Association between Smoking and periodontal disease.pptx

Smoking

1. Smoking and its effects on the Periodontium and Periodontal therapy

2. 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

3. 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

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 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,PGE 2 MMPs

6. 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.

7. ATTACHMENT LOSS AND SMOKING ( Grossi et al, 1994)

8. 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]

9. Stopping smoking (for 10 years) reduces risk of periodontitis to that of non-smokers The more you smoke the worse the periodontitis

10. Tobacco contains over 4,000chemicals, 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 INHALED SMOKE Nicotine Carbon monoxide Tar  all of which can cause disease

12. Nicotine action Raise blood pressure Vasoconstriction Psychological - social dependency Retards growth of gingival fibroblasts Reduces fibronectin & collagen Increases collagen breakdown

13. 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

14. 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

15. Effect of Smoking on Plaque

16. PERIODONTAL PATHOGENS The proportions of 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

17. SMOKING AND HOST RESPONSE 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 .

18. 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

19. EFFECT OF SMOKING ON GINGIVA

20. 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

21. Effect of Smoking on 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.

22. Oxygen Tension in the Gingival Tissues Smoking Decreases Tissue Oxygen Tissue oxygen decreases: 65 to 44 mmHg Tissue oxygen 40-50 mmHg —> infection Effects on the Gingival Vasculature H igh proportion of small vessels compared with large vessels in smokers than non-smokers

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

24. Smoking and gingival inflammation 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.

25. Smoking and periodontitis in 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.

26. Smoking and Periodontitis in 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.

27. Smoking and Acute Necrotizing Ulcerative Gingivitis (ANUG)

28. SMOKING influence the tissue response 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}

29. SMOKING AND SYSTEMIC HEALTH

30. 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

31. Smoking and Respiratory Disease 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

32. Smoking and Cancer Smoking causes 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

33. SMOKING – MORBIDITY (miller et 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

34. SMOKING AND ORAL HEALTH

35. 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 .

36. Abnormal Changes at Cancerization site Clinically: Leukoplakia Erythroplasia Dysplasia Carcinoma in situ

37. 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

38. 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

39. STAINING OF TEETH HALITOSIS DELAYED WOUND HEALING DRY SOCKET SMOKER’S FACE

40. EFFECT OF SMOKING IN 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 .

41. Effects Of Smoking On Periodontal Therapy

42. Non-surgical and Surgical Therapy Numerous studies have shown smoking compromises probing depth and/or attachment gain outcomes following non-surgical or surgical therapy. S mokers 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.

43. Antimicrobial Therapy in Smokers 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.

44. 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.

45. 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 majority of implant failures in smoking occurred prior to prosthesis delivery.

46. 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

47. TOBACCO CESSATION

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49. 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 .

50. Nicotine withdrawal: the 4 ‘D’s D elay acting on the urge to smoke D rink water slowly D eep breathe. D o something else (eg exercise)

51. PHARMACOTHERAPY Pharmacotherapy + 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

52. 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

53. 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%) 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

54. 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

55. 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

56. Impact of Smoking Cessation 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 .

57. CONCLUSION It 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.

58. To summarise ….

59. Thank you