smoking and periodontitis

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Smoking and Periodontitis Noreen Mohammed 5212322 G.11

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Page 1: Smoking and periodontitis

Smoking and Periodontitis

Noreen Mohammed5212322

G.11

Page 2: Smoking and periodontitis

Cigarette smoking is one of the most preventable sources of morbidity and premature death worldwide. In the United States, smoking is responsible for approximately one in five deaths . Smoking prevalence has been on the decline in recent years. In 1963, the per capita consumption was 4,354 cigarettes compared to an estimated 1,979 in 2002, a lower level not seen since the 1940s.

Page 3: Smoking and periodontitis

Pathology of smoking and periodontal diseaseOne hypothesis for the increased periodontal changes noted in smokers is that the periodontal pockets of smokers tend to be more anaerobic compared to nonsmokers . An anaerobic environment could conceivably promote the growth of Gram-negative periodontal pathogens in the subgingival plaque. However, the study using Gram staining techniques failed to show a significant difference in the subgingival microflora between smokers and nonsmokers

Page 4: Smoking and periodontitis

Disease masking is a term that has been applied to describe the appearance of the gingiva associated with chronic smokers . Typically, the diseased tissues of smokers tend to have a firmer appearance and less bleeding compared to that of nonsmokers. The term disease masking is used because the vasoconstrictive properties of tobacco smoke hide the inflammatory and destructive changes occurring within the periodontium .The periodontal tissues are compromised by the initial vasoconstriction,

resulting in decreased blood flow to the gingiva .

Page 5: Smoking and periodontitis
Page 6: Smoking and periodontitis

Signs and symptomsAcute necrotizing ulcerating gingivitis (ANUG) has also been shown to be clearly correlated to smoking, but no cause-and-effect relationship has been demonstrated . It is thought that both smoking and ANUG may be the result of underlying anxiety and stress. The condition involves primarily the free gingival margin, the crest of the gingiva, and the interdental papillae. Rarely, the lesions can spread to the soft palate and tonsillar areas, resulting in the condition known as Vincent's angina.

Page 7: Smoking and periodontitis

Nicotinic stomatitis, or smoker's palate, is another oral change that is characteristic of smokers. It is characterized by prominent mucous glands with inflammation of the orifices and a diffused erythema, or by a wrinkled, "cobblestone" appearance of the palate often described as a "dried lake bed" effect .This visual appearance is the result of thickening of the epithelium adjacent to the orifice in response to chronic irritation. The regression of these lesions upon smoking cessation has led many researchers to conclude a cause-and-effect relationship

Page 8: Smoking and periodontitis

EtiologyNicotine is one of the most studied components of tobacco products and the most pharmacologically active compound in tobacco smoke. It has been shown to have various mood-altering effects on its consumers. Nicotine is a poisonous alkaloid found in tobacco smoke and can enter the body by absorption through the oral mucosa and skin or inhalation via the lungs. Nicotine is also highly addictive. Only 2.5 percent of the 34 percent of smokers who attempt to quit smoking are successful. Nicotine has numerous detrimental effects on

periodontal cells .

Page 9: Smoking and periodontitis

Nicotine also promotes collagen breakdown. Periodontal cells exposed to nicotine have also been shown to have decreased growth and protein content, damaged cell membranes, and atypical shapes.18 Tobacco use has been implicated as a risk factor for alveolar bone loss .One hypothesis has been the possible stimulant effect of nicotine on osteoclastic activity, the cells most responsible for bone resorption.

Page 10: Smoking and periodontitis

Nicotine has also been thought to delay apoptosis. A delay in cell death has been thought to contribute to tumor production. Also, this delay would allow for osteoclasts to continue the resorptive process longer than their normal life cycle would have permitted. These factors may also contribute to the accelerated alveolar bone loss seen in smokers.

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ConclusionIn conclusion, whether it is direct heat from the cigarette, the vasoactive response from nicotine, or a change in the host response to periodontal pathogens, the mechanism by which smoking induces periodontal attachment loss is currently unknown. Smoking has not only been shown to increase the severity of periodontal disease, but also to decrease the response of the gingival tissues to periodontal therapy, resulting in a greater incidence of refractory disease. Obviously, there is a plethora of published information correlating periodontal diseases to both tooth loss and systemic manifestations.

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These systemic manifestations include increased risk of coronary artery disease; diabetes; osteopenia; and premature, low-birth-weight babies. Further, it has been demonstrated in numerous studies that smoking cessation leads to improved periodontal health and improved response to periodontal therapy, thus improving overall health. Therefore, it would greatly benefit our patients if we, as dental professionals, made a deliberate effort to promote smoking-cessation programs as well as educate our community on the benefits of not smoking.

Page 13: Smoking and periodontitis

ReferencesTrends in tobacco use: American Lung Association Epidemiology. American Lung Association Epidemiology and Statistics Unit Research and Scientific Affairs. June 2003.

Preber H, Kant T, Bergstrom J. Cigarette smoking, oral hygiene, and periodontal health in Swedish Army conscriptsBergstrom J, Eliasson S. Cigarette smoking and alveolar bone height in subjects with a high standard of oral

hygiene .

Page 14: Smoking and periodontitis

Thank you