sem 7 smoking and periodontium

8/12/2019 Sem 7 Smoking and Periodontium

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EFFECTS OF TOBACCO AND

SMOKING ON PERIODONTIUM

PRESENTED BY

MANASA. AII YR PG


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CONTENTS

Introduction

Assessment of smoking

Prevalence

Smoking and ANUG

Effects of smoking on plaque, calculus and gingival tissues Smoking and periodontitis

Effects on host response

Effects on periodontal therapy

Smoking cessation Smoking and periodontal health In future

Conclusion


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INTRODUCTION


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Composition of tobacco

CDC 2004


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The gas phase - carbon monoxide, ammonia, formaldehyde, hydrogencyanide, and many other toxic and irritant compounds, including morethan 60 known carcinogens such as benzo(a)pyrene anddimethylnitrosamine.

The particulate phase - nicotine, tar (itself mae up of many toxicchemicals), benzene, and benzo(a)pyrene.

Tar is inhaled with the smoke and in its condensate form, is the sticky brown substancethat stains fingers and teeth yellow/brown.

Nicotine, an alkaloid, is found within the tobacco leaf and evaporates when thecigarette is lighted. It is quickly absorbed in the lung and reaches the brain within 10 to19 seconds. Nicotine is highly addictive and causes a rise in blood pressure, increasedheart rate and respiratory rate, and peripheral vasoconstriction.

Toxic components of tobacco


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Pack-years = (number of packs smoked per day) (number of years ofsmoking)

Smokers have smoke 100 cigarettes in their lifetime an currently

smoke.Former smokers have smoke 100 cigarettes in their lifetime an o

not currently smoke.Nonsmokers have not smoke 100 cigarettes in their lifetime an o

not currently smoke.CDC 2004


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Serum cotinine levels which is a metabolite of nicotine

Reliable method


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Gelesky 1999, smoking meets the majority of criteria given for causationof a disease.

True risk factor for periodontitis.

It has been associated with two to three fold increases in the odds ofdeveloping clinically detectable periodontitis and subsequent tooth loss.(Tonnetti 1998)

An overwhelming body of data from multiple cross-sectional andlongitudinal studiesconducted have demonstrated pocket depth andclinical attachment loss were more prevalent and severein patient whosmoke compared with non-smokers. (Carranza 11thed..)

Smoking - true risk factor


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Smoking - true risk factor

Smoking is the second strongest modifiable risk factorfor periodontaldisease after the first one which is the microbial dental plaque. (Nurcan

Buduneli 2012)


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There are 1.1 billion smokers worldwide and 182 million (16.6%) of themlive in India (Sinha 2003)

Tobacco is used in smoking and smokeless forms in India. Among tobacco

users, 34% smoke Bidis, 31% are regular cigarette smokers, and 35% usesmokeless tobacco. (Preetha 2007)

The prevalence of smoking among 13-15 year old school going students inIndia ranges from 19.7-34.5%

Prevalence of smoking


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Smoking and Acute Necrotizing Ulcerative

Gingivitis (ANUG)

An association between necrotizing forms of periodontal disease andtobacco smoking was reported as early as 1947 and has long beenconsidered an etiologic factor in ANUG.

It influence the tissue response to irritation.

Karadachi et al. 1974 - smoking activates the release of epinephrine andpromotes contraction of peripheral vessels reducing blood flow to thegingiva

Preexisting gingivitis

emotional/psychic stresssmoking


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Smoking and Acute Necrotizing Ulcerative

Gingivitis (ANUG)

sepsis, stress, and smoking

Severe reduction of blood flow

Loss of vitality of gingival epithelium

ANUG

Karadachi et al. 1974


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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 diseaseor becoming edentulous as do non smokers.

It was found that no significant difference in loss of alveolar bone heightwhen comparing male and female smokers.(Carranza 11thed)


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Cigarette Smoking and Oral Hygiene

Several studies demonstrated higher levels of oral debris in smokers thanin 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.

The toothbrushing efficiency of smokers was much less and the calciumconcentrationin the dental plaque of smokers was found to be

significantly higher than in nonsmokers(Bergstrom J 2000)


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Effect of Smoking on Plaque

The early studies that examined the relation between smoking and oralcleanlines consistently found that smokers had poorer oral hygiene thannon-smokers(Preber 1980, Feldman 1983).

Macgregor (1984) measured the area of stained plaque, and theproportion of gingival margin in contact with plaque in 64 smokers and 64non-smokers, matched for age and sex. In both sexes, smokers hadsignificantly more plaque than non-smokers, and there was a trend

towards increased plaque deposits with increasing cigarette consumption.


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Effect of Smoking on Plaque

Feldman (1985), in the study of periodontal measures, found significantlyless plaque in smokers than in nonsmokers.

Bergstrom and Eliasson (1987) similarly found no difference in mean Plindex scores amongst 285 subjects (31% smokers and 69% non-smokers).

Bergstrom and Preber (1986) studied the rate of plaque growth . Again,

there was no quantitative difference between the growth rates of plaquein smokers and non-smokers.


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Smoking and gingival inflammation

A reduction in clinical signs of gingivitis has been reported in smokers andthis effect has been shown to be independent of plaque levels(Markkanen 1984)

Heavy smokers may have greyish discoloration and hyperkeratosis of thegingiva: an increased number of keratinized cells has been found in thegingiva of smokers. Changes in the epithelium were described as keratotic,hyperkeratotic and hyperplastic (Bajagic V 2006)


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Smoking and gingival bleeding

smoking is known to produce peripheral vasoconstriction but in somesubjects this is preceded by vasodilatation. In any particular instance, theeffect produced is probably related to the degree of inhalation of thetobacco smoke and the rate of nicotine absorption (Muller HP 2002)

Nicotine from cigarette stimulates the sympathetic ganglia to produceneurotransmitters including catecholamines (Trauth JA 2001). These affectthe alpha-receptors on blood vessels which in turn causesvasoconstriction.


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Bergstrom et al. 1983 have found less gingival bleeding in smokers mayalso be attributable to the heavier keratinization of the gingivae in

Smokers Palmer and colleagues 1999 measured gingival blood flow, using a laser

Doppler technique, and their data did not support the view that smokingcompromised blood flow in the periodontal tissues. Tobacco use has alsobeen associated with reduced permeability of peripheral blood vessels.


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Interestingly, in smokers undergoing smoking cessation programs, gingivalbleeding and gingival blood flow, as well as gingival crevicular fluid flow,increase and normalize toward non-smoker levels after quitting.

(Nair 2003, Morozumi 2004)


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Smoking & Oxygen tension in gingival tissues

Oxygen saturation of hemoglobin is affected by cigarette smoking, andattempts have been made to measure this in the gingival tissues.

In healthy gingiva smokers appear to have lower oxygen saturation

determined by using tissue reflectance spectrophotometry, but in thepresence of inflammation converse was shown

They also examined oxygen tension in periodontal pockets anddemonstrated oxygen tension was significantly lower in smokers.

(Palmer 2005)


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Effects on the Gingival Vasculature

The vasculature has also been examined in histological andimmunocytochemical studies

It was found that high proportion of small vessels compared with large

vessels in smokers than non-smokers but no difference in the vasculaturedensity.

(Mirbod 2001)


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Smoking and oral microorganisms

Cigarette smoking could cause a lowering of the oxidation-reductionpotential (Eh), and this could cause an increase in anaerobic plaquebacteria (Kinane DF 1997).

There was a statistically significant increase in the proportion of Gram-positive to Gram-negative bacteria in 3-day-old plaque from smokers,when compared with the non-smokers (Stoltenberg JL 1993).


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Smoking and oral microorganisms

Tobacco smoke contains phenols and cyanides, which can account forantibacterial and toxic properties. Smokers harboured significantly higherlevels and were at significantly greater risk of infection with Tanarellaforsythensisthan non-smokers (Zambon JJ 1996).

Adjusting for disease severity, Porphyromonas gingivalis was also morelikely to subgingivally infect smokersthan non-smokers (Sayers NM 1999).However, there was not a significantly higher relative riskfor infectionwith this bacterium.


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Smoking and Calculus formation

There have been consistent reports of more calculus in smokers than innon-smokersfrom the earliest epidemiological studies (Martinez-Ganut P1995).

Some authors reported that significantly more pipe smokers than cigarettesmokers had supragingival calculus.This might be because the pH of pipesmoke is higher than that of cigarette smoke, and because pipe smokerscirculate the smoke around the mouth, whereas cigarette smoke tends tobe inhaled (Albandar JM 2000).

Moreover, the smoking cycle is much longer in pipe smokers than incigarette smokers, causing pipe smokers to salivate more (Bergstrom J2005).


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There is an increased calcium concentration in fresh saliva in smokersfollowing smoking (Khan GJ 2005).

Nicotine affects the exocrine glands by an initial increase in salivary and

bronchial secretions that are followed by inhibitionof the secretions.

The increased amount of calculus found in smokers might therefore bedue to an effect of tobacco smoke upon properties of saliva (Erdimir2006).


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The reasons for an elevated calcification rate in smokers are not known,but it has been speculated that it might be coincident with the increasedrisk in smokers for ectopic calcification.

(Bergstrom 2005)


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Smoking and periodontal disease

Multiple cross-sectional and longitudinal studies have demonstrated thatpocket depth, attachment loss, and alveolar bone loss are more prevalentand severe in patients who smoke compared with nonsmokers.

Prevalence:

Third National Health and Nutrition Examination Survey (NHANES III).

Of >12,000 individuals studied, 9.2% had periodontitis.

On average, smokers were four times as likely to have periodontitis as persons who hadnever smoked

Former smokers were 1.7 times more likely to have periodontitis than persons who hadnever smoked

(Tomar SL 2000)


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Dose-response relationship

In subjects - smoking 9 per day, the odds for having periodontitis were 2.8

subjects smoking - 31 per day were almost 6 times more likely to have periodontitis.

With former smokers, the odds of having periodontitis declined with the number ofyears since quitting.

(Tomar SL 2000)



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increased risk for smokers to have subgingival infection with Porphyromonas gingivalis

smokers were 3 times more likely to harbor A. actinomycetemcomitans.

Magor DL 2003, Luciana L 2004

No significant differences in the occurrence of Porphyromonas gingivalis,Prevotella intermedia,Tanarella forsythensis,Aggregetibacter actinomycetemcomitans and Treponema denticola

Kamma 1999, Darby 2000

greater probing depths and bone loss in smokers than non-smokers no difference was found in relationto tooth mobility

Feldmen 1983

not only significantly increased probing depths and alveolar bone loss, but also increased tooth mobilityin smokers

Bergstrom 1991

dose relationship between the effect of cigarette consumption and periodontal attachment loss

Grossi 1994, Haffaji 2001, Obrodovic 2007

smokers suffer from more tooth loss than non-smokers

Daniell 1983, Osterberg 1986, Holme G 1994, Mc Leod 1997, Calsina 2002


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So the relationship is causal.

The results of the cohort studies, in particular those that have evaluatedthe dose-response effects, offer convincing evidence that the relationbetween smoking and destructive periodontal disease is causal, i.e.,smoking can cause the disease.

(Jan Bergstrom 2004)


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Smoking & destructive periodontal disease:

relative risk

Based on current evidence, the relative risk for a smoker to attractdestructive periodontal disease can be estimated to be 5- to 6-foldelevated in comparison with a non-smoker.

RR (Relative risk) is also epenent on the amount of exposure

A smoker who has smoked 20 cigarettes a day for over 20 years runs a 20-fold increased risk.

(Hyman, Bergstrom 2003)


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Smoking and gingival recession

Gingival recession in smokers was greater than that in non-smokers andthe difference was statistically significant.

Significant positive associations were noted between gingival recessionand age, and between gingival recession and plaque index betweensmokers and non-smokers

(Nikolaos Andreas 2011)


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Host response in gingivitis

Evidence From Studies on Gingival Crevicular Fluid (GCF)

Smoking may result in lower resting GCF flow rate(Persson 1999)

The increase in GCF during an experimental gingivitis may be less in smokers (Bergstrom1986)

Higher levels of TNF-(Bostrom 1998)

Decreased levels of IL-1 an IL-1 (Rawlinson 2003) and enzyme elastase in GCF

Lower levels of cytokines, enzymes, and possibly polymorphonuclear leukocytes

(PMNs). (Rawlinson 2003)

This correlates with the lower levels of inflammation observed clinicallyand within the tissues.


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Inflammatory & immune responses in smoking

Microbialvirulance

Hostresponse


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Inflammatory & immune responses in smoking

Microbialvirulance

Hostresponse

Smoking


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Smoking and Fibroblast Function

Gingival Fibroblasts (Palmer 2005) Periodontal Fibroblasts

production of Type 1 collagen andfibronectin collagenase activity

Periodontal ligament (PDL) fibroblastsgrowth andAttachment was inhibitedby nicotine at high concentrations (over 1

mg/ml) (James 1991)

Cellular changes

disruption of cell orientationchanges in cytoskeletonpresence of large vacuolessignificant reduction in cell viability

Nicotine at highconcentrations (100 ng/ml to25g/ml)(Giannopovlou C 1999)

cytotoxic by inhibiting the vacuolation andproliferation of fibroblastsPDL cell proliferation and protein synthesis wereinhibitedCell attachment was significantly less on rootsurfaces


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Potential mechanisms of smoking action

Nicotine metabolites can concentrate in the periodontium and theireffects

the promotion of vasoconstriction

the impairment of the functional activity of polymorphs and macrophages.

The numbers of neutrophils in peripheral blood are also increased by tobaccouse and their migration through capillary walls.

Bergstrom 2004


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PMN function

Important role in the defense of the marginal periodontal tissues againstbacterial invasion.

PMN activity to be severely depressed by a solution of tobacco-smokewhere as phagocytosis and bactericidal activity were not affected.(Corberand 1980)

Smokers have higher blood PMN counts than do non-smokers andchemotaxis of PMN s from smokers was suppressed relative to

nonsmokers (Mac Ferlene 1992)


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Adhesion molecules and smoking

Elevated levels of soluble intercellular adhesion molecule-1 (sICAM-1)in

the gingival crevicular fluid (GCF) of smokers - tissue destructive activityvia enzymes such as elastase (Rezavandi K 2002).

On otherhand protease inhibitor molecules alpha-1 antitrypsin and alpha-2 macroglobulin are suppressed in smokers, suggesting that thedestructive action of certain proteases, such as elastase, may be increased(Persson 2001)

Smoking & cytokine levels


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Smoking & cytokine levels

GCF levels of Tumor necrosis factor-alpha (TNF-) aninterleukin-8 (IL-8 ) seem to be increased in smokers.

Bostrom L 1998, Giannopolou C 2003,

Levels of IL-4 and IL-1, 13,5,6 are epresse.

Bostrom L 1998, Giannopolou C 2003,

GCF levels of IL-1and IL-1ra- decreased in smokers

Rawlinson 2003

GCF levels of IL-1 nd IL-1ra- no influence of smoking

Giannopolou C 2003

I i t f RANK/RANKL/OPG t


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Impairment of RANK/RANKL/OPG system smoking was reported to reduce

salivary osteoprotegerinconcentrations in untreated and

also treated chronic periodontitispatients (Buduneli et al.2008).

Nicotine and lipopolysaccharide(LPS) effects on the expression of

macrophage colony-stimulatingfactor (M-CSF), osteoprotegerin(OPG), and prostaglandin E2 (PGE2)have been evaluated by Tanaka etal. (2006)in osteoblasts andosteoclast-like cells.

OPG expression was increased inthe initial stages with nicotine andLPS but decreased in the laterstages

Impairment of RANK/RANKL/OPG system


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Lappin et al. (2007) reporteddecreased serum OPG levels and

greater soluble receptor activatorof nuclear- factor kappa B ligand(sRANKL) sRANKL/OPG ratios insmoker patients in themaintenance program than the

non-smoker counterparts.

Negative correlation betweenpack-years and total OPG amountin peri-implant crevicular fluid was

detected in clinically healthyimplants (Arkanet al. 2008).


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The plasma data reported by zaka etal. (2010)are in line with the study byTang et al. (2009) reporting similarsRANKL and OPG levels in GCF samplesof never smokers, former smokers andcurrent smokers.

In later study the only significantdifference could be found in GCF OPGlevels of the high pack-years group andnever smokers.


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Smoking and MMP levels

Pathogens in microbial dental plaque are capable of stimulating host cells

to increase their matrix metalloproteinase (MMP) release which isconsidered among the indirect mechanisms of tissue destruction seenduring periodontitis(Sorsa et al. 2006).

Periodontal tissues are infiltrated mainly by neutrophilic granulocytes andPMN which play an important role in the development of inflammatoryinjury.

Tobacco-induced degranulation events in neutrophils, tobacco-induced

alterations to the microbial flora, and tobacco induced increases in pro-inflammatory cytokine burden could each, influence MMP-8 levels in theperiodontal tissues of smokers.

St di MMP 8 i k


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Studies on MMP -8 in smokers

Knuutinen et al. (2002) noted anincreased MMP-8 concentration in

the resulting fluid infiltrate insmokers

Sder et al. (2002) found a positivecorrelation between elastase

complexed to 1-antitrypsin andMMP-8 concentrations in the

gingival crevicular fluid (GCF) ofsmokers in individuals with various

persistent periodontal diseases.

Persson et al. (2003) reported that GCFMMP-8 levels remained unchanged in

the smokers following surgical

treatment for periodontitis, whereasdecreased levels were observed in thenon-smokers, suggesting a tobacco-

induced MMP-8 burden.

(zaka et al. 2011), serum MMP-8concentrations did not differ

significantly between the smokersand non-smokers.


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Predisposing to cardiovascular disease..

In a recent study (zaka et al. 2011), it was hypothesised that smokingmay affect MMPs and neutrophil degranulation products in the systemiclevel eventually leading more severe periodontal tissue destruction andsystemic inflammation predisposing to cardiovascular diseases (Pussinenet al. 2007).

the serum concentrations of MMP-8, MMP-9, TIMP-1, NE, and MPO wereevaluated comparatively in smoker versus non-smoker patients withchronic periodontitis as well as periodontally healthy subjects.

The findings of significantly elevated serum MMP-9, MPO, NE togetherwith decreased TIMP-1 in smoker patients with chronic periodontitis thannon-smoker counterparts support the idea that smoking together withperiodontal destruction may expose/predispose to cardiovasculardiseases.


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Predisposing to COPD & Atherosclerosis..

MPO was suggested as an early marker of systemic inflammation in smokers


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ICTP levels (Carboxyterminal-telopeptide

pyridinoline)

Carboxyterminal-telopeptide pyridinoline cross-links of type I collagen(ICTP) is released into the periodontal tissues as a consequence ofcollagen degradation and alveolar bone resorption (Seibel 2003).

ICTP was suggested to predict future bone loss, to correlate with clinicalparameters and putative periodontal pathogens and also to reducefollowing periodontal therapy (Giannobile 1999).


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osteocalcin

Osteocalcin (OC) is a calcium-binding protein of bone and the mostabundant noncollagenous protein of the mineralized tissue (Lian &Gundberg 1988).

Serum level of OC is considered as a marker of bone formation(Christenson 1997).

Serum levels of OC were reported to be lower in periodontitis patientscompared with healthy subjects suggesting lower osteoblastic activity andbone formation ability (Shi et al. 1996).


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Antibody production and smoking

some components of cigarette such as nicotine are immunosuppressive(Geng et al. 1996)

whereas some others are immunostimulatory such as tobaccoglycoprotein and metals (Francus et al. 1988, Brooks et al. 1990).

Serum immunoglobulin G (IgG) levels were reduced in smoker patientswith periodontitis (Quinn et al. 1998)

The number of B lymphocytes seemed to be similar in smokers and non-smokers but their function in peripheral blood was impaired in smokers


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Genetic Polymorphism and Smoking

Genetic variability, its relationship with periodontal disease, and itsinteraction with smoking

Tooth loss reported a positive genotype of IL-1 increasesthe risk for tooth loss by 2.7 times, while smoking

increases the risk by 2.9 times. When both werecombined, the risk increased to 7.7 times.

Mc Guire MK 1999

N-acetyletransferase 2 (NAT-2) polymorphism also

affects the population by altering the metabolism ofarylamines which may influence the immune responseand may act as an immunosuppressant.

Cullinan MP 2001

ff f k l b


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Effects of Smokeless Tobacco on

Periodontal Tissues

In studies done by Amarasena et al. 2003in a Sri Lankan population hasconfirmed quantified tobacco use may significantly increase bleeding onprobing and periodontal attachment loss

Other studies have also shown the negative effect of the areca nut on hostimmunity by affecting PMNs. (Hung SL 2001, 2002)

Areca nut extracts have also been shown to inhibit the growth,attachment, and matrix protein synthesis of cultured human gingivalfibroblasts (Chang 1998)


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Smoking and periodontal therapy


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smoking exerts a negative influence on the outcomefollowing non-surgicalas well as surgical periodontal therapy. (Bergstrom 2004)

smoking negatively influences the outcome following implant therapy andrisk for implant failure is increased in smoker patients (Bain 2003)

smokers contribute the vast majority of therapeutic failures or refractorycases (Magnusson 1994)


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Following non-surgical therapy including scaling, root planing andprofessional tooth cleaning, healing in terms of gingival bleeding reductionand pocket depth reduction was less favorable in smokers as compared to

nonsmokers. (Jansson 2002)

A study by Grossi et al. 1997 showed that current smokers have lesshealing and reduction in subgingival Tanarella forsythenssis andPorphyromonas gingivalis after treatment compared to former and non-

smokers, suggesting that smoking impair periodontal healing.

Ah et al. 1994, who reported less probing depth reduction and attachmentgain in smokers who had been treated by periodontal surgery,corroborated this finding that smokers were poor candidates for

successful periodontal care.


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A statistically significant difference was observed in the reduction ofprobing depth between smokers and non-smokers at 12 month post-surgical follow-up after Widman flap surgery on 4 to 6 mm pockets (preber

1990).

James and colleagues (1999) investigated the in vitro effect of nicotine onfibroblast activity. They found that it inhibited attachment and growth ofperiodontal ligament fibroblasts.


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Soft and Hard Tissue Grafting

recession sites were treated using connective tissue with a partialthickness pedicle graft (Harris JJ 1994) and a coronally positioned flapalone, or with a bioabsorbable membrane (Amarante ES 2000) found nodifference in root coverage between smokers and non-smokers.

When guided tissue regeneration procedures were used smokers hadsignificantly less root coverage (57%) compared to non-smokers (78%).

(Trombelli 1997)


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Implant Therapy

In the studies reviewed, 0% to 17% of implants placed in smokers werereported as failures as compared to 2% to 7% in non-smokers.

The 3-year data demonstrated 8.9% of implants placed in smokers failedas compared to 6% in individuals who had never smoked or had quit

smoking.

The majority of implant failures in smoking occurred prior to prosthesisdelivery.

(Georgia 2004)


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Methods of smoking cessation

Set a Quit Date

Will Power Alone

Self-Help Materials

This includes a variety of literature and online resources that patients canaccess. The dental team can be helpful in providing literature and guidingpatients towards resources they can access.

Brief Intervention Program in Primary Care



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Nicotine Replacement Therapy (NRT)


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Bupropion

This medication is used as an antidepressant at higher doses but iseffective for smoking cessation at lower doses. It is usually prescribedstarting 12 weeks before the quit date, initially at 150 mg once perday for 6 days then 150 mg twice daily for 79 weeks. There are

serious potential drug interactions so this medication should beprescribed by the patient's medical doctor.

Other Methods

intensive counseling, motivational interviewing, cognitive behavioral

therapy, hypnosis, and acupuncture.


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Environmental tobacco smoke & periodontitis

Among persons in the United States who had never used tobacco, thoseexposed to ETS were more likely to have periodontal disease than werethose not exposed to ETS.

Samuel James 2001

smoking and periodontal health in


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the future

smoking is associated with over 40 various diseases, it is evident that theperiodontal tissues share a susceptibility to smoking with 40 other tissuesor organs of the body.

The periodontal tissues react to or are influenced by functions that

regulate the body as a whole

As a consequence, destructive periodontal disease can be regarded as asystemic rather than a local isease.

(Bergstrom 2004)



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the future

The destruction by smoking of the periodontal tissues, resembles that oflung tissues.

The end stage of lung destruction isloss of respiratory function, and the

worsening of lung function isaccompanied by microbial infection

that often results in acute

exacerbations

End stage of periodontaldestruction is the loss ofmasticatory function, and along

with the gradual breakdown of theperiodontal tissues and ensuingpocket formation, root surfacesbecome microbially colonized or

infected.

Bergstrom 2004


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The basic steps are known as 5 As -: (Glynn and Manley)

ASK All your patients about tobacco use

ADVISE Tobacco users to quit

ASSESS - Tobacco users willingness to quit ASSISST Tobacco users in eveloping a quit plan

ARRANGETobacco users follow up contact


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Conclusion

Substantial progress has been made in our understanding of thepathogenesis of periodontal disease and host response to therapy. Clearly,the identification of individuals at high risk for periodontal disease and thefactors that place them at risk has significantly improved the clinicalmanagement of these patients.

The opportunity for dentists and dental hygienists to become more activein evaluation of tobacco use by patients and more aggressive in offeringcounseling and cessation services can positively impacts both the oral andgeneral health of dental patients. Of all the preventive servicestraditionally offered within a dental practice, those related to tobacco

cessation are by far the most beneficial to the patient relative to generalhealth and quality of life.


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Conclusion

Periodontal health and Prognosis for PERIODONTAL THERAPY substantiallyimprove when patients QUIT SMOKING


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REFERENCES

Carranza 11thedition D.F. Kinane and I.G. Chestnutt, Smoking And Periodontal Disease, critical

reviews In oral biology and medicine 2000, 11(3):356-365

Samuel James Arbes, Helga gstsdttir, Gary Douglas Slade.Environmental Tobacco Smoke and Periodontal Disease in the United

StatesAm J Public Health. 2001;91:253

257

Nurcan Buduneli, Effects of Tobacco Smoking on Chronic Periodontitis andPeriodontal Treatment,2012, chapter 5 , 82-96.

Ana Pejid, Radmila Obraovid, Ljiljana Kesid, Draginja KojovidSmokingAnd Periodontal Disease A Review Vol.14, No 2, 2007, pp. 5359

Vandana, K Laxman, Annaji Tobacco Use and Its Effects on thePeriodontium and Periodontal Therapy The Journal of ContemporaryDental Practice, Volume 9, No. 7, November 1, 2008, 1-11


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REFERENCES

Jan Bergstrm, Tobacco smoking and chronic destructive periodontaldisease. Odontology (2004) 92:18


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We as PERIODONTISTS Can and Should

MAKE the DIFFERENCE

sem 7 smoking and periodontium

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