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Smoking & periodontium


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These slides mainly gives information regarding effects of smoking in gums.

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Smoking & periodontium

  1. 1. Smoking and its effects on the Periodontium and Periodontal therapy
  2. 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. 3. INTRODUCTION 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. .
  4. 4. Tobacco smoking is a significant risk factor for periodontal disease Environmental &acquired risk factors [SMOKING] Ag Specific LPS pathogenic bacteria Ab Cytokines,PGE2 Host Connective immune tissue & inflambone MMPs matory metabolism response PMNs Genetic risk factors Clinical expression of disease, initiation progression
  5. 5. 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)
  6. 6. RISK ASSESSMENT ATTACHMENT LOSS Variable Estimated odds ratio Age 1.72 - 9.01 Smoking 2.05 - 4.75 Diabetes 2.32 P gingivalis 1.59 Education 0.65 (Grossi et al, 1994)
  7. 7. ATTACHMENT LOSS AND SMOKING 40 30 20 10 0 Pack years healthy low moderate high (Grossi et al, 1994) severe
  8. 8. 10 year prospective study of smoking and periodontitis [Bergstrom et al 2000] Smokers lost significantly more periodontal bone compared to nonsmokers (p<0.001)
  9. 9. 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 status to be more pronounced in younger women. [Goultschin et al.10]
  10. 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]
  11. 11. Stopping smoking (for 10 years) reduces risk of periodontitis to that of non-smokers 0-2 years -> OR=3.2 >10 years -> OR=1.2 The more you smoke the worse the periodontitis (dose response) Smoking <10 cigs/day OR = 2.8 Smoking >30 cigs/day OR = 6.9 [Tomar and Asma 2000]
  12. 12. 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
  13. 13. POTENT CARCINOGENS • Nitrosamines • Polycyclic aromatic hydrocarbons • Radiation-emitting polonium COMPONENTS OF INHALED SMOKE •Nicotine •Carbon monoxide •Tar all of which can cause disease
  14. 14. Nicotine action • Accelerates release of neurotransmitter dopamine in the brain’s NA* & increases metabolism in NA *NA = nucleus accumbens
  15. 15. •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
  16. 16. 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
  17. 17. 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
  18. 18. Effect of Smoking on Plaque
  19. 19. 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 of exogenous flora (Escheria coli and Candida albicans) have been reported in smokers
  20. 20. 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.
  21. 21. • 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).
  22. 22. 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)
  23. 23. Genetic Polymorphism and Smoking Investigators have looked at 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.*JCDP’08+
  25. 25. 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
  26. 26. Effect of Smoking on Gingival Blood Flow • In smokers, gingival blood flow was significantly increased by cigarette smoking. • However, 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.
  27. 27. 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 Vasculature researchers found a high proportion of small vessels compared with large vessels in smokers than non-smokers but no difference in the vasculature density. [journal CDP nov08]
  28. 28. 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
  29. 29. Smoking and Fibroblast Function Gingival Fibroblasts In vitro studies have shown reduction in the production of Type 1 collagen and fibronectin and an increase in the collagenase activity. Cellular changes like disruption of cell orientation, changes in cytoskeleton, presence of large vacuoles, and significant reduction in cell viability have been noticed.
  30. 30. 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. [Albander et al 99, Lie et al 98]
  31. 31. 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.
  32. 32. 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. [Haber et al]
  33. 33. 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.
  34. 34. 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 particularly important in the etiology of severe periodontal attachment loss. {NHANES}
  35. 35. There is a strong dose-response relationship between the amount smoked and the severity of periodontal destruction which further supports the role of smoking as a risk factor for periodontitis. The most marked difference between smokers and non-smokers in probing depths or attachment loss occurs in the maxillary lingual area and mandibular anterior area, suggesting a local effect of smoking.
  36. 36. Effects of Smokeless Tobacco on Periodontal 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.
  37. 37. Smoking and Acute Necrotizing Ulcerative Gingivitis (ANUG) An association between necrotizing forms of periodontal disease and tobacco smoking was reported as early as 1947 Preexisting gingivitis, emotional/psychic stress, and smoking forms a triad of interrelated predisposing factors in the etiology of the disease. .
  38. 38. 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}
  40. 40. 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).
  41. 41. 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
  42. 42. Smoking and Cancer Smoking 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
  43. 43. 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, and sudden 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.
  44. 44. 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
  45. 45. Interaction between smoking and systemic Health status and periodontitis The combination of smoking with other systemic factors further enhances the risk of periodontal destruction. .
  46. 46. •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
  48. 48. 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.
  49. 49. Abnormal Changes at Cancerization site • Clinically: – Leukoplakia – Erythroplasia – Dysplasia – Carcinoma in situ
  50. 50. 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
  51. 51. 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
  53. 53. Effects Of Smoking On Periodontal Therapy
  54. 54. 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+
  55. 55. 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. [Medicine and Biology Vol.14, No 2, 2007, pp. 53 – 59]
  56. 56. 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. (Nolan et al.,85; Preber & Bergström, 85a; 86; 90).
  57. 57. Non-surgical and Surgical Therapy Numerous studies have shown smoking compromises probing depth and/or attachment gain outcomes following non-surgical or surgical 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 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.
  58. 58. 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 subantimicrobial doxycycline (anticollagenase) therapy in combination with SRP in a group of severe periodontitis patients that included smokers.
  59. 59. 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.
  60. 60. 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.
  61. 61. 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
  63. 63. 64
  64. 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.
  65. 65. Nicotine withdrawal: the 4 ‘D’s Drink water slowly Deep breathe. Do something else (eg exercise) Delay acting on the urge to smoke
  66. 66. 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
  67. 67. NRT: Nicotine patches • • • 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 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!
  68. 68. 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 Bupropion • 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 antiarrhythmics • Nicotine replacement and buproprion should always be used in conjunction with behavior modification
  69. 69. 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
  70. 70. Smokers may move backwards or forwards, to and fro across the cycle many times before finally quitting Relapse Precontemplation Maintenance Cycle of change Action Contemplation Determination
  71. 71. 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.(JCDP’08)
  72. 72. 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.
  73. 73. Referances • Carranza’s clinical periodontology, tenth edition • Journal of contemporary dental practice2008 • • •
  74. 74. Thank you