Smoking and periodontal diseases

Smoking and
periodontal
disease

CONTENTS
 Introduction
 Constituents of tobacco smoke
 Mechanism of toxicity
 Tobacco as a risk factor
 Effect of smoking on :
 Plaque and oral flora
 Periodontal tissues
 Immunology
 Smoking and systemic status
 Effect of smoking on periodontal therapy
 Tobacco cessation
 Conclusion
 References

INTRODUCTION
 Tobacco smoking - detrimental habit
 In India Population
Males
Females
- 1.1 billion
53%47%
0.00%
10.00%
20.00%
30.00%
40.00%
Males
Females
Prevalence rate of smokers
NHFS
98-99
NHFS
05-06
25%
29%
3.2% 2.8%

Introduction
Deaths due to cancer
Other
causes
Due to
smoking
Deaths due to habit
50 %
30 %
0%
20%
40%
Death rate
32%
6%
M F

Introduction
 Different methods of tobacco smoking
Pipes

Introduction
Heavy smokers
> 20 / day
Former smokers
Quit within the last
10 years
Light smokers
< 20 / day

 Risk factor for systemic diseases
 Susceptibility to coronary artery
disease: 2-4 times
Introduction

Introduction
Smoking and periodontal disease
 Long-term chronic exposure
  in prevalence and progression
 Passive smoking – 30% of disease susceptibility

Introduction
Tobacco
smoking
Plaque and
oral flora
Periodontal
tissues
Homeostasis
and healing
potential
Systemic
health
Immune
response

CONSTITUENTS OF TOBACCO
SMOKE
 Complex mixture of substances – over 4000 known
constituents
 Phenols and cyanides – antibacterial and toxic
properties

Constituents
 Gaseous phase and particulate phase
 Tar and nicotine yields reduced due to use of filters
 Dose of tobacco intake – depends on the way an
individual smokes

Constituents
 Biochemical analyses of cotinine (Wall et al 1988)
 Measurements are more reliable – longer half life of
14-20 hours (Jarvis et al 1988)
 Cotinine concentrations of regular smokers
 Resting plasma nicotine levels : 5–50 ng/ml
Plasma and salivary
levels
~ 300 ng/ml
(14 ng/ml – 1000 ng/ml)
Urine concentrations ~ 1500 ng/ml

Constituents
Absorption of nicotine
 Rapidly absorbed into blood - 30% in free form
 Lipid-soluble
 Inhalation of tobacco smoke

Constituents
Action on organs
  blood pressure
  heart rate
  respiratory rate
  skin temperature
 Vasodilatation at other body sites

Constituents
Oral mucosa
 Slowly
 From cigarette smoke  pH 5.5  not well absorbed
 From cigar and pipe smoke  pH 8.5  good
absorption
(Benowitz 1988)

MECHANISMS OF TOXICITY
Vascular alteration
 antibody production
(IgG2P7)
Immunosuppressive
effect
Physical subgingival
environment
Nicotine on root surfaces
 bacterial adhesion to
epithelial cells

Mechanisms of toxicity
Impaired immune
response
Anaerobic
subgingival
infection
Connective tissue
cytotoxicity
Impaired wound
healing
 in severity of
periodontal
disease

TOBACCO AS A RISK FACTOR
 Based on Hill’s criteria (1965) for causation, reviewed
by Gelskey (1999)
Biologic
plausibility
Strength of
association
Consistency Specificity
Temporality
Biologic
gradient
Analogy

EFFECT OF SMOKING ON
PLAQUE
 Plaque development
 Oral flora
 Subgingival microflora
 Calculus formation
 Conclusion

PLAQUE
Effect of smoking on plaque development
 Higher prevalence of dental plaque in smokers
(Kristoffersen 1970, Preber et al 1980)
 In contrast, smoking did not appear to increase the
amount of plaque (Alexander 1970, Sheiham 1971)
 Experimental gingivitis models – rate of plaque
formation was similar (Bastiaan & Waite 1978, Bergstrom
1981)

Effect of smoking on plaque
Effect of smoking on the oral flora
 No significant trend for smokers to harbor
putative pathogens (Mager et al 2003, Lie et al 1998b)
 Increased counts of exogenous flora – E. coli and
C. albicans – have been reported in smokers

Effect of smoking on the subgingival microflora
 Cross-sectional investigations
 No influence of smoking on the occurrence of any
species
 Zambon et al 1996 - higher prevalence of
A. actinomycetemcomitans, T. forsythensis and
P. gingivalis
Risk of infection with T. forsythensis – 2.3 times
 Mager 2003 – A. actinomycetemcomitans

 Prevalence of B. forsythus and P. nigrescens
maxilla > mandible (Haffajee 2001)
 Cigarette smoking  lowers redox potential 
increase in anaerobic bacteria
 Eggert 2001 – effects of CO
Enhancing growth
of anaerobes
Formation of
advanced glycation
end products by
smoke

Effect of smoking on calculus formation
 More supragingival calculus deposits (Bergstrom 1999)
 Significantly more with pipe smokers than cigarette
 Reason:
 salivary flow rates
 calcium concentration, organic components

Conclusions
 Numerous species in oral cavity
 Varied sampling methods
 Common known species often investigated
 Trend:
Greater numbers of pathogens not correlating with
plaque levels

PERIODONTAL TISSUES
 Gingiva
 Gingival blood flow
 Gingival vasculature
 Gingival inflammation and bleeding
 Oxygen tension in gingival tissue
 Gingival and PDL fibroblasts
 Periodontitis
 Wound healing
 Conclusion

PERIODONTAL TISSUES
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)

Effect of smoking on periodontal
tissues
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)

tissues
Effect of smoking on gingival blood flow
Infusion of nicotine
•  gingival blood flow
• Recovery below baseline
levels
Transient decrease
(Clarke et al 1981)
Laser Doppler Flow study
• Gingival blood flow 
~25%
• Maintained for 5 min
• Gradually declined to
baseline values
Transient increase
(Baab & Oberg 1987)

tissues
 Reason:
Nicotine  Vasoconstrictive property
In some cases, smoking-induced elevation in blood
pressure overcomes vasoconstrictive effect of smoking.
Smoking decreases gingival blood flow

tissues
 Bergstrom et al 1983
Nicotine
Sympathetic ganglia  catecholamines
α - receptors  vasoconstriction
Peripheral blood vessels – periodontium
 gingival bleeding
Vasoconstriction
Keratinization

tissues
 Morozumi et al 2004 - following quitting
At 3 days – significant increase
At 4-8 weeks - small increases occurred

tissues
Effect on the gingival vasculature
  number of vessels
  endothelial ICAM-1 expression
(Rezavandi et al 2002)
not accompanied by an
equivalent increase in vascularity
Inflammation -

tissues
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

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

tissues
Oxygen tension in the gingival tissues
 Carbon monoxide – reduces O2 tension (Scott et al 2001)
 Oxygen saturation of haemoglobin – lower in healthy
gingiva, higher with inflammation (Hanioka et al 2000b)
 Pocket oxygen tension
Smokers Non-smokers
~ 21.9 mm Hg ~ 33.4 mm Hg

tissues
Effect on fibroblasts
 Nicotine affects
 Production of collagenous, non-collagenous proteins
(Giannopoulou 2001)
 Cell orientation and attachment (Raulin et al 1988)
Effect on human gingival fibroblasts
 Nicotine HGF
(Wendell 2001)
IL-6
IL-8
P. gingivalis

tissues
 25–100 ng/ml of nicotine
 Orientation of cells lost (Tanur et al 2000)
 10–75 g/ml of nicotine
 Inhibition of proliferation of gingival fibroblasts
  production of type 1 collagen and fibronectin
  collagenase activity in the culture media
 Cytoplasmic vacuolation
 Attachment disrupted (Tipton and Dabbous 1995)

tissues
 Effect of acrolein and acetaldehyde
 Inhibited cell attachment and cell proliferation
(Cattaneo et al 2000, Poggi et al 2002)
 EM changes:
o Disruption of cell orientation
o Presence of large vacuoles and residual bodies
o Reduction in cell viability
o Disruption of the cytoskeletal structures

tissues
 Root surface of tooth
 Alters fibroblast attachment
 Integrin expression
 Decrease collagen production
 Increase collagenase production
 Nicotine levels could be reduced following root planing
(Cuff et al 1989)

tissues
Effect on PDL fibroblasts
 Dose-dependent inhibition
 < 10 g/ml – no significant effect
 100 ng/ml-2 g/ml – inhibition of proliferation
 > 1mg/ml – vacuolation
(Giannopoulou et al 1999)
 High concentrations (5–25mM) - cytotoxicity (Chang
et al 2002)

tissues
Periodontitis
 Relative risk for smokers : 3.97
former smokers : 1.68
 Odds ratio – 1.5-7.3
 Cigar and pipe smokers - severity of disease
intermediate between current cigarette smokers and
nonsmokers

tissues
 Deeper probing depths and a larger number of deep
pockets (Feldman et al 1983, Bergstrom et al 2000a)
 Twin study - greater degree of alveolar bone loss and
tooth loss in smokers (Bergstrom in 1983)
 More attachment loss including more gingival
recession (Grossi et al 1994, Haffajee & Socransky 2001a)
 More teeth with furcation involvement (Mullally &
Linden 1996)

tissues
Wound healing
 Initial short-term healing after therapy (up to 6 weeks)
 Reduced cell function
 Reduced host defense response
 Reduced vascularity
 Medium to longer term healing (3 months - 1 year)
 Cellular and tissue differences

tissues
 Poorly functioning fibroblasts  gingival tissue
adaptation impaired
Poor healing
Persistence of
infection
Predisposition to
disease

tissues
Conclusions
 Long-term chronic effect
 Impairing the vasculature and revascularization
 Following abstinence, the vasculature does return to a
near- normal state

IMMUNOLOGY AND HOST
RESPONSE
 PMN function
 Lymphocyte function
 GCF
 Cytokines
 Other factors
 Conclusion

IMMUNOLOGY AND HOST
RESPONSE
Effect on PMN function
 Systemic neutrophilia
 No effect on oral and sulcular neutrophils
 Reduction in numbers (Eichel & Shahrik 1969, Pauletto et al
2000)

Effect of smoking on immunology
and host response
Express several receptors
Metabolites of Endogenous
smoke factors
34 subtype of nicotinic
receptors (Benhammou et al
2000)
IL-8, ICAM-1,
TNF-

and host response
PMN
function
Degradative
protease
formation
Neutrophil
respiratory
burst
PMN
migration
and
chemotaxis
Neutrophil
priming

and host response
Degradative protease formation from PMN
  elastase activity and MMP-8 activity – refractory
periodontitis (Soder B 1999)
 Lower elastase concentrations in GCF
PMNs are less functional (Wolff et al 1994) or are present
in reduced quantities

and host response
Neutrophil respiratory burst
 “Respiratory burst” – O2-dependent phagocytosis
 Cigarette smoke constituents may inhibit the
respiratory burst (Drost et al 1992, Sorensen et al 2004)
 Nicotine   IL-8   ROS, particularly ONOO-
(Iho et al 2003)
 Metallothionein – protective role
Responses – enhanced or suppressed ?

and host response
Neutrophil migration and chemotaxis
 Tobacco smoke exposure may impair f-actin kinetics
Hampers neutrophil motility and migration
(Ryder et al 2002)
 Neutrophil migration
  expression of adhesion integrins
  expression of selectins

and host response
 Neutrophil chemotaxis and phagocytosis (Seow et al
1994)
 Dose-dependent suppression
o Low concentrations – stimulatory to fMLP
o High concentrations - inhibitory
Neutrophils respond to multiple chemotactic stimuli
Results depend upon the experimental system used

and host response
Neutrophil priming (hyper-reactivity)
Koethe et al 2000, Matheson et al 2003
Cigarette smoke condensate (CSC)
2-fold increase in fMLP-receptor
expression
Subsequent stimulation with fMLP
Cells ‘‘primed’’
2-fold increase in superoxide and elastase
release
Hyperinflammatory response

and host response
 Neutrophil priming capabilities for TNF-alpha
(Gustafsson 2000, Bostrom et al 1998b)

and host response
Conclusions
 Neutrophils - critical role

and host response
Smoking And Lymphocyte Function
Immune system  recognize antigens  response
Lymphocytes
T lymphocytes NK cellsB lymphocytes

and host response
T lymphocytes
 Leucocytosis (Corre et al 1971, Hughes et al 1985)
 Loos et al 2004
 Non-smokers, light smokers or heavy smokers
 Total leucocyte count - highest in heavy smokers
 Increased neutrophil numbers

and host response
 Animal studies - chronic exposure of rats
 Vapour phase – no significant changes
 Particulate phase - confers immunosuppressive
properties
Nicotine, Benzo(a)pyrene,
Benzo(a)anthracene
Immunosuppressive
(Geng et al 1995, 1996)
Tobacco glycoprotein, Metals
Immunostimulatory
(Francus 1988, Brooks 1990)
Net effect - dependent upon dose and duration

and host response
 T cell function – controversial
 Reduction in proliferative response of lymphocytes
to mitogens (Chang et al 1990, Johnson et al 1990)
 No significant differences between control subjects,
periodontitis patients and smoking status (Loos et al
2004)

and host response
B cells and Immunoglobulins
 B cells + Cytokines  Plasma cells
(Th-derived)
 Chronic exposure to nicotine
Impairment of antigen-mediated T cell signalling
Inhibits antibody-forming cell responses
Immunosuppression
(Sopori et al 1998)

and host response
 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

and host response
 B cell function
 Decrease in proliferative response to B cell mitogens
and antigens (Sopori et al 1989)
 Smoking cessation, function returns to normal
(Reynolds et al 1991)
 Combustion by-products -  B cell function
 Tobacco glycoprotein - potent B cell mitogen
Net effect – depends on properties of tobacco

and host response
Natural killer (NK) cells
 Antibody-dependent cellular cytotoxicity
 Analogous to cytotoxic T cells
 Produce chemokines and cytokines
 Reduced activity in smokers (Tollerud et al 1989)
 Reversible on smoking cessation (Meliska et al 1995)

and host response
Conclusions
 Inconsistencies and variations in findings
 Inadequate knowledge of antigens and responses

and host response
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

and host response
 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)

and host response
Cytokines
 Cytokine overproduction  detrimental host response
 disease
 Higher levels of TNF- (Bostrom et al 1998)
 Dose-dependent effect of smoking on IL-1, IL-8, and
MCP-1 levels (Kuschner et al 1996)

and host response
 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)

and host response
The balance between protection and destruction is mediated
largely by the type of cytokine pattern secreted by these cells.

and host response
Other Factors
 2-macroglobulin and 1-anti-trypsin levels
 Lower concentrations in heavy smokers (Persson 2001)
 ICAM-1 levels (Fraser et al 2001)
Smokers Non-smokers
Serum 331 ng/ml 238 ng/ml
GCF 83 ng/ml 212 ng/ml

and host response
Conclusions
 Logic – factors associated with tissue destruction
should be higher
 However, lower levels with most cytokines
Clinically, low levels of inflammation observed
May indicate higher levels of activity
GCF could be an end product of the destructive process

SMOKING AND SYSTEMIC
STATUS
 Smoking + systemic factors =  risk of disease
 Erie County study
 In diabetics, more periodontal attachment loss
 Odds ratio for attachment loss - 30 times more
o Diabetes and heavy smoking
o > 45 years of age
o P. gingivalis or T. forsythensis
 Postmenopausal women
 AIDS / HIV +ve

Smoking and systemic status
Gene polymorphisms
IL-1 genotype & smokers
(McGuire & Nunn, 1999)
  bleeding on probing (Lang 2000)
  probing depth and attachment loss
Risk factor Risk of tooth loss
IL-1 positive genotype 2.7
Smoking 2.9
IL-1 positive + smoking 7.7

N-acetyltransferase 2 (NAT2)
 Tobacco smoke Arylamines
 Detoxification
 Immunosuppressant
 Polymorphism  rapid or slow acetylators
 Severe periodontal conditions – slow acetylators
 NAT2 genotype-positive   bone loss (Kocher 2002)
NAT2

Cytochrome P450 and glutathione S-transferase
enzymes
 Neutralization of toxic substances
 Polymorphism  risk of periodontitis

PERIODONTAL THERAPY
 Non-surgical therapy
 Antimicrobial therapy
 Surgical therapy
 Tissue grafts
 Implant therapy
 Maintenance therapy
 Recurrent/refractory disease

PERIODONTAL THERAPY
Non-surgical therapy
 Non-surgical therapy is less effective in smokers and
non-smokers
 Less reduction in probing depth
Smaller levels of gain in clinical attachment

therapy
 Grossi et al 1996 – 3-month study
 Pocket depth reduction - 1.29 vs 1.76 mm
 Good plaque control – differences are less significant
Smokers respond less well to nonsurgical therapy

therapy
Antimicrobial therapy
 Antimicrobial therapy as an adjunct
 Widely used host modulators - tetracycline antibiotics
 Anti-inflammatory
 Anti-collagenase activity
 Anti-oxidant
 Enhanced results with:
 Locally delivered minocycline microspheres

therapy
 Little effect of systemic metronidazole (Soder et al)
 Systemic amoxicillin and metronidazole – better results

therapy
Surgical therapy
 Smokers treated with surgical periodontal therapy
 Less probing depth reduction
 Smaller gains in CAL
 Less gain in bone height
 Kaldahl 1996 – 7-year follow up
 Deterioration of furcation areas
 Level of recession - worse in smokers (Martinez-Canut et
al 1995, Gunsolley et al 1998)

therapy
Tissue grafts
 Heavy cigarette smoking decreases the amount of root
coverage
 Harris’ study (n=100)
 CT with partial thickness pedicle graft
 Light smokers - 97%
Heavy smokers - 99%
Non-smokers - 98%
 CT graft - more resistant to effects of smoking

therapy
 Smoking - negative impact on outcomes of GTR,
DFDBA
 GTR with ePTFE membrane
 Smokers - 57%
 Non-smokers - 78%
 Trombelli et al 1997

therapy
Implant therapy
 Bain 1993 – 6-year follow-up study
Success rate - > 95% (non-smokers)
< 89% (smokers)
 Implant failure is 2.5 times greater (Wilson 1999)
 Smoking cessation - 1/3rd as many failures as
compared to smokers

therapy
 Light smoking - no effect on machined or dual acid-
etched surface implants (Bain 2002)
 Maxillary implants
 risk for peri-implantitis
 Failures – twice more
 Lindquist et al 1996 - 15-year longitudinal study
 Greater marginal bone loss around mandibular
implants

therapy
Maintenance therapy
 2 times the risk of losing teeth
 Scabbia 2001 - more residual pockets
Effects of smoking on treatment outcomes - long lasting

therapy
Recurrent/refractory disease
 Smokers do not respond favorably  recurrent or
continuing disease
 MacFarlane et al 1992 – 90% of subjects who showed
poor results were smokers

therapy
Conclusion
 Smoking  detrimental effect on periodontal therapy

TOBACCO CESSATION
 Intervention models for dental practice
1. Brief
2. Comprehensive
3. Pharmacotherapy
 Relapse prevention
 Effect of cessation on PDL status and treatment outcomes

TOBACCO CESSATION
 Tobacco is harmful to health
 Success  long-term abstinence  6 months

Tobacco Cessation
Brief Intervention Program
 Agency for Health Care Research and Quality
(Fiore MC et al 2000)
Brief
Intervention
Program
ASK
ADVISE
ASSESSASSIST
ARRANGE

Tobacco Cessation
Comprehensive Intervention Program
 Expanding the scope of intervention
 Expanding the five A’s
1. Ask
2. Advise
3. Assess
4. Assist (2-14% effectiveness)
5. Arrange

Tobacco Cessation
Pharmacotherapy
 Nicotine replacement therapies
 Others
 Sustained-release bupropion
 Clonidine, nortriptyline
OTC products
 Nicotine
chewing gum
 Lozenges
 Patches
On
prescriptions
 Nasal sprays
 Inhalers

Tobacco Cessation
Indications
 Patient’s health history
 Current nicotine exposure
 Past experience with cessation

Tobacco Cessation
Nicotine replacement and combinations
 < 20 / day – patch – 7–22 mg for 4 weeks or longer
> 20 / day – combination; patch + other products
 No use of any other form of tobacco when on a
cessation program
 Bupropion –
 1st 3 days : 150 mg OD
 upto 7-12 weeks : BID
 Safe upto 6 months

Tobacco Cessation
Relapse prevention
 Withdrawal symptoms after tobacco cessation
 Relapse – high
 Long-term abstinence
 Alternate treatment modalities

Tobacco Cessation
Effect of cessation on PDL status and treatment outcomes
 Rate of bone and attachment loss slows
 Disease severity – intermediate
 Former smokers respond to therapy similar to never
smokers (Kaldahl et al 1996)
 Bain 2002 - implant failures

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.

REFERENCES
 Jan Lindhe, Niklaus P. Lang, Thorkild Karring. 5th Edition.
Clinical Periodontology and Implant Dentistry. Blackwell
Munksgaard 2008.
 Rose LE, Genco RJ, Cohen DW, Mealy BL. Periodontal Medicine.
B.C. Decker Inc 2000.
 Palmer RM, Wilson RF, Hasan AS, Scott DA. Mechanisms of
action of environmental factors – tobacco smoking. J Clin
Peridontol 2005; 32 (Suppl. 6): 180–195.
 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.

References
 Georgia K. Johnson, Margaret Hill. Cigarette smoking and the
periodontal patient. J Periodontol 2004; 75: 196–209.
 Francisco Rivera-Hidalgo. Smoking and periodontal disease.
Periodontology 2000, Vol. 32, 2003, 50–58.
 D.F. Kinane and I.G. Chestnutt. Smoking and Periodontal Disease.
CROBM 2000 11: 356.
 Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza’s
Clinical Periodontology. 10th Edition. Saunders Elsevier 2007.

References
 Mark I. Ryder. The influence of smoking on host responses in
periodontal infections. Periodontology 2000, Vol. 43, 2007,
267–277.
 Boström L, Bergström J, Dahle´n G, Linder LE. Smoking and
subgingival microflora in periodontal disease. J Clin Periodontol
2001; 28: 212–219.
 Antonella Labriola, Ian Needleman & David R. Moles. Systematic
review of the effect of smoking on nonsurgical periodontal
therapy. Periodontology 2000, Vol. 37, 2005, 124–137.
 Vivian I. Binnie. Addressing the topic of smoking cessation in a
dental setting. Periodontology 2000, Vol. 48, 2008, 170–178.

Find out
• Smokeless tobacco
• Different forms of smoking
• Plasma/GCF/urine levels of tobacco
• NNN – nitrosonornicotine
• Effect of smoking on maintenance therapy
• Add from carranza…genco???
• Format
• Read soben peter
• Add contents of smoke from SP
• Elastase levels
• Functions of elastase, ICAM-1
• Lindhe treatment aspect
• Carranze perio therapy

Smoking and periodontal diseases

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