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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.

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