Smoking and its effects on thePeriodontium and Periodontal therapy

CONTENTS• Introduction• Epidemiological evidence• Toxic subtances in tobacco• Mechanism for negative effects of smoking on

periodontium• Effect of smoking on gingival & periodontal tissues• Smoking and periodontitis in adults• Smoking and ANUG• Smoking and systemic health• Smoking and oral health• Effect on periodontal therapy• Cessation of smoking• Conclusion

Periodontal disease is defined as inflammatory destruction of periodontal tissue and alveolar bone supporting the teeth.

Progression and severity of the disease depends on complex interactions between several risk factors such as microbial, immunological, environmental and genetic factors, as well as age, sex, and race.

.

INTRODUCTION

Tobacco smoking is a significant risk factor for periodontal disease

Specific

pathogenic bacteria

Host immune inflam-matory response

Connective tissue &bone metabolism

Clinical expression of disease,initiation progression

Environmental &acquired risk factors[SMOKING]

Genetic risk factors

Ag

LPS

Ab

PMNs

Cytokines,PGE2

MMPs

EPIDEMIOLOGICAL EVIDENCE

• Cross-sectional and case-control studies demonstrate a moderate to strong association between smoking and periodontitis[Hill’s criteria].

• Smokers are 4x as likely to develop periodontitis as non-smokers.

• Smoking may be responsible for more than half of the periodontal disease among adults.

• Up to 90% of refractory periodontitis patients are smokers. (MacFarlane et al, 1992)

RISK ASSESSMENT - ATTACHMENT LOSSVariable Estimated odds ratioAge 1.72 - 9.01Smoking 2.05 - 4.75Diabetes 2.32P gingivalis 1.59Education 0.65(Grossi et al, 1994)

healthy low moderate high severe

403020100

Pack years

ATTACHMENT LOSS AND SMOKING

(Grossi et al, 1994)

10 year prospective study of smoking andperiodontitis[Bergstrom et al 2000]

Smokers lost significantly more periodontalbone compared to non-smokers (p<0.001)

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

The effects of smoking on periodontal statusto be more pronounced in younger women.

[Goultschin et al.10]

PREVALENCE OF MODERATE AND SEVERE PERIODONTITIS

• Current smokers - 25.7%• Former heavy smokers - 20.2%• Cigar/pipe smokers - 17.6%• Non-smokers - 13.1% [ Albandar et al 2000]

Stopping smoking (for 10 years) reduces risk ofperiodontitis to that of non-smokers0-2 years -> OR=3.2>10 years -> OR=1.2

The more you smoke the worse the periodontitis(dose response)Smoking <10 cigs/day OR = 2.8Smoking >30 cigs/day OR = 6.9[Tomar and Asma 2000]

Tobacco contains over 4,000chemicals, many of which are harmful. These include:

Benzene- solvent used in fuel manufactureFormaldehyde- highly poisonous, colourless liquid used to preserve dead bodiesAmmonia- chemical found in cleaning fluids. Used in cigarettes to increase the delivery of nicotineHydrogen cyanide-poisonous gas used in the manufacture of plastics, dyes, and pesticides.- Often used as a fumigant to kill ratsCadmium- extremely poisonous metal found in batteriesAcetone- solvent found in nail polish remover

COMPONENTS OF INHALED SMOKE

•Nicotine

•Carbon monoxide

•Tar

all of which can cause disease

POTENT CARCINOGENS• Nitrosamines• Polycyclic aromatic hydrocarbons• Radiation-emitting polonium

Nicotine action

• Accelerates release of neurotransmitter dopamine in the brain’s NA*& increases metabolism in NA

*NA = nucleus accumbens

•Nicotine retards growth of gingival fibroblasts reduces fibronectin & collagen increases collagen breakdown

Other actions are:•raise blood pressure•stimulants•vasoconstriction•psychological - social dependency•physical dependancy - craving

CARBON MONOXIDE-ACTIONS

•Carbon monoxide is a poisonous gas found in car fumes, which reduces the amount of oxygen carried in the blood.

•Oxygen is vital for the body’s organs to function efficiently.

• The reduction in oxygen changes the consistency of the blood, making it thicker and putting the heart under increased strain as it pumps blood around the body

TAR-actions

•Tar contains many substances proven to cause cancer.

•Irritants found in tar damage the lungs causing narrowing of the tubes(bronchioles) and damaging the small hairs (cilia) that protect the lungs from dirt and infection

Effect of Smoking on Plaque

PERIODONTAL PATHOGENS

The proportions of subjects positive for A. actinomycetemcommitans, P. gingivalis, and T. forsythesis were higher among smokers.{Zambon et al.(1996),using a fluorescence technique

in a Cross sectional study from

Erie County Study population}

Furthermore, increased counts ofexogenous flora (Escheria coli and Candidaalbicans) have been reported in smokers

SMOKING AND HOST RESPONSE• Smoking decreases salivary IgA and

serum IgG,and specifically reduces IgG2 levels against A.a.commitans (Bennet & Read, 82; Barbour et al.,97).

• The ability of tobacco products to decrease the proliferating capacity of T and B lymphocytes might contribute to this diminished production of protective antibodies.

• Smoking can exert deleterious effects on polymorphonuclear leukocytes (PMN) and other neutrophil functions such as chemotaxis & phagocytosis so that they cannot efficiently deal with the bacterial infection

(Kenney et al., 1977; Eichel & Shahrik, 1969; Selby et al., 1992).

• Impaired phagocytosis function of neutrophils among smokers with refractory periodontitis. (MacFarlane et al., 1992).

In addition, tobacco smoking may modify the production of pro-inflammatory cytokines IL-1 and TNF-ᾳ which are considered key regulators of the host response to microbial challenge. ( Kornman et al. ,1997)

Genetic Polymorphism and Smoking

Investigators have looked at genetic variability,its relationship with periodontal disease, and itsinteraction with smoking. Tooth loss reported a positive genotype of IL-1increases 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 to7.7 times.[JCDP’08]

EFFECT OF SMOKING ON GINGIVA

Cigarette Smoking and Gingival Bleeding

Smokers expressed less gingival bleeding than non-smokers

This is also proved to be dose dependant This may be due to vasoconstrictive effect of

nicotine. Clarke et al 1984

Effect of Smoking on Gingival Blood Flow

• In smokers,gingival blood flow was significantly increasedby cigarette smoking.

• However, intravenousadministration of nicotine reduces the marginaltemperature of gingival sites suggesting adecrease in gingival blood flow which lead tothe hypothesis this phenomenon is caused byvasoconstriction induced by nicotine and stress.

Oxygen Tension in the Gingival Tissues

• Smoking Decreases Tissue Oxygen• Tissue oxygen decreases: 65 ± 7 to 44 ± 3 mmHg

[Jensen, et al. Arch Surg, 1991]• Tissue oxygen 40-50 mmHg —> infection

Effects on the Gingival Vasculatureresearchers found a high proportionof small vessels compared with large vessels insmokers than non-smokers but no difference inthe vasculature density.[journal CDP nov08]

Evidence From Studies on (GCF) Smoking may result in lower resting GCF flow rate. The increase in GCF during an experimental gingivitis may be less

in smokers. Studies have shown higher levels of TNF-α and decreased levels of

IL-1α and IL-1β ,enzyme elastase in GCF when compared between smokers and nonsmokers.

This research has demonstrated there are lower levels of cytokines, enzymes, and possibly polymorphonuclear leukocytes (PMNs).

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

Kinane and Radvar 1997

Smoking and Fibroblast FunctionGingival FibroblastsIn vitro studies have shown reduction in theproduction of Type 1 collagen and fibronectinand an increase in the collagenase activity.

Cellular changes like disruptionof cell orientation, changes in cytoskeleton,presence of large vacuoles, and significantreduction in cell viability have been noticed.

Smoking and gingival inflammation

Smokers may present with lowerlevels of gingival inflammation than nonsmokers.

Furthermore,development of gingival inflammation inresponse to experimental plaque accumulation(experimental gingivitis) was less pronouncedin smokers than in non-smokers.

[Albander et al 99, Lie et al 98]

Periodontal fibroblast PDL fibroblast growth, attachment and

integrin expression was inhibited by nicotine at high concentrations (≥1 mg/ml)

Nicotine at high concentrations (100 ng/ml to 25μg/ml) to be cytotoxic by inhibiting the vacuolation and proliferation of fibroblasts. [Giannopovlou et al.27]

PDL cell proliferation and protein synthesis were also inhibited in a dose dependent manner.

Cell attachment was significantly less on root surfaces obtained from heavy smokers compared with nonsmokers.

Smoking and periodontitis in young adults(≤35 years)

Several studies have shown young adult smokersaged 19-30 years had a higher prevalence andseverity of periodontitis compared to non-smokersdespite similar or lower plaque levels.

The prevalence of periodontitis,defined as having a site with attachment lossof ≥2 mm and probing depths of ≥4 mm, wasthree to four times higher in young smokerscompared to non-smokers.[Haber et al]

Smoking and Periodontitis in Adults

Current smokers have deeper probingdepths, greater attachment loss, more boneloss, and fewer teeth.

Smokers also exhibitmore supragingival calculus deposits.

Smokers were four times more likely to haveperiodontitis as compared to non-smokers.

Among 20-49 year-olds, the adjusted odds ratio for a mean attachment loss of 1 to 1.99 mm among current smokers was 2.29, whereas the odds ratio for attachment loss ≥3 mm was over 18.43.

This suggests smoking is particularlyimportant in the etiology of severe periodontal attachment loss.

{NHANES}

There is a strong dose-response relationshipbetween the amount smoked and the severity ofperiodontal destruction which further supports therole of smoking as a risk factor for periodontitis.

The most marked difference between smokersand non-smokers in probing depths or attachmentloss occurs in the maxillary lingual area andmandibular anterior area, suggesting a localeffect of smoking.

Effects of Smokeless Tobacco onPeriodontal Tissues

It involves chewing a quid that includes betel leaf,lime, areca nut, and tobacco.

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.

Arecanut extracts have also been shown to inhibit the growth, attachment, and matrix protein synthesis of cultured human gingival fibroblasts.

Smoking and Acute Necrotizing UlcerativeGingivitis (ANUG)

An association between necrotizing formsof periodontal disease and tobacco smokingwas reported as early as 1947 Preexisting gingivitis, emotional/psychic stress,and smoking forms a triad of interrelatedpredisposing factors in the etiology of the disease..

SMOKING

influence the tissueresponse to irritation. activates the release of epinephrine

promotes contraction of peripheral vessels

reducing blood flow to the gingiva

loss of vitality to the gingival epithelium

onset of ANUG .{Karadachi et al}

SMOKING AND SYSTEMIC HEALTH

Smoking and cardiovascular system•Smoking causes coronary heart disease, atherosclerosis, arteriosclerosis, heart attack the leading cause of death

•Cigarette smoking causes reduced circulation by narrowing the blood vessels (arteries) and puts smokers at risk of developing peripheral vascular disease

•Smoking causes abdominal aortic aneurysm (i.e., a swelling or weakening of the main artery of the body—the aorta—where it runs through the abdomen).

Smoking and Respiratory DiseaseSmoking causes lung cancer.

Smoking causes lung diseases (e.g., emphysema, bronchitis, chronic airway obstruction) by damaging the airways and alveoli (i.e., small air sacs) of the lungs.

Smoking and brain

Can cause stroke which may be fatal or cause mental and physical disability

Smoking and CancerSmoking causes the following cancers:1

*Acute myeloid leukemia*Bladder cancer*Cancer of the cervix*Cancer of the esophagus*Kidney cancer*Cancer of the larynx (voice box)*Lung cancer*Cancer of the oral cavity (mouth)*Pancreatic cancer*Cancer of the pharynx (throat)*Stomach cancer

Smoking and Other Health Effects

Smoking has many adverse reproductive and early childhood effects, including increased risk for—infertility,preterm delivery,stillbirth,low birth weight, andsudden infant death syndrome (SIDS).

Smoking is associated with the following adverse health effects:Postmenopausal women who smoke have lower bone density than women who never smoked.

SMOKING – MORBIDITY (miller et al 1999)50% of total cancer deaths84% of lung cancer deaths30% of heart disease deaths23% of respiratory deaths80% of bronchitis and emphysema deaths

Interaction between smoking and systemicHealth status and periodontitis

The combination of smoking with other systemicfactors further enhances the risk of periodontaldestruction.

.

•Studies say that 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.(JCDP nov,2008)

•Smoking also increases the risk of attachment and/or bone loss in AIDS and HIV serotype patients.

•Periodontitis also may worsen the systemic status of an individual

SMOKING AND ORAL HEALTH

Tobacco use in all forms, especially cigarette smoking, is the number one risk factor for oral cancer.Possible mechanisms are•Irritants and toxic substances in tobacco•Change in Ph•Change in immune response•Dryness due to heat produced while smoking

The most common form of cancer is Squamous cell carcinoma.

•The most common sites of the oral cancer is the tongue and the floor of the mouth.• The other common sites are buccal vestibule, buccal mucosa, gingiva and rarely hard and soft palate.• Cancer of bucco-pharyngeal mucosa is common in smokers.

Abnormal Changes at Cancerization site

• Clinically:– Leukoplakia– Erythroplasia– Dysplasia– Carcinoma in situ

OTHER LESIONS:SMOKER’S PALATE• Palate becomes white with tiny red spots-raised

duct opening of salivary glands [dried mud appearance]

SMOKER’S MELANOSIS• Brown spots on oral mucosa

HAIRY TONGUE• Overgrowth of papilla on the surface of tongue

COATED TONGUE• Tongue coated with food particles, bacteria and

debris from epithelium

DENTAL CARIES AND EROSION

• Smoking stimulates saliva flow immediately, does not affect saliva in long term

• Decrease Ph and buffering action

Dental caries Erosion

GINGIVAL RECESSION

• STAINING OF TEETH

• HALITOSIS

• DELAYED WOUND HEALING

• DRY SOCKET

• SMOKER’S FACE

Effects Of Smoking OnPeriodontal Therapy

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.

[JCDP’08]

Toothbrushing efficiency of smokers was much less andthe calcium concentration in the dental plaque of smokers was found to be significantly higher than in nonsmokers.

[Medicine and Biology Vol.14, No 2, 2007, pp. 53 – 59]

EFFECT OF SMOKING IN WOUND HEALINGSmoking hasbeen shown to impair revascularization during soft and hard tissue wound healing,which is critical for periodontal plastic, regenerative, and implant procedures. (Nolan et al.,85; Preber &Bergström, 85a; 86; 90).

Non-surgical and Surgical TherapyNumerous studies have shown smokingcompromises probing depth and/or attachmentgain outcomes following non-surgical or surgicaltherapy.

The numerical differences betweensmokers and non-smokers become morepronounced in probing depths ≥5 mm, wheresmokers demonstrated 0.4 mm to 0.6 mmless improvement in clinical attachment levelsfollowing scaling and root planning.

Following flap debridement surgery, smokers experienced upto 1 mm less improvement in clinical attachmentlevels in probing depths that were initially ≥7mm.

Antimicrobial Therapy in Smokers

• Because of the diminished treatment response insmokers, clinicians may recommend adjunctive antimicrobial therapy for smokers.

• Because subgingival pathogens are more difficult to eliminate in smokers following SRP.

• Systemic amoxicillin and metronidazole or locally delivered minocycline microspheres enhanced the results of mechanical therapy.

• A recent study reported a positive response to sub-antimicrobial doxycycline (anticollagenase) therapy in combination with SRP in a group of severe periodontitis patients that included smokers.

Soft and Hard Tissue Grafting

• In guided tissue regeneration procedures smokers had significantly less root coverage(57%) compared to nonsmokers (78%)

• Smoking is detrimental to regenerative therapy in interproximal and furcation defects, whether treatment includes the use of osseous graft, bioabsorbable membrane, or a combination.

• The results have shown less than 50% as much improvement in clinical attachment levels in smokers, which amounted to differences ranging from 0.35 mm to 2.9 mm.

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.

Maintenance phase

• ↑pocket depth• ↓gain in clinical attachment level• Deeper and more residual pockets after flap

surgery

Refractory disease• ↑recurrence and ↑need for re treatment and antibiotic therapy• ↑tooth loss after surgical therapy

TOBACCO CESSATION

64

The “5 A’s” To Intervention

• ASK about tobacco use.• ADVISE to quit.• ASSESS willingness to make a

quit attempt.• ASSIST in quit attempt.• ARRANGE for followup.

Nicotine withdrawal: the 4 ‘D’s

Delay acting on the urge to smoke

Drink water slowly

Deep breathe.

Do something else (eg exercise)

PHARMACOTHERAPYPharmacotherapy + behavioural counselling improves long-term quit rates

Smokers of 10 or more cigarettes a day who are ready to stop should be encouraged to use pharmacologial support as a cessation aid

Nicotine replacement• Begin NRT on the quit date, (apply patches the night before)

• Use a dose that controls the withdrawal symptoms

• NRT provides levels of nicotine well below smoking

• Prescribe in blocks of two weeks

• Arrange follow up to provide support

• Use a full dose for 6 to 8 weeks then stop

NRT: Nicotine nasal sp • Nasal sprays more closely mimic nicotine from cigarettes• Common side effects with nasal sprays include nasal and throat

irritation, coughing and oral burning

NRT: Nicotine gum• Instruct the patient to ‘chew and park’• Absorption may be impaired by coffee and some acidic drinks • Common side effects with gum include gastrointestinal disturbances and jaw pain• Dentures may be a problem!

• Patches provide a slow, consistent release of nicotine throughout the day

• Available in various shapes and sizes,• Common side effects with patches include skin sensitivity and

irritation

NRT: Nicotine patches

• Begin bupropion a week before the quit date

• Normal dose 150mg bd, (reduce in elderly, liver/renal disease)

• Contra-indicated in patients with epilepsy, anorexia nervosa, bulimia, bipolar disorder or severe liver disease.

• The most common side effects are insomnia (up to 30%), dry mouth (10-15%), headache (10%), nausea (10%), constipation (10%), and agitation (5-10%)

• Interaction with antidepressants, antipsychotics and anti-arrhythmics

• Nicotine replacement and buproprion should always be used in conjunction with behavior modification

Bupropion

Nicotine Tabs• Nicotine tablets deliver 2-mg or 4-mg dosages of nicotine over

30-minutes• Common side effects with gum include burning sensations in

the mouth, sore throat, coughing, dry lips, and mouth ulcers

Nortryptiline• Tri-cyclic antidepressant

• Not licensed for smoking cessation

• Low cost

• Side-effects include sedation, dry mouth, light-headedness, cardiac arrhythmia

• Contra-indicated after recent myocardial infarction

Varenicline• Begin varenicline a week before the quit date, increasing dose

gradually.

• Alleviates withdrawal symptoms, reduces urge to smoke

• Common side effects include: nausea (30%), insomnia, (14%), abnormal dreams (13%), headache (13%), constipation (9%), gas (6%) and vomiting (5%).

• Contra-indicated in pregnancy

Pre-contemplation

Contemplation

Determination

Action

Maintenance

Relapse

Cycle of change

Smokers may move backwards or forwards, to and fro across the cycle many times before finally quitting

Impact of Smoking Cessation on PeriodontalStatus and Treatment Outcomes

•While smoking cessation does not reversethe past effects of smoking, the rate of bone andattachment loss slows after patients quit smokingand the severity of their disease is intermediatecompared to current and non-smokers.

•It is encouraging to note former smokers respondto non-surgical and surgical therapy in a mannersimilar to nonsmokers.

•Similarly, implant success rates for past smokerswere similar to nonsmokers.(JCDP’08)

CONCLUSIONIt is clear that smokers• Present with periodontitis at an early age• Difficult to treat them with conventional therapy• Continue to have progressive or recurrence of periodontitis

leading to tooth loss The opportunity for dentists to become more active in

evaluation of tobacco use by patients and more aggressive in offering counseling and cessation services can positively impact both the oral and general health of dental patients.

Referances

• Carranza’s clinical periodontology, tenth edition

• Journal of contemporary dental practice2008

• www.digital.library.edu.au• www.slideworld.org• www.tobaccoinduceddiseases.com

Thank you