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Smoking and Periodontal Disease presentation
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- 2. Introduction • Tobacco smokingis an addictive habit first introduced in Europe. Smoking is now recognized as the most important cause of preventable death and disease. • Currently, the most of adult population smoke cigarettes. However, nowadays, the smokers are changing to lower-tar brands. • Consumption is rising in developing countries, particularly where tobacco production brings great economic benefits.
- 3. • Smoking isassociated with a wide spectrum of diseases including:- Stroke, coronary artery disease, peripheral artery disease, gastric ulcer and cancers of the mouth, larynx, esophagus, pancreas, bladder and uterine cervix. It is also a major cause of chronic obstructive pulmonary disease and a risk factor for low birth weight babies. Approximately 50% of regular smokers are killed by their habit and smoking causes 30% of cancer deaths.
- 4. • Cigarette smokeis a very complex mixture of substances with over 4000 known constituents. These include:- carbon monoxide, hydrogen cyanide, reactive oxidizing radicals, a high number of carcinogens, and the main psychoactive and addictive molecule – nicotine • Many of these components could modify the host response in periodontitis.
- 5. • Inter-subject smokingvariation includes frequency of inhalation, depth of inhalation, length of the cigarette stub left, presence or absence of a filter, and the brand of cigarette. • The patient's exposure to tobacco smoke can be measured in several ways including interviewing the subject using simple questions or more sophisticated questionnaires and biochemical analyses.
- 6. • The testsinclude exhaled carbon monoxide in the breath, which is commonly measured in smoking cessation clinics, and cotinine (a metabolite of nicotine) in saliva, plasma/serum, or urine. • Cotinine measurements are more reliable in determining a subject's exposure to tobacco smoke because the half-life is 14-20 hours compared with the shorter half-life of nicotine which is 2-3 hours.
- 7. • The meanplasma and salivary cotinine concentrations of regular smokers are approximately 300ng/ml and urine concentrations are about 1500 ng/ml. • Nonsmokers typically have plasma/saliva concentrations under 2ng/ml, but this may be raised slightly due to environmental exposure (passive smoking).
- 8. Nicotine Effect………. • Inhalationof tobacco smoke allows very rapid absorption of nicotine into the blood and transport to the brain, which is faster than an intravenous infusion. • Nicotine in tobacco smoke from most cigarettes is not well absorbed through the oral mucosa because the nicotine is in an ionized form as a result of the pH (5.5). • In contrast cigar and pipe smoke is more alkaline (pH 8.5), which allows good absorption of un-ionized nicotine through the buccal mucosa.
- 9. • Nicotine isabsorbed rapidly in the lung where the smoke is well buffered. • The administration of nicotine causes :- A rise in the blood pressure, an increase in heart rate, an increase in respiratory rate and decreased skin temperature due to peripheral vasoconstriction. • However, at other body sites, such as skeletal muscle, nicotine produces vasodilatation.
- 10. Periodontal Disease InSmokers • Pindborg (1947) was one of the first investigators to study the relationship between smoking and periodontal disease. • He discovered a higher prevalence of acute necrotizing ulcerative gingivitis The typical appearance of necrotizing ulcerative gingivitis in a heavy smoker with poor oral hygiene.
- 11. Smokers with periodontitis,have: 1. Deeper probing depths and a larger number of deep pockets 2. More attachment loss including more gingival recession 3. More alveolar bone loss 4. More tooth loss 5. Less gingivitis and less bleeding on probing 6. More teeth with furcation involvement
- 12. Smoking and gingivalinflammation • A reduction in clinical signs of gingivitis has been reported in smokers and this effect is independent of plaque levels. • Heavy smokers may have grayish 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.
- 13. Smoking and gingivalbleeding • Smoking is known to produce peripheral vasoconstriction, in some subjects, this is preceded by vasodilatation. • Degree of inhalation of tobacco smoke and the rate of nicotine absorption. Nicotine from cigarettes stimulates the sympathetic ganglia to produce neurotransmitters including catecholamines.
- 14. These affect thealpha-receptors in blood vessels which in turn causes vasoconstriction. The vasoconstriction of peripheral blood vessels caused by smoking can also affect the periodontal tissue as smokers have less overt signs of gingivitis than nonsmokers and clinical signs of gingival inflammation such as redness, bleeding, and exudation are not evident in smokers. The vasoconstrictive actions of nicotine may be responsible for the decreased gingival blood flow.
- 15. Effects of Smokingon the Etiology and Pathogenesis of Periodontal Disease
- 16. Smoking and oral microorganisms •Smoking has important effects on oral bacteria. • Cigarette smoking could cause a lowering of the oxidation-reduction potential, and this could cause an increase in anaerobic plaque bacteria. • There was a statistically significant shift in the proportion of Gram-positive to Gram-negative bacteria in 3-day-old plaque from smokers when compared with non-smokers.
- 17. • Tobacco smokecontains phenols and cyanides, which can account for antibacterial and toxic properties. • Smokers harbored significantly higher levels and were at significantly greater risk of infection with Tanarella forsythia than non-smokers. • Adjusting for disease severity, Porphyromonas gingivalis was also more likely to subgingivally infect smokers than non-smokers
- 18. Effects on thehost response • Nicotine metabolites can concentrate in the periodontium and their effects include the promotion of vasoconstriction; and 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.
- 19. Physiology • Clinical signsof inflammation are less pronounced in smokers than in nonsmokers. • This may result from alterations in the inflammatory response in smokers, as outlined previously, or from alterations in the vascular response of the gingival tissues. • Although no significant differences in the vascular density of healthy gingiva have been observed between smokers and nonsmokers, the response of the microcirculation to plaque accumulation appears to be altered in smokers compared with nonsmokers.
- 20. • With developinginflammation, a rise in GCF flow, bleeding on probing, and gingival blood vessels are less in smokers than nonsmokers. In addition, the oxygen concentration in healthy gingival tissues appears to be less in smokers than nonsmokers, although this condition is reversed in the presence of moderate inflammation. • Subgingival temperatures are lower in smokers than nonsmokers, and recovery from the vasoconstriction caused by local anesthetic administration takes longer in smokers.
- 21. • These cumulativedata suggest that significant alterations are present in the gingival microvasculature of smokers compared with nonsmokers and that these changes lead to decreased blood flow and decreased clinical signs of inflammation. • This explains the long observed phenomenon of a transient increase in gingival bleeding when a smoker quits.
- 22. Effects of Smokingon Response to Periodontal Therapy
- 23. • Following non-surgicaltherapy, healing in terms of gingival bleeding reduction and pocket-depth reduction was less favorable in smokers. • The clinical results showed a statistically significant reduction of pocket depth and number of diseased sites in both smokers and non-smoker patients. • These findings are in agreement with recent long- term results which suggest that tobacco smoking interferes with the healing process following non- surgical periodontal therapy.
- 24. • James andcolleagues investigated the in vitro effect of nicotine on fibroblast activity. They found that it inhibited attachment and growth of periodontal ligament fibroblasts. • The results of these studies all indicate that smoking has a deleterious effect on wound healing and may help to explain why smokers respond less favourably to periodontal therapy.
- 25. Maintenance Therapy • Thedetrimental effect of smoking on treatment outcomes appears to be long-lasting and independent of the frequency of maintenance therapy. • After four different modalities of therapy, including scaling and root planing, modified Widman flap surgery, and osseous surgery, maintenance therapy was performed by a hygienist every 3 months for 7 years. • Smokers consistently had deeper pockets than nonsmokers and less gain in attachment when evaluated each year for the 7-year period.
- 26. • Even withmore intensive maintenance therapy, Smokers possess deeper and more residual pockets than nonsmokers, even though no significant differences in plaque or bleeding on probing scores were found. • Smokers also tend to experience more periodontal breakdown than nonsmokers after therapy.
- 27. • In studiesof patients who failed to respond to conventional therapy, including different combinations of oral hygiene instruction, scaling and root planing, surgery, and antibiotics, approximately 90% of these poorly responding patients were smokers. • It is clear from these studies that smokers (1) may present with periodontal disease at an early age, (2) may be difficult to treat effectively with conventional therapeutic strategies, and (3) may continue to have progressive or recurrent periodontitis. For this reason, smoking cessation counseling must be a cornerstone of periodontal therapy in smokers.
- 28. Smoking Cessation • Variousmethods for helping patients to quit smoking in the dental environment have been described. • ASK: Ask the patient about their smoking status. • This should be part of the medical history.
- 29. • ADVISE: Advisesmokers of the associations between oral disease and smoking. Be informative, honest, and helpful but not judgmental. • ASSESS: Assess the patient's interest and readiness to attempt smoking cessation. Patients may not yet be in an action phase to quit smoking, which is why it is always important to make these assessments every time you see the patient. • ASSIST: Assist the patient in their quit attempt. If you are trained, many techniques can be used. Alternatively, assist the patient in seeking the help they need.
- 30. • ARRANGE: Arrangefollow-up or referral to professional smoking cessation services. The most important aspect of this is to keep in regular contact particularly around the quit date and in the immediate period after.
- 31. Effects of SmokingCessation on Periodontal Treatment Outcomes • Studies have demonstrated that smokers have significantly worse periodontal status (deeper probing depths, more attachment loss, and bone loss) than either former smokers or nonsmokers and usually have poorer treatment outcomes.
- 32. • There arevery few intervention studies on the effect of smoking cessation on periodontal treatment outcomes (i.e., studies in which smokers were helped to quit and the effect on periodontal status was then assessed). • Two short-term studies have indicated that smoking has a negative impact on the gingival vasculature and that these changes are reversible upon quitting smoking.
- 33. • One interventionstudy has assessed the impact of smoking cessation on outcomes after nonsurgical periodontal treatment. • This study employed dental hygienists who were trained as smoking cessation advisors and achieved a 20% quit rate at 12 months in a population of smokers who also had periodontitis using a variety of strategies, including Counseling, Nicotine Replacement Therapy, and Bupropion.
- 34. Nicotine Replacement Therapy •Nicotine replacement therapy (NRT) gives you nicotine – in the form of gum, patches, sprays, inhalers, or lozenges – but not the other harmful chemicals in tobacco. • NRT can help relieve some of the physical withdrawal symptoms so that you can focus on the psychological (emotional) aspects of quitting.
- 35. • To conclude,smoking is the major risk factor for periodontitis, and smoking cessation should be an integral part of periodontal therapy in patients who smoke and needs to be considered a priority for the management of periodontitis in smokers.
- 36. References • Carranza’s clinicalPeriodontology 11th Ed • Jan Lindhe • Ana Pejčić, Radmila Obradović, Ljiljana Kesić, Draginja Kojović : SMOKING AND PERIODONTAL DISEASE A REVIEW, Medicine and Biology Vol.14, No 2, 2007, pp. 53 – 59 • Bergstrom J, Eliasson S, Dock J. Exposure to tobacco smoking and periodontal health. J Clin Perio 2000; 27: 61- 68.
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