2. 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
12. CONSTITUENTS OF TOBACCO
SMOKE
Complex mixture of substances – over 4000 known
constituents
Phenols and cyanides – antibacterial and toxic
properties
13.
14. 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
15. 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
23. 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
24. EFFECT OF SMOKING ON
PLAQUE
Plaque development
Oral flora
Subgingival microflora
Calculus formation
Conclusion
25. EFFECT OF SMOKING ON
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)
26. 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
27. Effect of smoking on plaque
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
28. Effect of smoking on plaque
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
29. Effect of smoking on plaque
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
30. Effect of smoking on plaque
Conclusions
Numerous species in oral cavity
Varied sampling methods
Common known species often investigated
Trend:
Greater numbers of pathogens not correlating with
plaque levels
31. EFFECT OF SMOKING ON
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
32. EFFECT OF SMOKING ON
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)
33. 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)
34. Effect of smoking on periodontal
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)
35. Effect of smoking on periodontal
tissues
Reason:
Nicotine Vasoconstrictive property
In some cases, smoking-induced elevation in blood
pressure overcomes vasoconstrictive effect of smoking.
Smoking decreases gingival blood flow
36. Effect of smoking on periodontal
tissues
Bergstrom et al 1983
Nicotine
Sympathetic ganglia catecholamines
α - receptors vasoconstriction
Peripheral blood vessels – periodontium
gingival bleeding
Vasoconstriction
Keratinization
37. Effect of smoking on periodontal
tissues
Morozumi et al 2004 - following quitting
At 3 days – significant increase
At 4-8 weeks - small increases occurred
38. Effect of smoking on periodontal
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 -
39. Effect of smoking on periodontal
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
40. Effect of smoking on periodontal
tissues
gingival
redness
Fewer gingival
vessels
GCF
Less bleeding
sites
Suppression of the
normal inflammatory
response
(Bergstrom 1986)
41. Effect of smoking on periodontal
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
42. Effect of smoking on periodontal
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
43. Effect of smoking on periodontal
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)
44. Effect of smoking on periodontal
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
45. Effect of smoking on periodontal
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)
46. Effect of smoking on periodontal
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)
47. Effect of smoking on periodontal
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
48. Effect of smoking on periodontal
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)
49. Effect of smoking on periodontal
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
50. Effect of smoking on periodontal
tissues
Poorly functioning fibroblasts gingival tissue
adaptation impaired
Poor healing
Persistence of
infection
Predisposition to
disease
51. Effect of smoking on periodontal
tissues
Conclusions
Long-term chronic effect
Impairing the vasculature and revascularization
Following abstinence, the vasculature does return to a
near- normal state
53. 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
54. EFFECT OF SMOKING ON
IMMUNOLOGY AND HOST
RESPONSE
PMN function
Lymphocyte function
GCF
Cytokines
Other factors
Conclusion
55. EFFECT OF SMOKING ON
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)
56. Effect of smoking on immunology
and host response
Express several receptors
Metabolites of Endogenous
smoke factors
34 subtype of nicotinic
receptors (Benhammou et al
2000)
IL-8, ICAM-1,
TNF-
57. Effect of smoking on immunology
and host response
PMN
function
Degradative
protease
formation
Neutrophil
respiratory
burst
PMN
migration
and
chemotaxis
Neutrophil
priming
58. Effect of smoking on immunology
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
59. Effect of smoking on immunology
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 ?
60. Effect of smoking on immunology
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
61. Effect of smoking on immunology
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
62. Effect of smoking on immunology
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
63. Effect of smoking on immunology
and host response
Neutrophil priming capabilities for TNF-alpha
(Gustafsson 2000, Bostrom et al 1998b)
64. Effect of smoking on immunology
and host response
Conclusions
Neutrophils - critical role
65. Effect of smoking on immunology
and host response
Smoking And Lymphocyte Function
Immune system recognize antigens response
Lymphocytes
T lymphocytes NK cellsB lymphocytes
66. Effect of smoking on immunology
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
67. Effect of smoking on immunology
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
68. Effect of smoking on immunology
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)
69. Effect of smoking on immunology
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)
70. Effect of smoking on immunology
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
71. Effect of smoking on immunology
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
72. Effect of smoking on immunology
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)
73. Effect of smoking on immunology
and host response
Conclusions
Inconsistencies and variations in findings
Inadequate knowledge of antigens and responses
74. Effect of smoking on immunology
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
75. Effect of smoking on immunology
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)
76. Effect of smoking on immunology
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)
77. Effect of smoking on immunology
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)
78. Effect of smoking on immunology
and host response
The balance between protection and destruction is mediated
largely by the type of cytokine pattern secreted by these cells.
79. Effect of smoking on immunology
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
80. Effect of smoking on immunology
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
82. 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
83. 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
84. Smoking and systemic status
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
85. Smoking and systemic status
Cytochrome P450 and glutathione S-transferase
enzymes
Neutralization of toxic substances
Polymorphism risk of periodontitis
87. EFFECT OF SMOKING ON
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
88. Effect of smoking on periodontal
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
89. Effect of smoking on periodontal
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
90. Effect of smoking on periodontal
therapy
Little effect of systemic metronidazole (Soder et al)
Systemic amoxicillin and metronidazole – better results
91. Effect of smoking on periodontal
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)
92. Effect of smoking on periodontal
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
93. Effect of smoking on periodontal
therapy
Smoking - negative impact on outcomes of GTR,
DFDBA
GTR with ePTFE membrane
Smokers - 57%
Non-smokers - 78%
Trombelli et al 1997
94. Effect of smoking on periodontal
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
95. Effect of smoking on periodontal
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
96. Effect of smoking on periodontal
therapy
Maintenance therapy
2 times the risk of losing teeth
Scabbia 2001 - more residual pockets
Effects of smoking on treatment outcomes - long lasting
97. Effect of smoking on periodontal
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
98. Effect of smoking on periodontal
therapy
Conclusion
Smoking detrimental effect on periodontal therapy
99. TOBACCO CESSATION
Intervention models for dental practice
1. Brief
2. Comprehensive
3. Pharmacotherapy
Relapse prevention
Effect of cessation on PDL status and treatment outcomes
101. Tobacco Cessation
Brief Intervention Program
Agency for Health Care Research and Quality
(Fiore MC et al 2000)
Brief
Intervention
Program
ASK
ADVISE
ASSESSASSIST
ARRANGE
102. 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
106. 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
108. 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
109. 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.
110. 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.
111. 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.
112. 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.
116. 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
Editor's Notes
Total population : Males, Females
Smokers : Males, Females
Deaths : Males, Females
Deaths due to smoking : Males, Females
Mk chart
N-formylmethionyl-leucyl-phenylalanine – neutrophil chemoattractant
fMLP – chemotactic to PMNs – causes them to release lysosomal enzymes
APC are peripheral dendritic cells, monocyte-derivatives, and B-cells.
T cells recognize diverse antigens using a low-affinity transmembranous complex, the T -cell antigen receptor (TCR). Antigens are recognized by T-cells in association with either MHC Class I or Class II molecules on the surface of the antigen presenting cell.
B-cells recognize diverse antigens using the B-cell antigen receptor (BCR), which is a high-affinity antigen receptor.
NK cells - Large granular non-T non-B lymphocyte-like cells
NK-cells possess several classes of antigen receptors, including killer inhibitory receptors (KIR) and killer activating receptors (KAR). These receptors will recognize antigens associated with MHC Class I molecules, MHC Class I molecules themselves, or certain other surface glycoproteins.
A. actinomycetemcomitans, P. intermedia, F. nucleatum and T. denticola
Mitogen = cell activator
Smoking has a detrimental effect on periodontal therapy resulting in increased possibility of treatment failure and cessation of smoking may improve disease condition as well as response to treatment.