EFFECTS OF TOBACCO AND SMOKING ON PERIODONTIUM

PRESENTED BY MANASA. A II YR PG

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

INTRODUCTION

Composition of tobacco

CDC 2004

Toxic components of tobacco

The gas phase - carbon monoxide, ammonia, formaldehyde, hydrogen cyanide, and many other toxic and irritant compounds, including more than 60 known carcinogens such as benzo(a)pyrene and dimethylnitrosamine. The particulate phase - nicotine, tar (itself made up of many toxic chemicals), benzene, and benzo(a)pyrene.
Tar is inhaled with the smoke and in its condensate form, is the sticky brown substance that stains fingers and teeth yellow/brown. Nicotine, an alkaloid, is found within the tobacco leaf and evaporates when the cigarette is lighted. It is quickly absorbed in the lung and reaches the brain within 10 to 19 seconds. Nicotine is highly addictive and causes a rise in blood pressure, increased heart rate and respiratory rate, and peripheral vasoconstriction.

Assessment of smoking

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

Smokers have smoked 100 cigarettes in their lifetime and currently smoke. Former smokers have smoked 100 cigarettes in their lifetime and do not currently smoke. Nonsmokers have not smoked 100 cigarettes in their lifetime and do not currently smoke.
CDC 2004

Assessment of smoking

Serum cotinine levels which is a metabolite of nicotine

Reliable method

Smoking - true risk factor

Gelesky 1999, smoking meets the majority of criteria given for causation of a disease. True risk factor for periodontitis. It has been associated with two to three fold increases in the odds of developing clinically detectable periodontitis and subsequent tooth loss. (Tonnetti 1998) An overwhelming body of data from multiple cross-sectional and longitudinal studies conducted have demonstrated pocket depth and clinical attachment loss were more prevalent and severe in patient who smoke compared with non-smokers. (Carranza 11th ed..)

Smoking - true risk factor

Smoking is the second strongest modifiable risk factor for periodontal disease after the first one which is the microbial dental plaque. (Nurcan Buduneli 2012)

Prevalence of smoking
There are 1.1 billion smokers worldwide and 182 million (16.6%) of them live 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% use smokeless tobacco. (Preetha 2007) The prevalence of smoking among 13-15 year old school going students in India ranges from 19.7-34.5%

Smoking and Acute Necrotizing Ulcerative Gingivitis (ANUG)

An association between necrotizing forms of periodontal disease and tobacco smoking was reported as early as 1947 and has long been considered an etiologic factor in ANUG.
Preexisting gingivitis

smoking

emotional/psychic stress

It influence the tissue response to irritation. Karadachi et al. 1974 - smoking activates the release of epinephrine and promotes contraction of peripheral vessels reducing blood flow to the gingiva

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

Interaction Between Smoking and Systemic Health Status

In an Erie County Pennsylvania study the combination of diabetes and heavy smoking in an individual over the age of 45 years who harbored P. gingivalis or T. forsythesis resulted in an odds ratio of attachment loss 30 times that of a person lacking these risk factors Smoking also increases the risk of attachment and/or bone loss in AIDS and HIV serotype patients.

Vandana 2008

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 disease or becoming edentulous as do non smokers. It was found that no significant difference in loss of alveolar bone height when comparing male and female smokers. (Carranza 11th ed)

Cigarette Smoking and Oral Hygiene

Several studies demonstrated higher levels of oral debris in smokers than in non-smokers. Increased levels of debris observed in smokers have been tentatively attributed to personality traits leading to decreased oral hygiene habits, increased rates of plaque formation, or a combination of the above. The toothbrushing efficiency of smokers was much less and the calcium concentration in the dental plaque of smokers was found to be significantly higher than in nonsmokers (Bergstrom J 2000)

Effect of Smoking on Plaque

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

Macgregor (1984) measured the area of stained plaque, and the proportion of gingival margin in contact with plaque in 64 smokers and 64 non-smokers, matched for age and sex. In both sexes, smokers had significantly more plaque than non-smokers, and there was a trend towards increased plaque deposits with increasing cigarette consumption.

Effect of Smoking on Plaque

Feldman (1985), in the study of periodontal measures, found significantly less plaque in smokers than in nonsmokers. Bergstrom and Eliasson (1987) similarly found no difference in mean Pl index 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 plaque in smokers and non-smokers.

Smoking and gingival inflammation

A reduction in clinical signs of gingivitis has been reported in smokers and this effect has been shown to be independent of plaque levels (Markkanen 1984) Heavy smokers may have greyish discoloration and hyperkeratosis of the gingiva: an increased number of keratinized cells has been found in the gingiva of smokers. Changes in the epithelium were described as keratotic, hyperkeratotic and hyperplastic (Bajagic V 2006)

Smoking and gingival bleeding

smoking is known to produce peripheral vasoconstriction but in some subjects this is preceded by vasodilatation. In any particular instance, the effect produced is probably related to the degree of inhalation of the tobacco smoke and the rate of nicotine absorption (Muller HP 2002) Nicotine from cigarette stimulates the sympathetic ganglia to produce neurotransmitters including catecholamines (Trauth JA 2001). These affect the alpha-receptors on blood vessels which in turn causes vasoconstriction.

Smoking and gingival bleeding

Bergstrom et al. 1983 have found less gingival bleeding in smokers may also 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 smoking compromised blood flow in the periodontal tissues. Tobacco use has also been associated with reduced permeability of peripheral blood vessels.

Smoking and gingival bleeding

Interestingly, in smokers undergoing smoking cessation programs, gingival bleeding and gingival blood flow, as well as gingival crevicular fluid flow, increase and normalize toward non-smoker levels after quitting. (Nair 2003, Morozumi 2004)

Smoking & Oxygen tension in gingival tissues

Oxygen saturation of hemoglobin is affected by cigarette smoking, and attempts 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 the presence of inflammation converse was shown They also examined oxygen tension in periodontal pockets and demonstrated oxygen tension was significantly lower in smokers. (Palmer 2005)

Effects on the Gingival Vasculature

The vasculature has also been examined in histological and immunocytochemical studies It was found that high proportion of small vessels compared with large vessels in smokers than non-smokers but no difference in the vasculature density. (Mirbod 2001)

Smoking and oral microorganisms

Cigarette smoking could cause a lowering of the oxidation-reduction potential (Eh), and this could cause an increase in anaerobic plaque bacteria (Kinane DF 1997). There was a statistically significant increase in the proportion of Grampositive to Gram-negative bacteria in 3-day-old plaque from smokers, when compared with the non-smokers (Stoltenberg JL 1993).

Smoking and oral microorganisms

Tobacco smoke contains phenols and cyanides, which can account for antibacterial and toxic properties. Smokers harboured significantly higher levels and were at significantly greater risk of infection with Tanarella forsythensis than non-smokers (Zambon JJ 1996). Adjusting for disease severity, Porphyromonas gingivalis was also more likely to subgingivally infect smokers than non-smokers (Sayers NM 1999). However, there was not a significantly higher relative risk for infection with this bacterium.

Smoking and Calculus formation

There have been consistent reports of more calculus in smokers than in non-smokers from the earliest epidemiological studies (Martinez-Ganut P 1995). Some authors reported that significantly more pipe smokers than cigarette smokers had supragingival calculus. This might be because the pH of pipe smoke is higher than that of cigarette smoke, and because pipe smokers circulate the smoke around the mouth, whereas cigarette smoke tends to be inhaled (Albandar JM 2000).

Moreover, the smoking cycle is much longer in pipe smokers than in cigarette smokers, causing pipe smokers to salivate more (Bergstrom J 2005).

Smoking and Calculus formation

There is an increased calcium concentration in fresh saliva in smokers following smoking (Khan GJ 2005). Nicotine affects the exocrine glands by an initial increase in salivary and bronchial secretions that are followed by inhibition of the secretions. The increased amount of calculus found in smokers might therefore be due to an effect of tobacco smoke upon properties of saliva (Erdimir 2006).

Smoking and Calculus formation

The reasons for an elevated calcification rate in smokers are not known, but it has been speculated that it might be coincident with the increased risk in smokers for ectopic calcification. (Bergstrom 2005)

Smoking and periodontal disease

Multiple cross-sectional and longitudinal studies have demonstrated that pocket depth, attachment loss, and alveolar bone loss are more prevalent and 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 had never smoked

Former smokers were 1.7 times more likely to have periodontitis than persons who had never smoked

(Tomar SL 2000)

Smoking and periodontal disease

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 of years since quitting.

(Tomar SL 2000)

Smoking and periodontal disease

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 relation to tooth mobility
Feldmen 1983

not only significantly increased probing depths and alveolar bone loss, but also increased tooth mobility in smokers
Bergstrom 1991

smokers suffer from more tooth loss than non-smokers

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

dose relationship between the effect of cigarette consumption and periodontal attachment loss
Grossi 1994, Haffaji 2001, Obrodovic 2007

So the relationship is causal.

The results of the cohort studies, in particular those that have evaluated the dose-response effects, offer convincing evidence that the relation between smoking and destructive periodontal disease is causal, i.e., smoking can cause the disease. (Jan Bergstrom 2004)

Smoking & destructive periodontal disease: relative risk

Based on current evidence, the relative risk for a smoker to attract destructive periodontal disease can be estimated to be 5- to 6-fold elevated in comparison with a non-smoker. RR (Relative risk) is also dependent on the amount of exposure A smoker who has smoked 20 cigarettes a day for over 20 years runs a 20fold increased risk. (Hyman, Bergstrom 2003)

Smoking and gingival recession

Gingival recession in smokers was greater than that in non-smokers and the difference was statistically significant. Significant positive associations were noted between gingival recession and age, and between gingival recession and plaque index between smokers and non-smokers (Nikolaos Andreas 2011)

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 (Bergstrom 1986) Higher levels of TNF- (Bostrom 1998) Decreased levels of IL-1 and 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 clinically and within the tissues.

Inflammatory & immune responses in smoking

Microbial virulance

Host response

Inflammatory & immune responses in smoking

Microbial virulance

Smoking

Host response

Smoking and Fibroblast Function

Gingival Fibroblasts (Palmer 2005) Periodontal Fibroblasts

production of Type 1 collagen and fibronectin collagenase activity

Periodontal ligament (PDL) fibroblasts growth and Attachment was inhibited by nicotine at high concentrations (over 1 mg/ ml) (James 1991)
Nicotine at highconcentrations (100 ng/ml to 25g/ml) (Giannopovlou C 1999)
cytotoxic by inhibiting the vacuolation and proliferation of fibroblasts PDL cell proliferation and protein synthesis were inhibited Cell attachment was significantly less on root surfaces

Cellular changes
disruption of cell orientation changes in cytoskeleton presence of large vacuoles significant reduction in cell viability

Potential mechanisms of smoking action

Nicotine metabolites can concentrate in the periodontium and their effects
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 tobacco use and their migration through capillary walls.
Bergstrom 2004

PMN function
Important role in the defense of the marginal periodontal tissues against bacterial invasion. PMN activity to be severely depressed by a solution of tobacco-smoke where as phagocytosis and bactericidal activity were not affected. (Corberand 1980) Smokers have higher blood PMN counts than do non-smokers and chemotaxis of PMN s from smokers was suppressed relative to nonsmokers (Mac Ferlene 1992)

Adhesion molecules and smoking

Elevated levels of soluble intercellular adhesion molecule-1 (sICAM-1) in the gingival crevicular fluid (GCF) of smokers - tissue destructive activity via enzymes such as elastase (Rezavandi K 2002).

On otherhand protease inhibitor molecules alpha-1 antitrypsin and alpha2 macroglobulin are suppressed in smokers, suggesting that the destructive action of certain proteases, such as elastase, may be increased (Persson 2001)

Smoking & cytokine levels

GCF levels of Tumor necrosis factor-alpha (TNF-) and interleukin-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 depressed.

Bostrom L 1998, Giannopolou C 2003,

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

Rawlinson 2003

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

Giannopolou C 2003

Impairment of RANK/RANKL/OPG system

smoking was reported to reduce salivary osteoprotegerin concentrations in untreated and also treated chronic periodontitis patients (Buduneli et al.2008). Nicotine and lipopolysaccharide (LPS) effects on the expression of macrophage colony-stimulating factor (M-CSF), osteoprotegerin (OPG), and prostaglandin E2 (PGE2) have been evaluated by Tanaka et al. (2006) in osteoblasts and osteoclast-like cells.

OPG expression was increased in the initial stages with nicotine and LPS but decreased in the later stages

Impairment of RANK/RANKL/OPG system

Lappin et al. (2007) reported decreased serum OPG levels and greater soluble receptor activator of nuclear- factor kappa B ligand (sRANKL) sRANKL/OPG ratios in smoker patients in the maintenance program than the non-smoker counterparts. Negative correlation between pack-years and total OPG amount in peri-implant crevicular fluid was detected in clinically healthy implants (Arkan et al. 2008).

Impairment of RANK/RANKL/OPG system

Higher sRANKL, lower OPG concentrations in saliva of untreated/treated smokers than nonsmokers (Buduneli et al. 2008)

Significantly lower plasma OPG concentrations were detected in smoker chronic periodontitis patients than the smoker healthy controls (zaka et al. 2010).

Impairment of RANK/RANKL/OPG system

The plasma data reported by zaka et al. (2010) are in line with the study by Tang et al. (2009) reporting similar sRANKL and OPG levels in GCF samples of never smokers, former smokers and current smokers. In later study the only significant difference could be found in GCF OPG levels of the high pack-years group and never smokers.

Smoking and MMP levels

Pathogens in microbial dental plaque are capable of stimulating host cells to increase their matrix metalloproteinase (MMP) release which is considered among the indirect mechanisms of tissue destruction seen during periodontitis (Sorsa et al. 2006). Periodontal tissues are infiltrated mainly by neutrophilic granulocytes and PMN which play an important role in the development of inflammatory injury. Tobacco-induced degranulation events in neutrophils, tobacco-induced alterations to the microbial flora, and tobacco induced increases in proinflammatory cytokine burden could each, influence MMP-8 levels in the periodontal tissues of smokers.

Studies on MMP -8 in smokers

Knuutinen et al. (2002) noted an increased MMP-8 concentration in the resulting fluid infiltrate in smokers
Sder et al. (2002) found a positive correlation between elastase complexed to 1-antitrypsin and MMP-8 concentrations in the gingival crevicular fluid (GCF) of smokers in individuals with various persistent periodontal diseases.

Persson et al. (2003) reported that GCF MMP-8 levels remained unchanged in the smokers following surgical treatment for periodontitis, whereas decreased levels were observed in the non-smokers, suggesting a tobaccoinduced MMP-8 burden.

(zaka et al. 2011), serum MMP-8 concentrations did not differ significantly between the smokers and non-smokers.

Predisposing to cardiovascular disease..

In a recent study (zaka et al. 2011), it was hypothesised that smoking may affect MMPs and neutrophil degranulation products in the systemic level eventually leading more severe periodontal tissue destruction and systemic inflammation predisposing to cardiovascular diseases (Pussinen et al. 2007). the serum concentrations of MMP-8, MMP-9, TIMP-1, NE, and MPO were evaluated comparatively in smoker versus non-smoker patients with chronic periodontitis as well as periodontally healthy subjects. The findings of significantly elevated serum MMP-9, MPO, NE together with decreased TIMP-1 in smoker patients with chronic periodontitis than non-smoker counterparts support the idea that smoking together with periodontal destruction may expose/predispose to cardiovascular diseases.

Predisposing to COPD & Atherosclerosis..

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

ICTP levels (Carboxyterminal-telopeptide

pyridinoline)
Carboxyterminal-telopeptide pyridinoline cross-links of type I collagen (ICTP) is released into the periodontal tissues as a consequence of collagen degradation and alveolar bone resorption (Seibel 2003). ICTP was suggested to predict future bone loss, to correlate with clinical parameters and putative periodontal pathogens and also to reduce following periodontal therapy (Giannobile 1999).

osteocalcin
Osteocalcin (OC) is a calcium-binding protein of bone and the most abundant 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 patients compared with healthy subjects suggesting lower osteoblastic activity and bone formation ability (Shi et al. 1996).

ICTP & Osteocalcin levels in smoking

salivary OC levels were lower in smokers than non-smokers. ICTP levels in non-smoker chronic periodontitis patients were higher than non-smoker controls smoker healthy control group revealed higher ICTP levels than non-smoker counterparts (zaka et al. 2011) There were no significant differences in saliva ICTP concentrations between the smoker and non-smoker patient groups (Grlek et al. 2009)

Antibody production and smoking

some components of cigarette such as nicotine are immunosuppressive (Geng et al. 1996) whereas some others are immunostimulatory such as tobacco glycoprotein and metals (Francus et al. 1988, Brooks et al. 1990). Serum immunoglobulin G (IgG) levels were reduced in smoker patients with periodontitis (Quinn et al. 1998) The number of B lymphocytes seemed to be similar in smokers and nonsmokers but their function in peripheral blood was impaired in smokers

Genetic Polymorphism and Smoking

Genetic variability, its relationship with periodontal disease, and its interaction with smoking Tooth loss reported a positive genotype of IL-1 increases the risk for tooth loss by 2.7 times, while smoking increases the risk by 2.9 times. When both were combined, the risk increased to 7.7 times.

Mc Guire MK 1999 N-acetyletransferase 2 (NAT-2) polymorphism also affects the population by altering the metabolism of arylamines which may influence the immune response and may act as an immunosuppressant.
Cullinan MP 2001

Effects of Smokeless Tobacco on Periodontal Tissues

In studies done by Amarasena et al. 2003 in a Sri Lankan population has confirmed quantified tobacco use may significantly increase bleeding on probing and periodontal attachment loss Other studies have also shown the negative effect of the areca nut on host immunity 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 gingival fibroblasts (Chang 1998)

Smoking and periodontal therapy

 smoking exerts a negative influence on the outcome following non-surgical as well as surgical periodontal therapy. (Bergstrom 2004) smoking negatively influences the outcome following implant therapy and risk for implant failure is increased in smoker patients (Bain 2003) smokers contribute the vast majority of therapeutic failures or refractory cases (Magnusson 1994)

 Following non-surgical therapy including scaling, root planing and professional tooth cleaning, healing in terms of gingival bleeding reduction and 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 less healing and reduction in subgingival Tanarella forsythenssis and Porphyromonas gingivalis after treatment compared to former and nonsmokers, suggesting that smoking impair periodontal healing. Ah et al. 1994, who reported less probing depth reduction and attachment gain in smokers who had been treated by periodontal surgery, corroborated this finding that smokers were poor candidates for successful periodontal care.

 A statistically significant difference was observed in the reduction of probing depth between smokers and non-smokers at 12 month postsurgical 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 on fibroblast activity. They found that it inhibited attachment and growth of periodontal ligament fibroblasts.

Antimicrobial Therapy in Smokers

This practice may be justified by evidence suggesting subgingival pathogens are more difficult to eliminate in smokers following scaling and root planing (Grossi 1997) Soder et al. 2001 concluded there was little adjunctive effect of systemic metronidazole on non-surgical therapy in smokers A few studies have reported adjunctive systemic amoxicillin and metronidazole or locally delivered minocycline microspheres enhanced the results of mechanical therapy. (Heasman 2006)

A study reported a positive response to sub-antimicrobial doxycycline (anticollagenase) therapy in combination with scaling and root planning in smokers with severe chronic periodontitis (Novak 2002)

Soft and Hard Tissue Grafting

recession sites were treated using connective tissue with a partial thickness pedicle graft (Harris JJ 1994) and a coronally positioned flap alone, or with a bioabsorbable membrane (Amarante ES 2000) found no difference in root coverage between smokers and non-smokers. When guided tissue regeneration procedures were used smokers had significantly less root coverage (57%) compared to non-smokers (78%). (Trombelli 1997)

Regenerative therapy in interproximal and furcation defects

Whether treatment includes the use of osseous graft alone, bioabsorbable membrane alone, or bioabsorbable membranes in combination with osseous grafts. less than 50% as much improvement in clinical attachment levels in smokers compared to nonsmokers, which amounted to differences ranging from 0.35 mm to 2.9 mm. (Cortellini 1996)

Implant Therapy
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. The 3-year data demonstrated 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. (Georgia 2004)

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 can access. The dental team can be helpful in providing literature and guiding patients towards resources they can access. Brief Intervention Program in Primary Care

Methods of smoking cessation

Nicotine Replacement Therapy (NRT)

Methods of smoking cessation

Bupropion This medication is used as an antidepressant at higher doses but is effective for smoking cessation at lower doses. It is usually prescribed starting 12 weeks before the quit date, initially at 150 mg once per day for 6 days then 150 mg twice daily for 79 weeks. There are serious potential drug interactions so this medication should be prescribed by the patient's medical doctor. Other Methods intensive counseling, motivational interviewing, cognitive behavioral therapy, hypnosis, and acupuncture.

Impact of Smoking Cessation on Periodontal Status and Treatment Outcomes

There is abundant evidence to indicate the rate of bone and attachment loss slows after patients quit smoking and the severity of their disease is intermediate compared to current and non-smokers. Haffajee 2001, Tomer 2000, Bergstrom 2000, Albender 2000. Former smokers respond to non-surgical and surgical therapy in a manner similar to those who have never smoked (Grossi 1997) Implant success rates for past smokers were similar to those who have never smoked (Georgia 2004)

Environmental tobacco smoke & periodontitis

Among persons in the United States who had never used tobacco, those exposed to ETS were more likely to have periodontal disease than were those not exposed to ETS. Samuel James 2001

smoking and periodontal health in the future

smoking is associated with over 40 various diseases, it is evident that the periodontal tissues share a susceptibility to smoking with 40 other tissues or 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 a systemic rather than a local disease. (Bergstrom 2004)

smoking and periodontal health in the future

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

The end stage of lung destruction is loss of respiratory function, and the worsening of lung function is accompanied by microbial infection that often results in acute exacerbations

End stage of periodontal destruction is the loss of masticatory function, and along with the gradual breakdown of the periodontal tissues and ensuing pocket formation, root surfaces become microbially colonized or infected.

Bergstrom 2004

 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 developing a quit plan ARRANGE Tobacco users follow up contact

Conclusion
Substantial progress has been made in our understanding of the pathogenesis of periodontal disease and host response to therapy. Clearly, the identification of individuals at high risk for periodontal disease and the factors that place them at risk has significantly improved the clinical management of these patients. The opportunity for dentists and dental hygienists to become more active in evaluation of tobacco use by patients and more aggressive in offering counseling and cessation services can positively impacts both the oral and general health of dental patients. Of all the preventive services traditionally offered within a dental practice, those related to tobacco cessation are by far the most beneficial to the patient relative to general health and quality of life.

Conclusion

Periodontal health and Prognosis for PERIODONTAL THERAPY substantially improve when patients QUIT SMOKING

REFERENCES
Carranza 11th edition 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 States Am J Public Health. 2001;91:253257 Nurcan Buduneli, Effects of Tobacco Smoking on Chronic Periodontitis and Periodontal Treatment,2012, chapter 5 , 82-96. Ana Pejid, Radmila Obradovid, Ljiljana Kesid, Draginja Kojovid Smoking And Periodontal Disease A Review Vol.14, No 2, 2007, pp. 53 59 Vandana, K Laxman, Annaji Tobacco Use and Its Effects on the Periodontium and Periodontal Therapy The Journal of Contemporary Dental Practice, Volume 9, No. 7, November 1, 2008, 1-11

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

We as PERIODONTISTS Can and Should MAKE the DIFFERENCE

Thank you