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CONTENTS

1. Introduction

2 Effects of smoking on prevalence & severity of

periodontitis

3. Interaction between smoking and systemic health

status

4. Effects of smoking on etiology & pathogenesis of

periodontitis

a) microbiology

b) immunology

c) local effects of nicotine

5. Genetic polymorphism

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6. Effects of smoking on periodontal therapy

a) Nonsurgical therapy & Surgical therapy

c) Antimicrobial therapyd) Hard and soft tissue grafting

e) Implant therapy

f) Maintainance therapy

7. Recurrent disease

8. Impact of smoking cessation on periodontal

status & treatment outcome

9. Role of dental health professionals in tobacco

cessation

10. Tobacco -intervention models.

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Introduction

Tobacco smoking is very common, with cigarettes

being the main product. smoked in an European union

, average of 29% of the adult population. The figure ishigher formen (34%) than for women (24%).

Most smokers start the habit as teenagers, with the

highest prevalence in the 20-24 yearold age group.

Higher smoking in the lower socio-economic groups

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Smoking is associated with a wide spectrum of

disease including stroke, coronary artery disease,

peripheral artery disease, gastric ulcer and cancers of

the mouth, larynx, esophagus, pancreas, bladder and

uterine cervix.

it is also a major cause of chronic obstructive

pulmonary disease and a risk factor for low birth

weight babies.Approximately 50% of regular smokers

are killed by their habit and smoking causes 30% of

cancer deaths.

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Cigarette smoke is a very complex mixture of

substances with over 4000 known constituents these

include carbon monoxide, hydrogen cyanide, reactiveoxidizing radicals, a high number of carcinogens and

the main psychoactive and addictive molecule nicotine

(Benowitz 1996). Many of these components could

modify the host response in periodontitis.

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Tobacco smoke has a gaseous phase and solid phase which

contains tar droplets.

Filters tar & nicotine

However, there has been little change in the tar and nicotine

content of the actual tobacco and the dose an individual

receives is largely dependent upon the way in which they

smoke (Benowitz 1989).

Inter subject smoking variation includes: frequency of

inhalation, depth of inhalation, length of the cigarette stub left,

presence or absence of a filter and the brand of cigarette

(Bencam 1988).

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1.Interviewing the subject using simple question or more

sophisticated questionnaires

2. Biochemical analysis of exhaled CO in thebreadth which is commonly measured in smoking

cessation clinics, and cotinine (a metabolite of nicotine)

in saliva, plasma/serum or urine (Wall et al. 1988).

Measurement of tobacco smokeexposure

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Cotinine measurements are more reliable in determining a

subject exposure to tobacco smoke because the half life is

14-20 hrs compared with shorter half life of nicotine which

is 2-3 hours.

The mean plasma and salivary cotinine concentration ofregular smokers are approximately 300 ng/ml and urine

concentrations are about 1500ng/ml.

Non-smokers typically have plasma/saliva concentrations

under 2ng/ml, but this may be raised slightly due to

environmental exposure (passive smoking).

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Inhalation of tobacco smoke allows very rapid absorption

of nicotine into the blood and transport to the Brain, which

is faster than an intravenous infusion.

Nicotine in tobacco smoke from most cigarettes is not wellabsorbed through the oral mucosa because the nicotine is

in an ionized form as a result of the pH (5.5).

In contrast, cigar and pipe smoke is more alkaline (pH

8.5), which allows good absorption of unionized nicotine

through the buccal mucosa (Benowitz 1988)

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blood pressure, heart rate, respiratoryrate

skin temperature due to peripheral

vasoconstriction.

However, at other body sites, such as skeletal muscle,

nicotine produces vasodilatation.

Nicotine

Clarke and co-workers (1981)--- decrease in gingival bloodflow in a rabbit model.

Baab and Oberg using Doppler flowmetry ------ an immediate

but transient increase in relative gingival blood flow during

smoking

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The authors hypothesized that the steep rise in heart rate and

blood pressure due to smoking could lead to an increase in the

gingival circulation during smoking.

These results were confined by Meekin et al. (2000) who

showed that subjects who smoked only very occasionally

experienced an increase in blood flow to the head, whereas

regular smokers showed no change in blood flow,

demonstrating tolerance in the regular smoker.

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EFFECTSOFSMOKINGON PREVALENCE &SEVERITYOF PERIODONTALDISEASE

Gingivitis

Controlled clinical studies & cross-sectional studies

have demonstrated that smokers present

decreased expression of clinical inflammation in

the presence of plaque accumulation compared

with nonsmokers

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Periodontitis

An overwhelming body of data points to smoking as

a major risk factor forincreasing the prevalence and

severity periodontal destruction.

Multiple cross-sectional and longitudinal studies have

demonstrated that pocket depths, attachment loss,

and alveolar bone loss are more prevalent and

severe in patients who smoke compared with

nonsmokers.

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An assessment of the relationship between cigarette

smoking and periodontitis was performed in more than

12,000 dentate individuals over age 18 years as part of

NHANES III

Periodontitis was defined as one or more sites with clinical

attachment loss of 4 mm or greater and pocket depth of

4mm or greater.

Using criteria established by the CDC,

''Current smokers" were defined as those who had

smoked 100 or more cigarettes over lifetime of the

interview;

''Former smokers had smoked 100 or more cigarettes in

their lifetime but were not currently smoking; and

Nonsmokers" had not smoked 100 or more cigarettes

their life time..

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Of the 12,000 individuals studied9.2% hadperiodontitis. This represented approximately 15

million cases of periodontitis in the United States.

On an average, smokers were four times as likely

to have periodontitis compared to persons who

had never smoked after adjusting for age, gender,

race/ethnicity, education, and income/poverty ratio

Former smokers were 1.68 times more likely to have

periodontitis than persons who had never smoked

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This study also demonstrated a dose response

relationship b/w cigarettes smoked per day and odds of

having periodontitis.

In subjects smoking nine or fewer cigarettes per day, theodds for having periodontitis was 2.79, whereas subjects

smoking 31 0r more cigarettes per day were almost six

times more likely to have periodontitis .with former

smokers, the odds of having Periodontitis declined with

the number of years since quitting

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INTERACTION BETWEENSMOKING &SYSTEMIC

HEALTH STATUS

Diabetics were approximately twice as likely to exhibit

periodontal attachment loss compared to non-diabetics

and the combination of diabetes and heavy smoking in an

individual over the age of 45yrs resulted in an odds ratioof attachment loss that was 30 times that of a person

lacking these risk factors.

Smoking also increases the risk of attachment and/or

bone loss in postmenopausal women and AIDS and HIV-

Seropositive patients.

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sEFFECTSOFSMOKINGONETIOLOGY &PATHOGENESISOF PERIODONTALDISEASE

microbiology

In a study of 615 patients using immunoassay, the

prevalence of A. A comitans, P. gingivalis, P. intermedia,and Eikenella corrodens was not found to be

significantly different between smokers and nonsmokers

In contrast, other studies have shown differences in the

microbial composition of subgingival plaque between

smokers and non smokers.

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In a study of 798 subjects with different histories, it was found

that smokers had significantly levels of bacteroides forsythus

and that smokers were 2.3 times to harbor T.forsythia than

nonsmokers and former smokers.

Of particular interest was the observation that smokers do not

respond to mechanical therapy as nonsmokers; this is

associated with increased levels of T. forsythia, A. A comitans

and P. gingivalis remaining in the pockets after therapy in the

smoking group when compared with nonsmokers..

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Many discrepancies between the findings of

microbiologic studies are a function of the methodology

involved including bacterial counts versus proportions

or prevalence of bacteria, number of sites sampled and

the pocket depths selected, the sampling technique, the

disease status of the subject/and the methods of

bacterial enumeration and data analysis.

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In an attempt to over-come some of these problems, a

recent study sampled subgingival plaque from all teeth with

the exception of third molars in 272 adult subjects,

including 50 current smokers, 98 past smokers, and 124

nonsmokers.

Using checkerboard DNA-DNA hybridization/ technology to

screen for 29 different subgingival species, it was found

that members of the orange and red complexes were

Significantly more prevalent in current smokers than in nonsmokers and former smokers

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The increased prevalence of these periodontal pathogens

was caused by the colonization of shallow sites (pocket

depth 4mm), with no differences among smokers, former

smokers, and nonsmokers in pockets 4mm or greater, in

addition, these pathogenic bacteria were more prevalent in

the maxilla than the mandible.

In particular palatal surface of maxillary teeth &the upper

&lower incisor regions (Haffajee &socransky2001)

These data suggest that smokers have a greater extent of

colonization by periodontal pathogens than nonsmokers orformer smokers and this colonization may lead an increased

prevalence of periodontal breakdown.

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Smoking exerts a major effect on the protective

elements of the immune response, resulting in anincrease in the extent and severity of periodontal

destruction. The deleterious effects of smoking appear to

result in part from a down regulation of the immune

response to bacterial challenge

Immunology

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The neutrophil is an important component of the host response to

bacterial infection, and alterations in neutrophil number or Function

may result in localized and systemic infections.

Critical function of neutrophil include

Chemotaxis, phagocytosis,and killing by oxidative and non oxidative mechanisms.

Neutrophils obtained from the peripheral blood, oral cavity, or saliva

of smokers or exposed in vitro to whole tobacco smoke or nicotine

have been shown to demonstrate functional alterations in

chemotaxis, phagocytosis and the oxidative burst.

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SMOKERS

Nicotine

impede the recruitment of important host

defense cells to the area of inflammation

ICAM-1

ELAM-1

Neutrophil elastase & MMP-8.

Neutrophil

(koundouros et al,

1996,palmer et al1999,Scott et al

2000)

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EFFECTSOFSMOKING & TOBACCOON

NEUTROPHILCHEMOTAXIS (Robinset al 1991)

C5aNeutrophils

CR3 C5a des Arg

degraded

+

GcG

Chemotactic activity

CFI

SMOKE

Accumulation of neutrophils in the lung

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EFFECTS OF SMOKING & TOBACCOON

NEUTROPHIL-MEDIATED TISSUE DAMAGE

Human neutrophil elastase (HNE) is a serine protease Capable of

degrading a wide variety of connective tissue macromolecules

such as fibronectin, proteoglycan, collagen, and laminin.

The 02 produced by neutrophils may inactivate l-PI and lead to

increased HNE activity.

EFFECTS OF TOBACCO & SMOKING ON NEUTROPHIL-

MEDIATED DNA DAMAGE

Neutrophil derived reactive oxidants are also potential carcinogens

which directly damage DNA& compromise DNA repair mechanism.

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EFFECTSOFTOBACCO & SMOKINGONMACROPHAGES

Macrophage cell numbers

Cellularity

macrophage-colony-

stimulating factorChemotaxis

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a) EFFECTSOFSMOKING & TOBACCOONCYTOKINE

PRODUCTION BYMACROPHAGES

Smokeless tobacco suppresses LPS-induced IL-1

production by peripheral blood monocytes, suggesting that

products of tobacco combustion are not required for the

suppression of cytokine production

IL-6 and TNF

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b) EFFECTSOFSMOKING & TOBACCOONTHE PRODUCTIONOFLIPIDMEDIATORS

Macrophage-derived lipid mediators are the eicosanoids,

platelet-activating factor (PAF), and platelet activating

factor-like lipids (PAF-LL).

Levels of prostaglandin E2 (PGE2) are similar in

smoker and non-smoker BALF. In contrast, both

smokeless tobacco and nicotine potentiates the capacityof LPS to stimulate PGE2 production by peripheral

blood monocytes in in vitro experiments (Payne et al,

1994).

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In human system both chronic and acute smoking results inincreased plasma levels of PAF like lipids.

C) EFFECTS OF SMOKING & TOBACCO ON

PHAGOCYTOSIS

Phagolysosomes are larger in AM from smokers

compared with non-smokers, indicating that, regardless

of its effect on phagocytosis smoking suppresses thecatabolism of ingested Particles

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D) EFFECTSOFSMOKING & TOBACCOONTUMORICIDAL

ACTIVITY & OXYGENMETABOLISM

Tobacco smoke compromises macrophage cytotoxicity. Both intact AM

(contact-medi-ated) and supernatant- (cytokine-mediated) mediatedcytolysis of A549 cells are reduced in AM from smokers compared with

AM from non-smokers.

The decrease in tumoricidal activity may relate to decreased production

of TNF by smoker AM.

Reduced oxygen metabolism in AM from smokers could result in a

reduction in oxygen-mediated tissue damage and inflammation.

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Expression of the cathepsins

Process and present antigens

Class II MHC complex

Antigen presentation to T-lymphocytes

E) EFFECTS OF SMOKING & TOBACCOON ANTIGENPRESENTATION

Immune response

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3)a.EFFECTSOFSMOKING & TOBACCOONTHE NUMBER OFNK

CELLSsignificant decrease in the proportion of circulating NK cells in Caucasian

subjects, and this appears to persist for many years after the cessation of

smoking

b) EFFECTOFTOBACCOANDSMOKINGONNKCELLS

CYTOLYTICACTIVITY

The lytic capacity of NK cells varies from study to study but the

general consensus is that cigarette smoking reduces peripheral bloodNK cell cytotoxic activity. A recent report shows that smokers who

abstain from smoking for 31 days exhibit higher levels of peripheral

blood NK cell activity than smokers who continue to smoke during the

same period

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c) MECHANISMFOR THESUPPRESSIONOFNKCELL

ACTIVITY BYSMOKING

It is possible that antibodies to tobacco antigens may form

immune complexes which activate immunoregulatory cells such

as monocytes to secreate NK cell-inhibitory molecules

4) EFFECTS OF TOBACCOAND SMOKING ON B-LYMPKOCYTE

FUNCTION AND IMMUNOGLOBULIN PRODUCTION

A) Effects of tobacco and smoking on immunoglobulin levels in

serum

Studies suggest that smoking reduces the concentration ofimmunoglobulin G in human serum. The levels of IgG in serum tend to

increase when subjects stop smoking

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B) Effects of tobacco and smoking on B-lymphocyte

functionThe levels of serum IgG are reduced

in vitro experiments indicate that B-cells isolated from smokers'

peripheral blood have reduced proliferative responses to both

polyclonal B-cell activators (mitogens) and antigens (Sopori et al,

1989; Savage et al, 091- Goud et al, 1992). These data suggest that

B-cells are present in the peripheral blood of smokers but are

functionally compromised

Interestingly, there is a syndrome in which smokers actually exhibit

increased numbers of peripheral blood B cells. Persistent PolyclonalLymphocytosis (PPL) is a rare disorder which primarily affects women

who are heavy smokers and express HLA DR7 MHC antigen.

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5) EFFECTS OF SMOKING AND TOBACCO ON T-

LYMPHOCYTES

The effects of tobacco and smoking on the numbers of peripheral

blood T-cells are controversial. Most of these studies focus on the

number ofCD4+ (helper) T-cells, and variable reports of decreased,

increased or no changes in the numbers of these cells are available.

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EFFECTOFTOBACCO & SMOKINGONTHENUMBERSOFT-

LYMPHOCYTES IN PERIPHERAL BLOODAND BALF

Reduces the proliferative response of peripheral blood and BALF

lymphocytes to both antigens and T-cell mitogens (Chang et at, 19%;

Johnson tt al. I990).

B) EFFECTOFTOBACCO & SMOKINGONT-LYMPHOCYTE

CYTOKINE PRODUCTION

smokers' T-cells would produce smaller amounts of cytokine than T-cells

from non-smokers.

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LOCALEFFECTSOFNICOTINE

The oral tissues of smokers are exposed to high nicotine concentrations

that negatively affect local cell populations, gingival crevicular fluid nicotine

concentrations can be up to nearly 300 times that of nicotine plasma

concentrations in smokers (20 ng/ml).

With developing inflammation, increases in GCF flow, Bleeding on

probing & gingival blood vessels are less in smokers than nonsmokers. In

addition the oxygen conc in healthy gingival tissues appears to be less in

smokers.

Subgingival temperature are lower & recovery from the vasoconstrictioncaused by LA administration takes longer time in smokers

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Nicotine binds to root surface in smokers, and in vitro studies show it

can alterfibroblast attachment and integrin expression, and decrease

collagen production while increasing collagenase production. Root

surfaces of teeth extracted from smokers show reduced periodontal

ligament (PDL) fibroblast attachment as compared to those from non-

smokers.

Furthermore, animal studies have shown that local nicotine delivery

negatively impacts bone healing, which may be related to inhibited

expression of various growth factors and delayed revascularization.

These findings might help explain the diminished treatment response

to surgical periodontal procedures, especially those involving tissueregeneration.

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Cultured gingival keratinocytes and fibroblasts exposed tonicotine produce higher amounts of the proinflammatory

cytokines 1L-1 and 1L-6, respectively.( johnson GK, organ CC,

wendell KJ, stein SH)

Furthermore, there is evidence of a synergistic effect on

inflammatory mediator production when bacterial

Lipopolysaccharide is combined with nicotine. Taken together,

these Factors could contribute to the increased tissue destruction

observed in smokers (wendell KJ, stein SH et al)

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GENETIC POLYMORPHISMANDSMOKING

Studies looking at tooth loss reported that a positive genotype forIL-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 7.7times

In a study of 154 patients, the authors evaluated the possible

pharmacogenetic interaction of arylamines produced in tobacco

smoke and the N-acetyltransferase 2 (NAT2) profile of patients

with periodontal disease.

The inactivation of arylamines by acetylation may be involved in

detoxification of tobacco smoke

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The NAT2 polymorphism affects the population, making

individuals into rapid or slow acetylators. Results indicated that

patients with the most severe periodontal condition were the slowacetylators (risk ratio of more than 2).

The authors speculate that the altered metabolism of arylamines

may influence the immune response and may act as

immunosuppressants.

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EFFECTSOFSMOKINGON PERIODONTAL

THERAPY

Non- surgical and Surgical Therapy

Studies show that probing depth reduction and clinical attachment

level improvements in smokers are 50% to 75% those of non-

smokers following non-surgical and surgical periodontal 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 inclinical attachment levels following scaling and root planing.

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Following flap debridement surgery, smokers

experienced up to 1 mm less improvement in clinical

attachment levels in probing depths initially >7 mm.

In terms of dose response, heavy smokers (>20

cigarettes per day) to respond less favorably than light

smokers (

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Antimicrobial Therapy in Smokers

Because of the diminished treatment response in smokers,

clinicians may recommend adjunctive antimicrobial therapy for

smokers. This practice may be justified by evidence that

suggests subgingival pathogens are more difficult to eliminate in

smokers following scaling and root planing.

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Soder et al concluded that there was little adjunctive effect of

systemic metronidazole on non-surgical therapy in smokers.

On the other hand, in studies where adjunctive systemic

amoxicillin and metronidazole or locally delivered minocycline

microspheres enhanced the results of mechanical therapy, there

was a greater difference between the control and experimental

treatments within smokers as compared to within non-smokers.

These enhanced results might be due to antimicrobial actions,

and in the case of tetracycline derivatives, anticollagenaseactiv-ity.

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A recent study reported a positive response to sub-

antimicrobial doxycycline (anticollagenase) therapy in

combination with scaling and root planing in a group of severe

periodontitis patients that included smokers;

however, the comparative effectiveness of this host-modulatory therapy in smokers versus non-smokers has not

been reported.

Unique regimens that sequence systemic antimicrobial therapy

or combined local antimicrobial delivery with host-modulatory

therapy might offer clinicians and patients options that addressmicrobial and host response alterations in smokers.

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Soft and Hard TissueGrafting

In Harris' study of 100 consecutively treated recession sites using a

connective tissue with partial-thickness pedicle graft there was no

difference in the percentage of root coverage achieved between

light smokers (97%) heavy smokers (99%) or non-smokers(98%).

On the other hand, when expanded polytetrafluoroethylene

mem-branes were utilized in GTR pro-cedures at recession sites,

smokers had significantly less root coverage(57%) compared to

non-smokers (78%).

The superior blood supply afforded by the subepithelial connectivetissue graft might be more resistant to the effects of smoking as

compared to the nonresorbable barrier membrane.

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Smoking is detrimental to regenerative therapy whether treatment

includes osseous qrafts, membranes alone, membranes in combination

with osseous grafts.

In these studies, the results have shown less than 50%as much

improvement in clinical attachment levels in smokers compared to non

smokers which amounted to differences ranging from 0.35 mm to 2.9

mm.

In studies that evaluated osseous changes by sound probing or reentry,

vertical bone gain in smokers ranged from 0.1 to 0.5 mm, whereas non-

smokers demon-strated 0.9 to 3.7 mm improvement.

In terms of stability of treatment results, Cortellini et al found, that stability

was related to patient factors; patients who smoked, were non-compliant

with recall, and had deteriorating oral hygiene lost attachment (2.2 to 2.4

mm) following both guided tissue regeneration and scaling and root

planing treatment modalities.

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Implant Therapy

Based on a multivariate statistical model adjusted for age, gender, and jaw

position, smoking is significantly associated with implant failure. In the

studies reviewed, 0% to 17% of implants placed in smokers were reported

as failures as compared to 2% to 7% in non-smokers, with the majority of

studies showing at least twice as many failed implants in smokers.

The largest data set on the influence of smoking on implant success

comes from the DICRG of the Department of veterans Affairs (DVA); this is

an 8-year, randomized, prospective clinical study that includes more than

2,900 implants in more than 800 patients at 32 clinical centers.

The 3-year data demonstrated that 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; thereafter the differences between smokers and non-

smokers tended to disappear.

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The DlCRG reported that the percentage of maxillary implant failures

among smokers (10.9%) was almost twice that reported for non-

smokers or past smokers (6.4%). number of studies show little

difference in implant loss between smokers and non-smokers in the

mandible.

It is important to note that even with an increased number of implant

failures in smokers, the percentage of successful implants in most

studies still ranged from the upper 80s to low 90s.

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MaintenanceTherapy

The detrimental effects of smoking on treatment outcomes appear to be

long-lasting and independent of the frequency of maintenance therapy.

After four different modalities of therapy, including scaling, scaling and

root planing, modified Widman flap surgery, and osseous surgery,

maintenance therapy was performed by an hygienist every 3 months

for 7 years.

Smokers consistently had deeper pockets than nonsmokers and less

gain in attachment when evaluated each year for the 7 year period.

Heavy smokers (>20 cigarettes/day) had more plaque than light

smokers, former smokers and non smokers.

Even with more intensive maintenance therapy given every month for6

months after flap surgery, smokers had deeper and more residual

pockets than nonsmokers, even though no significant differences in

plaque or bleeding on probing scores were found.

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Recurrent (Refractory) Disease

Because of the difficulty in controlling periodontal disease in smokers,

many smokers become refractory to traditional periodontal treatment

and tend to show more periodontal breakdown than nonsmokers after

therapy.

The question has been raised as to whether patients are truly

refractive to therapy or whether the therapy administered was

insufficient to control the dis-ease process.

It is now thought that patients formerly considered refractive to

therapy actually undergo con-tinuous or recurrent disease; for thisreason, the diagnosis of "refractory periodontitis" has been removed

as a distinct classification

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Impact of SmokingC

essation on Periodontal Status andTreatment Outcomes

While smoking cessation does not reverse the past effects of

smoking, there is abundant evidence that the rate of bone and

attachment loss slows after patients quit smoking, and that theirdisease severity is intermediate to that of current and non smokers.

It is encouraging to note that former smokers respond to non

surgical and surgical therapy in a manner similar to never smokers.

In fact, among patients who had quit smoking 1yr or more prior to

scaling and root planing, there was no relationship between thenumber of years since cessation and changes in probing depth or

clinical attachment levels.

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According to Bain, if patients quit smoking 1 week before and. 8 weeks

after implant placement, early implant failures similar to non-smokers.

Due to the highly addictive nature of nicotine, most patients will not beable to comply with a "cold-turkey" approach. Therefore, clinical studies

should examine implant success rates in patients employing other

smoking cessation strategies that include behavioral management and

pharmaco-therapy.

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ROLEOFDENTAL HEALTH PROFESSIONALS INTOBACCO

CESSATION

Dentistry has a strong history of commitment to preventive education as

a routine part of patient treatment. Dentists and dental hygienists have

training in Patient education that can be applied easily to tobacco use

intervention methodologies.

The practice of periodontics offers multiple opportunites for interaction

with patients: during active treatment and especially in the ongoing long-

term maintenance phase of care. Because of the negative impact of

tobacco use on periodontal treatment, an additional motivation for

cessation can be demonstrated over time and used effectively to helppatients ultimately achieve a tobacco-free life.

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Nicotine dependence is classified as chemical addiction by theAmerican

Psychiatric Association in the Diagnostic and Statistical Manual of MentalDisorders 1994(DSM-1V).

the main motivation behind continued use is relief of withdrawal

symptoms.

The symptoms can include irritability, anx-iety, decreased heart rate,increased appetite, food cravings, restlessness, and difficulty

concentrating.

A systematic approach that combines behavioral counseling with

pharmacotherapy has been shown to achieve the highest rates of

cessation, although each is also effective alone. These types of approaches used together address both the nicotine withdrawal symptoms

and the psychological factors that must be faced to achieve abstinence

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TOBACCO INTERVENTION-MODELSFOR THEDENTAL

PRACTICE

Brief Intervention Program

There are several barriers that have been identified which interfere

with delivery of tobacco use intervention. .A lack of information

about treatment options, time constraints, lack of compensation,

and unrealistic expectations are common reasons that preventpractitioners from offering these services.

In offices where time an issue or where practitioners lack

confidence in pursuing more comprehensive programs, a usefulmodel for brief intervention that uses a five-step approach is

recommended by the Agency for Health Care Research and

Quality

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The program is known as the five A's for smoking cessation, it

includes:

Ask - systemati-cally identifying the tobacco use status of all

patients;

Advise - strongly advising all who use tobacco prod-ucts to stop;

Assess - evaluating the patient's willing-ness to quit;

Assist - offering assistance in quitting; and

Arrange - following up on the patient's cessation efforts, especiallyearly in the process.

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The emphasis in this brief intervention is to offer information,

encouragement, and support to patients, and to provide information

about resources that may help the patient become tobacco free.

All smokers benefit from the advice of a trusted health professional; in

up to 10% of cases, the simple statement of encouragement to stop

smoking will cause the patient to give up smoking.

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Comprehensive Intervention Program

A model for a comprehensive program in the dental office includesusing the five A's and expanding the scope of intervention. The most

ideal person to implement this program in the dental office is a dental

hygienist.

Implementing office systems to systematically identify tobacco users

and to update tobacco use information regularly is a critical

component of a comprehensive program in the dental office. It

provides an opportunity to give regular reinforcement of the specific

harmful effects of tobacco use.

A cessation program tailored to the patient's needs should be offered,one that ideally combines counseling, pharmacological therapy using

both nicotine replacement and other medications, and supportive

follow-up.

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Expanding the Five A's forComprehensive interventlon

ASK;Identification of the patient's tobacco use status (current, former,

or never) is the first step in all interventions. Once a patient is

identified as a tobacco user, additional information on the

patient's level of addiction is useful.

The fagerstrom test is easily administered and commonly used

to assess nicotine dependence levels. The Fagerstrom test is

scored based on answer to questions about timing of the first

cigarette smoked in the day, difficulty in not smoking in forbidden

areas, most important cigarette during the day, number of

cigarettes smoked per day, timing of most inters smoking, andsmoking when ill. Higher scores indi-cate more addicted

smokers.

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Advise.All oral health professionals should advise patients who smoke of the

associations between the oral disease and smoking, and advise them thatsmoking cessation would be beneficial.

A good time to discuss this is after the periodontal examination has been

completed and during a review of the etiologic factors involved in

periodontal diseases.

Facts regarding the strength of smoking as a risk factor for disease, its

impact on treatment, and the positive impact of cessation are statements

that can be included in a manner that is informative and not judgmental.

The patient, responses during this discussion will provide insight into theirinterest in cessation and level of readiness for cessation. Educational

resource for patients are available from several organization including AAP,

ADA,ACS etc. There are also numerous sites available on the Internet for

information and support for smokers who are trying to quit.

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AssessThe next step is to identify the patient's interest and readiness to

attempt tobacco cessation.

A transtheoretical model for readiness to change is useful for

evaluation of addictive behaviors, and is used frequently for

tobacco cessation counseling.

It is a five stage model that identifies behavior changes as a

process involving movement through these categories This

model is described as a spiral, and includes precontemplation,

contemplation, preparation, action, and maintenance.

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The most effective interventions can occur when the patient is in the

preparation or action stage, but all patients can benefit from appropriate

counseling based on their current stage of change.

Intervention should be considered successful if some moment is made

in the stages of change model even if it does not lead immediately to

cessation.

Patients in the precontemplative or contemplate stages are currentlyunwilling to stop using tobacco and any intervention should focus on

education reassurance, and motivation to consider cessation.

Patients in the preparation stage are willing to attempt cessation and are

ready for behavioral intervention and pharmacological therapy.

When patients are in active or maintanence stage, relapse prevention is

critical to continued abstinence. Patient may cycle through these stages

multiple times before they achieve success in becoming tobacco free.

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AssistA style of behavior change counseling that has grown in popularity is

motivational interviewing, a method that helps patients explore and

resolve ambivalence about changing behaviors.

The principles and techniques are particularly useful for health care

practitioners who are not formally trained in counseling. Motivational

interviewing is described as the process of resolving ambivalence,

using the patient's own reasons for concern and arguments for

change.

It involves creating collaborative effort with the patient to overcomeadditive behaviors.

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There are many other alternatives in behavioral therapy that have

been studied and used successfully in tobacco use counseling.Some behavioral therapy attempts to break the association between

smoking and pleasant events. Stimulus control helps the developed

behaviors to identify cues that trigger smoking and then to create

strategies to cope with these cues.

Another popular technique is hypnosis which uses suggestion,focused attention, and the therapeutic relationship to attempt to alter

the patient's behavior.

Overall, the use of behav-ioral techniques has been shown to have

2% to 14% effectiveness in cessation, defined as tobacco free for atleast 6 months. The best use of behavioral intervention might be in

combination with pharmacological treatment.

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Arrange.

If the patient made a commitment to smoking cessation, follow-up from

the office is critical.

Methods of maintaining contact with the patient can range from

appointments for office visits for monitoring and continued counseling,to letters or telephone calls confirming quit dates and encouraging

follow-through with cessation.

The most difficult time for patients is usually during the first week of

cessation .Research shows that cessation rates are positivelyinfluenced by follow-up contact.

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PharmacotherapyThe use of pharmacotherapy in tobacco cessation begins in the

1980s, when nicotine replacement therapy was introduced.

The U.S. Food and Drug Administration (FDA) currently approves

nicotine chewing gum, nicotine lozenges ,nicotine patches,

nicotine nasal sprays and nicotine inhalers for use in patients whoare attempting cessation. The patches, chewing gum, and

lozenges are available as over the -counter products; the inhaler

and nasal spray require prescriptions.

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Nicotine replacement products act as nicotine delivery systems in lieu

of tobacco and can decrease withdrawal symptoms. One nonnicotine

medication, sustained-release bupropion is also approved for tobacco

cessation pharmacotherapy. In larger doses, bupropion is used as an

antidepressant.

These medications have been proven safe and effective, and have

been extensively studied alone, in combination, and as an adjunct to

behavioral therapy. Barring complications, all patients attempting

cessation should be treated with at least one form of pharmacotherapy.

In general, the addition of medication to behavioral therapy doublescessation rates.

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Nicotine replacement products and sustained release bupropion

considered first-line therapies .

Clonidine and nortriptyline are second-line pharmacotherapies that

have been studied for cessation therapy, but have more side effects

and are not approved at this time by the FDA for use in tobacco

cessation.

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Indications forUse of Pharmacotherapy

In creating a personalized treatment plan for tobacco cessation, the

patient's health history is important the presence of other health

problems may influence the approach that is used, and consultationand cooperative treatment in conjunction with the patient's physician

are always appropriate.

The use of nicotine replacement products should be related to the

patient's current nicotine exposure, and to past experiences with

cessation..

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There are 3 mg of nicotine available in a single cigarette. On

average, a smoker gets approximately 1 mg from a cigarette

leisurely smoked over about a 5minute period.

However, smokers who smoke more rapidly and inhale deeply canget up to 3mg of nicotine from a cigarette. The ability to

subconsciously titrate nicotine dosages is one of the reasons that

patients who claim they have decreased the number of cigarettes

smoked per day are still able to maintain the same blood levels of

nicotine with fewer cigarettes, and successfully prevent withdrawal

symp-toms.

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Nicotine Replacement Therapy

There are a variety of nicotine replacement products available,

including gum, lozenge, patch, nasal spray and inhaler.

The selection of the type of nicotine replacement should be

individualized based on the patients smoking habits andpreferences for patients who smoke a pack (20 cigarettes or less a

day) the patch is the most popular form of replacement.

Nicotine patches provide a steady delivery of nicotine throughout

the time that the patch is in contact with the skin.

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Some patients may experience sleep disturbances if they wear

the patch at night, but those effects often disappear over time.

Removing the patch at night is always an option.

Nicotine patches come in several different dosages ranging from

7 to 22 mg. After the patient has been smoke free for at least 4

weeks or longer, tapering to lesser-strength patches at 2-week

intervals has been recommended.

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Nicotine Replacement Combinations

Patients who smoke more than 20 cigarettes per day or who havehad unsuccessful cessation attempts might benefit from a

combination of nicotine replace-ment products to increase the blood

levels of nicotine.

Several combinations have been studied, but the usual

recommendation is using the patch for constant nicotine blood

levels, and adding one of the other products (gum, nasal spray,

lozenge, or inhaler) as an addition for acute needs.

While the patient is using nicotine replacement products, they should

not use any other form of tobacco. If the patient has not stopped

using tobacco products while using nicotine replacement, thetherapy should be stopped, and a new treatment plan formulated

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Bupropion

Use of sustained-release bupropion has been shown to assist incessation attempts, both alone and in addition to nicotine

replacement products.

The mechanism of action is unknown, but may be related to

enhancement of dopamine and norepinephrine levels.

Side effects include a lowering of the seizure threshold so patients

with known seizure disorders are not candidates for use.

Contraindications; History of eating disorders, or concomitant use

of weilbutrin or monoamine oxidase inhibitors.

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Although it is considered a first-line of pharmacotherapy for smoking

cessation and can be used alone, it is effective when used incombination with nicotine replacement products, and may be

particularly helpful with heavy smokers or smokers who have

experienced multiple failed cessation attempts.

bupropion use should be initiated at least 2 weeks prior to the patientcessation date and subsequent initiation of nicotine replacement

therapy ,such as the patch therapy should start with 150 mg once per

day for 3 days then twice per day with at least 8 hours b/w doses.

the length of treatment can range from 7-12 weeks but bupropion

can safely be used for up to 6 months for maintenance therapy.

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Relapse Prevention

Since nicotine dependence is chronic, the tendency for relapse ishigh. Instead of seeing relapse as failure, it can be viewed by the

practitioner as an indication that alternate treatment approaches might

be indicated, just as the treatment of particularly challenging

periodontal conditions requires a treatment plan unique patient's

circumstances.

Smokers often experience several attempts at cessation before long-

term abstinence is achieved and are more likely to have success

when they have help with quitting. All former tobacco users in the

practice should be regularly encouraged to remain abstinent .for

patients who have recently quit, discussion should include the benefitsof cessation, the success they have had, , the problem they have

encountered .Scheduling follow up visits sending notes and making

telephone calls of support are examples of activities that can help

patients remain abstinent.

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Thank u