Smoking and Periodontal disease.

Epidemiology

Epidemic that is in both developed and developing nations. Singapore smoking prevalence rate from 20% (37% males and 3% females) in 1984 to 12.6% (21.9% males and 3.4% females) in 2004.

The smoking prevalence among Singaporean men and women are among the lowest in the world when compared with countries such as Canada, Australia, United Kingdom, United States, South Korea, Japan, Thailand, Italy, Germany and Switzerland.

However, smoking still causes a higher risk of disease in Singapore:

- 90% of lung cancer cases in males occur among smokers

- 80-90% of COPD deaths caused by smoking

- 40% of deaths due to cerebrovascular disease are related to smoking

- Up to 90% of refractory periodontis patients are smokers

Smoking and the Periodontium

Overall, smoking is probably the single most significant, modifiable risk factor for periodontal diseases. The incidence of periodontitis is 4.9 percent for never smokers, 10.5 percent for former smokers, and 15.6 percent for current smokers. The evidence suggests that more than one-half (8.1 million cases) of the chronic periodontitis cases in the United States are attributable to cigarette smoking.

There is an abundance of scientific evidence that smoking has an additive effect on the progression of periodontal disease and is detrimental to healing after periodontal therapy. One of the earliest studies to show a relationship between smoking and periodontal health was conducted on Swedish army soldiers. The subjects who smoked were shown to be at greater risk for gingivitis, but no differences were noted in bone loss or increased periodontal pocketing. However, another study demonstrated that the alveolar bone height was significantly reduced in smokers compared to nonsmokers.

Likewise, Haber and Kent demonstrated that smokers were 2.7 times more likely to have moderate to advanced periodontal disease.

Also, smoking has been shown to significantly increase the risk of tooth loss from periodontal disease. The effect appears to be dose-related, with heavy smokers exhibiting a significantly greater risk of tooth loss from periodontal disease compared to nonsmokers and lighter smokers. A paper by Grossi et al 1994 shows that attachment loss is correlated to pack years.

Pathology of smoking and Periodontal disease

Common hypothesis is that periodontal pockets of smokers tend to be more anaerobic compared to nonsmokers. Anaerobic environment could conervably promote growth of gram-ve periodontal pathogens in the subgingival plaque. However, a study using gram staining techniques failed to show a significant difference in subgingival microflora between smokers and nonsmokers.

Another hypothesis is that smoking alters host response by impairing normal functions such as neutrophil actions in neutralizing infection and alters the host response, resulting in destruction of the surrounding healthy periodontal tissue.

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. This masks the normal early signs of periodontal problems by decreasing gingival inflammation, erythema, and bleeding despite the presence of the disease.

Acute necrotizing ulcerating gingivitis (ANUG) has also been shown to be clearly correlated to smoking, but no cause-and-effect relationship has been demonstrated.14 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.

Treatment usually consists of mechanical debridement and systemic antibiotic treatment.treatment.

Nicotine

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.

Nicotine has numerous detrimental effects on periodontal cells. Periodontal cells exposed to nicotine have also been shown to have decreased growth and protein content, damaged cell membranes, and atypical shapes. Tobacco use has been implicated as a risk factor for alveolar bone loss. Nicotine has also been thought to delay apoptosis. A delay in cell death has been thought to contribute to tumor production.

Cigar, pipe, water-pipe and cannabis smoking have similar adverse effects on periodontal health as cigarette smoking. Passive smoking is also an independent periodontal disease risk factor. Smokeless tobacco is associated with localized periodontal disease.

Efforts

Smokers respond less favourably to both non-surgical and surgical treatments and have higher failure rates and complications following dental implantation. Smoking cessation may halt the disease progression and improve the outcome of periodontal treatment.

Conclusion

Smoking cessation counselling should be an integral part of periodontal therapy and prevention.

Biblography

- Carranza's clinical periodontology 10th edition

- https://www.moh.gov.sg/content/moh_web/home/diseases_and_conditions.html

- Alpar B, Leyhausen G, Saptonik A, Gunay H, Guertsen W. Nicotine-induced alterations in human primary periodontal ligament and gingival fibroblast cultures. Clin Oral Invest 1998; 2:40-46.

- Grossi SG, Genco RJ, Machtei EE. Assessment of risk for periodontal disease II. Risk indicators for alveolar bone loss. J Periodontol 1995; 66:23-29.