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![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](https://image.slidesharecdn.com/smokingandperiodontaldisease-251010060729-088e629f/75/Association-between-Smoking-and-periodontal-disease-pptx-5-2048.jpg)
![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.](https://image.slidesharecdn.com/smokingandperiodontaldisease-251010060729-088e629f/75/Association-between-Smoking-and-periodontal-disease-pptx-6-2048.jpg)
![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]](https://image.slidesharecdn.com/smokingandperiodontaldisease-251010060729-088e629f/75/Association-between-Smoking-and-periodontal-disease-pptx-8-2048.jpg)
![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](https://image.slidesharecdn.com/smokingandperiodontaldisease-251010060729-088e629f/75/Association-between-Smoking-and-periodontal-disease-pptx-38-2048.jpg)
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Association between Smoking and periodontal disease.pptx
- 1. Smoking and itseffects on the Periodontium and Periodontal therapy
- 2. CONTENTS • Introduction • Epidemiologicalevidence • 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
- 3. Periodontal disease isdefined 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
- 4. • “CURRENT SMOKERS”– 100 cigarettes or more over their lifetime & is still smoking at the time of interview • “FORMER SMOKERS” – 100 cigarettes or more in their lifetime, but not smoking now. • “NON SMOKERS” - < than 100 cigarrets in their lifetime.
- 5. Tobacco smoking isa 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
- 6. EPIDEMIOLOGICAL EVIDENCE • Cross-sectionaland 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.
- 7. healthy low moderatehigh severe 40 30 20 10 0 Pack years ATTACHMENT LOSS AND SMOKING (Grossi et al, 1994)
- 8. PREVALENCE OF MODERATEAND SEVERE PERIODONTITIS • Current smokers - 25.7% • Former heavy smokers - 20.2% • Cigar/pipe smokers - 17.6% • Non-smokers - 13.1% [ Albandar et al 2000]
- 9. Stopping smoking (for10 years) reduces risk of periodontitis to that of non-smokers The more you smoke the worse the periodontitis
- 10. Tobacco contains over4,000chemicals, many of which are harmful. These include: Benzene - solvent used in fuel manufacture Formaldehyde - highly poisonous, colourless liquid used to preserve dead bodies Ammonia - chemical found in cleaning fluids. Used in cigarettes to increase the delivery of nicotine Hydrogen cyanide -poisonous gas used in the manufacture of plastics, dyes, and pesticides. - Often used as a fumigant to kill rats Cadmium - extremely poisonous metal found in batteries Acetone - solvent found in nail polish remover
- 11. COMPONENTS OF INHALEDSMOKE •Nicotine •Carbon monoxide •Tar all of which can cause disease
- 12. Nicotine action • Raiseblood pressure • Vasoconstriction • Psychological - social dependency • Retards growth of gingival fibroblasts • Reduces fibronectin & collagen • Increases collagen breakdown
- 13. CARBON MONOXIDE-ACTIONS •Carbon monoxideis 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
- 14. TAR-actions •Tar contains manysubstances 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
- 16. Effect of Smokingon Plaque
- 17. PERIODONTAL PATHOGENS The proportionsof subjects positive for A. actinomycetemcommitans, P. gingivalis, and T. forsythesis were higher among smokers. Furthermore, increased counts of exogenous flora (Escheria coli and Candida albicans) have been reported in smokers
- 18. SMOKING AND HOSTRESPONSE • Smoking decreases salivary IgA and serum IgG,and specifically reduces IgG2 levels. • The ability of tobacco products to decrease the proliferating capacity of T and B lymphocytes might contribute to this diminished production of protective antibodies.
- 19. • Smoking canexert deleterious effects on polymorphonuclear leukocytes (PMN) and other neutrophil functions such as chemotaxis & phagocytosis so that they cannot efficiently deal with the bacterial infection •
- 20. EFFECT OF SMOKINGON GINGIVA
- 21. Cigarette Smoking andGingival 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
- 22. Effect of Smokingon Gingival Blood Flow Intravenous administration of nicotine reduces the marginal temperature of gingival sites suggesting a decrease in gingival blood flow which lead to the hypothesis this phenomenon is caused by vasoconstriction induced by nicotine and stress.
- 23. Oxygen Tension inthe Gingival Tissues • Smoking Decreases Tissue Oxygen • Tissue oxygen decreases: 65 to 44 mmHg • Tissue oxygen 40-50 mmHg —> infection Effects on the Gingival Vasculature High proportion of small vessels compared with large vessels in smokers than non-smokers
- 24. Evidence From Studieson (GCF) Smoking may result in lower resting GCF flow rate. The increase in GCF during an experimental gingivitis may be less in smokers. This correlates with the lower levels of inflammation observed clinically and within the tissues.
- 25. Smoking and gingivalinflammation Smokers may present with lower levels of gingival inflammation than nonsmokers. Furthermore, development of gingival inflammation in response to experimental plaque accumulation (experimental gingivitis) was less pronounced in smokers than in non-smokers.
- 26. Smoking and periodontitisin young adults (≤35 years) Several studies have shown young adult smokers aged 19-30 years had a higher prevalence and severity of periodontitis compared to non-smokers despite similar or lower plaque levels. The prevalence of periodontitis, defined as having a site with attachment loss of ≥2 mm and probing depths of ≥4 mm, was three to four times higher in young smokers compared to non-smokers.
- 27. Smoking and Periodontitisin Adults Current smokers have deeper probing depths, greater attachment loss, more bone loss, and fewer teeth. Smokers also exhibit more supragingival calculus deposits. Smokers were four times more likely to have periodontitis as compared to non-smokers.
- 28. Smoking and AcuteNecrotizing Ulcerative Gingivitis (ANUG)
- 29. SMOKING influence the tissue responseto 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}
- 30. SMOKING AND SYSTEMICHEALTH
- 31. Smoking and cardiovascularsystem • 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
- 32. Smoking and RespiratoryDisease Smoking 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
- 33. Smoking and Cancer Smokingcauses the following cancers: *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
- 34. SMOKING – MORBIDITY (milleret al 1999) 50% of total cancer deaths 84% of lung cancer deaths 30% of heart disease deaths 23% of respiratory deaths 80% of bronchitis and emphysema deaths
- 35. SMOKING AND ORALHEALTH
- 36. Tobacco use inall 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.
- 37. Abnormal Changes atCancerization site • Clinically: – Leukoplakia – Erythroplasia – Dysplasia – Carcinoma in situ
- 38. 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
- 39. DENTAL CARIES ANDEROSION • Smoking stimulates saliva flow immediately, does not affect saliva in long term • Decrease Ph and buffering action Dental caries Erosion GINGIVAL RECESSION
- 40. • STAINING OFTEETH • HALITOSIS • DELAYED WOUND HEALING • DRY SOCKET • SMOKER’S FACE
- 41. EFFECT OF SMOKINGIN WOUND HEALING Smoking has been shown to impair revascularization during soft and hard tissue wound healing, which is critical for periodontal plastic, regenerative, and implant procedures.
- 42. Effects Of SmokingOn Periodontal Therapy
- 43. Non-surgical and SurgicalTherapy Numerous studies have shown smoking compromises probing depth and/or attachment gain outcomes following non-surgical or surgical therapy. Smokers demonstrated 0.4 mm to 0.6 mm less improvement in clinical attachment levels following scaling and root planning. Following flap debridement surgery, smokers experienced upto 1 mm less improvement in clinical attachment levels in probing depths that were initially ≥7mm.
- 44. Antimicrobial Therapy inSmokers • Because of the diminished treatment response in smokers, 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.
- 45. Soft and HardTissue 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.
- 46. Implant Therapy • Inthe studies reviewed, 0% to 17% of implants placed in smokers were reported as failures as compared to 2% to 7% in non-smokers. • The majority of implant failures in smoking occurred prior to prosthesis delivery.
- 47. Maintenance phase • ↑pocketdepth • ↓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
- 48.
- 49.
- 50. 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.
- 51. Nicotine withdrawal: the4 ‘D’s Delay acting on the urge to smoke Drink water slowly Deep breathe. Do something else (eg exercise)
- 52. PHARMACOTHERAPY Pharmacotherapy + behaviouralcounselling 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
- 53. NRT: Nicotine nasalsp • 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
- 54. • Begin bupropiona 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%) • 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
- 55. 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
- 56. Pre- contemplation Contemplation Determination Action Maintenance Relapse Cycle of change Smokers maymove backwards or forwards, to and fro across the cycle many times before finally quitting
- 57. Impact of SmokingCessation on Periodontal Status and Treatment Outcomes •While smoking cessation does not reverse the past effects of smoking, 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. •It is encouraging to note former smokers respond to non-surgical and surgical therapy in a manner similar to nonsmokers. •Similarly, implant success rates for past smokers were similar to nonsmokers.
- 58. CONCLUSION It is clearthat 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.
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Editor's Notes
- #12 The nucleus accumbens is the pleasure and reward center of the brain. The amygdala (from Greek word for almond) is associated with emotions of fear, lust, and curiosity. http://www.benbest.com/science/anatmind/anatmd9.html