has
more time of entry into the epithelial cells
or the circulation
5. Allergens such as pollen also accumulate
leading to further inflammation of the
airways, reduced air-flow in and out of the
lungs and possible asthma attacks

19. COTININE
» Metabolite of nicotine-- reflects the extent of
the systemic distribution of nicotine in smokers
» Measured in preference to nicotine because
greater half-life (20 hrs)
20

20. EFFECT OF
SMOKING ON
ORAL HEALTH
21

21. » PERIODONTAL PATHOGENS:
• Higher proportions of A.
actinomycetemcomitans, P.gingivalis,T. forsythes
in smokers (Zambon, 1996)
• Increased counts of exogenous flora– E. coli, C.
albicans
• ORANGE and RED COMPLEX pathogens – more
prevalent in current smokers
» Affect salivary flow – easier for oral microbes to
stick to teeth and gingiva.
» Even smokeless tobacco products can irritate
gingiva, causing it to loosen around teeth, making
it easier for bacteria to settle in and
develop calculus.
22
EFFECTOFSMOKINGONPLAQUE

22. » Smoking may affect the host response by altering the immune response in local tissue.
» Smoke exposure impairs f-actin kinetics, resulting in the damage of the neutrophil cytoskeleton (Ryder et
al.1998).
» Decreased salivary IgA and serum IgG levels, specifically IgG2 levels against A.a.
» Increased production of PGE2 by monocytes in response to LPS.
» Deleterious effects on PMNs and other neutrophil functions such as chemotaxis & phagocytosis so that
they cannot efficiently deal with the bacterial infection (Selby et al., 1992).
» Impaired phagocytosis function of neutrophils among smokers with refractory periodontitis. (MacFarlane
et al., 1992).
» Tobacco smoking may modify the production of pro-inflammatory cytokines IL-1 andTNF-ᾳ which are
considered key regulators of the host response to microbial challenge.( Kornman et al. ,1997)
» 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 (JCPD ‘08)
23
SMOKINGANDHOSTRESPONSE

23. » 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
- Decreased subgingival temperature
» 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. 24

24. CLINICALCHANGESSEENATSITEOFINVOLVEMENT
» CARCINOMA:
- Leukoplakia
- Erythroplakia
- Dysplasia
- Carcinoma in situ
- OTHER LESIONS:
1. Smoker’s palate/ Nicotine stomatitis
2. Smoker’s melanosis
3. Hairy tongue
4. Coated tongue
25

25. CLINICALCHANGESSEENATSITEOFINVOLVEMENT
» DENTAL CARIES & EROSION
» Smoking stimulates saliva flow immediately—does not affect saliva long-term
» Decreased pH & buffering action
» STAININGOFTEETH
» HALITOSIS
» DELAYED WOUND HEALING
» DRY SOCKET
» SMOKER’S FACE
26
DENTAL CARIES
EROSION
GINGIVAL RECESSION

26. EFFECT OF
SMOKING ON
GINGIVA
27

27. EFFECTOFSMOKINGONGINGIVALBLOODFLOW
» 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)
» In smokers, gingival blood flow was significantly increased by cigarette smoking. However, I.V. 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.
» 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 GingivalVasculature:
Researchers found a high proportion of small vessels compared with large vessels in smokers than non-smokers but no
difference in the vasculature density.[JCDP Nov ‘08]
28

28. EVIDENCEFROMSTUDIESONGCF
» 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 ofTNF-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.
29
[Kinane & Radvar 1997]

29. » GINGIVAL FIBROBLASTS
• In vitro studies have shown reduction in the production ofType 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.
» 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]
» PERIODONTAL FIBROBLASTS
• PDL fibroblast growth, attachment and integrin expression was inhibited by nicotine at high concentrations (≥1 g/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]
• 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.
• 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.
30

30. SMOKING AND
PERIODONTITIS
IN ADULTS
31

31. CIGARETTESMOKINGANDPERIODONTITIS
» There’s a positive association between smoking and
measures of periodontal disease.
» The existence of potential confounding factors such as
socioeconomic status, education, and, ultimately, the
level of oral hygiene has been revealed in studies.
» Higher levels of oral debris in smokers than non-
smokers.
» Smokers have a significantly higher prevalence of
periodontal disease after correcting for potential
confounders; oral hygiene in particular.
» smokers have a tendency to display lower levels of oral
hygiene, oral hygiene and/ or socioeconomic factors
alone are unable to account totally for the observed
increase in prevalence and severity of periodontal
disease
32

32. SMOKELESSTOBACCOANDPERIODONTITIS
» 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.
» Studies have also shown the negative effect of
the areca nut on host immunity by affecting
PMNs.
» Areca nut extracts have also been shown to
inhibit the growth, attachment, and matrix
protein synthesis of cultured human gingival
fibroblasts.
33

33. CIGARETTESMOKINGANDPERIODONTITISINADULTS
» Current smokers have deeper probing depths, greater attachment loss, more bone loss, and fewer teeth.
» Smokers also exhibit more supragingival calculus deposits.
» Smokers were 4x more likely to have periodontitis as compared to non-smokers.
» 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 palatal area and mandibular anterior area, suggesting a local effect of smoking.
34

34. SMOKINGANDNECROTIZINGPERIODONTALDISEASES
» 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.
35

35. 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
NG
36

36. SMOKING AND
SYSTEMIC
HEALTH
37

37. SMOKING
HEALTH
RISKS
CATARACT
& VISION
LOSS
RHEUMATOID
ARTHRITIS
PERIODONTAL
DISEASE
CANCER
IMPOTENCE
ASTHMA
& COPD
ULCERS
CVD
REDUCED
LIFE
EXPECTANCY
CEREBRAL
STROKE
AGEING &
WRINKLES
38
- coronary heart disease
- Atherosclerosis
- Arteriosclerosis
- MI
- Peripheral vascular disease
- Abdominal aortic aneurysm
- Lung Ca.
- Emphysema
- Bronchitis
- Chronic airway obstruction
- Acute myeloid leukemia
- Bladder cancer
- Cervical ca.
- Esophageal ca.
- Renal ca.
- Laryngeal ca.
- Lung cancer
- Oral ca.
- Pancreatic cancer
- Pharyngeal ca.
- Stomach cancer
- Infertility
- Preterm delivery
- Stillbirth
- low birth weight
- sudden infant death
syndrome (SIDS).
In combination with
- Diabetes
- HIV/AIDS

38. EFFECT ON
PERIODONTAL
THERAPY
39

39. CIGARETTESMOKINGANDORALHYGIENE
» 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]
» 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
BiologyVol.14, No 2, 2007]
40

40. EFFECTOFSMOKINGONWOUNDHEALING
» 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).
41
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 planing.
- Following flap debridement surgery, smokers experienced upto 1 mm less improvement in clinical
attachment levels in probing depths that were initially ≥7mm.
[Rosa et al., 2014]

41. » Because of the diminished treatment response in smokers, clinicians may recommend adjunctive antimicrobial therapy
for smokers.
» 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 subantimicrobial doxycycline (anticollagenase) therapy in combination
with SRP in a group of severe periodontitis patients that included smokers.
42
ANTIMICROBIAL THERAPY IN SMOKERS
[Assem et al., 2017]

42. » 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, bio-absorbable 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.
43
SOFT AND HARD TSSUE GRAFTING
IMPLANT THERAPY
In the studies reviewed, 17% of implants placed in smokers were reported as failures as compared to 2% to 7% in non-
smokers.
• 3-year data demonstrates 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.
To increase implant survival in smokers, various protocols have been recommended:
1. Bain and Moy, 1993 suggested that
- the patient should cease smoking at least 1 week prior to surgery to allow reversal of the increased levels of platelet
adhesion and blood viscosity, as well as the short-term effects associated with nicotine.
- The patient should continue to avoid tobacco for at least 2 months after implant placement, by which time bone
healing would have progressed to the osteoblastic phase and early osseointegration would have been established.
2. Lambert et al. suggested that detrimental effects may be reduced by
- cessation of smoking
- using pre-operative antibiotics and
- hydroxyapatite-coated implants.
[Ionnau etal., 2015]

43. » Increased pocket depth
» Decreased gain in CAL
» Deeper and more residual pockets after flap surgery
44
MAINTENANCE PHASE
REFRACTORY DISEASE
- ↑recurrence and ↑need for re treatment and antibiotic therapy
- ↑tooth loss after surgical therapy

44. CESSATION OF
SMOKING
45

45. 46
Patient presents to a
dental practice
Does patient now use
tobacco?
Is patient now willing
to quit?
Did patient once use?
Provide
appropriate
treatment
Promote
motivation
to quit
Prevent
relapse
Encourage
continued
abstinence
YES
YES YES
NO
NO NO

46. THE5A’STOINTERVENTION
» ASK about tobacco use
» ADVISE to quit
» ASSESS willingness to make a quit attempt
» ASSIST in quit attempt
» ARRANGE for follow-up
47
- ASK
- ADVISE
- REFER

47. NICOTINEWITHDRAWAL:4D’S
» DRINK water slowly
» DEEP breath
» DO something else (e.g., exercise)
» DELAY acting on the urge to smoke
48

48. PHARMACOTHERAPY
» Pharmacotherapy + behavioral counselling improves long-term quit rates
» Smokers of 10 or more cigarettes a day who are ready to stop should be encouraged to
use pharmacological 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
49

49. » NRT: Nicotine nasal spray
» 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 patches
» 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 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 50

50. » Nicotine Tabs
» Nicotine tablets deliver 2-mg or 4-mg dosages of nicotine over 30-minutes
» Common side effects include burning sensations in the mouth, sore throat, coughing, dry lips, and mouth ulcers
» Bupropion
» Begin bupropion a week before the quit date
» Normal dose 150mg b.d., (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 antiarrhythmics
» Nicotine replacement and bupropion should always be used in conjunction with behavior modification
51

51. » Nortryptiline
» Tri-cyclic antidepressants
» 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
52

52. Smokersmaymovebackwardsor
forwards,toandfroacrossthecycle
manytimesbeforefinally
quitting
53
CYCLE
OF
CHANGE
RELAPSE
PRE-
CONTEMPLATION
CONTEMPLATION
DETERMINATION
ACTION
MAINTENANCE

53. IMPACTOFSMOKINGCESSATIONONPERIODONTALSTATUSAND
TREATMENTOUTCOMES
» 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) 54

54. CONCLUSION
55
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 periodontists 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 periodontitis patients.

55. 56
REFERENCES
1. CARRANZA’s Clinical Periodontology, 10th edition
2. Journal of contemporary dental Practice, 2008
3. Tobacco Use and Its Effects on the Periodontium and PeriodontalTherapy [Laxman,
November 1, 2008]
4. Smoking and Periodontal Disease, Hidalgo, Periodontology 2000
5. www.digital.library.edu.au
6. www.tobaccoinduceddiseases.com

56. Thank You