This document discusses the effects of smoking on periodontal disease. It states that smoking promotes a more anaerobic environment in the gingival pockets which can lead to increased growth of pathogens. Smoking also causes disease masking, where the tissues appear healthier than they are due to vasoconstriction reducing blood flow and inflammation. Specific oral conditions linked to smoking include acute necrotizing ulcerating gingivitis, nicotinic stomatitis, and accelerated alveolar bone loss. Nicotine is highlighted as the most pharmacologically active compound in cigarettes and can have detrimental effects on periodontal cells and promote collagen breakdown and delayed apoptosis of cells. The conclusion reiterates that smoking increases the severity of periodontal disease and

2. 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.

3. Pathology of smoking and
periodontal disease
One 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

4. 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.

6. Signs and symptoms
Acute 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.

7. 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

8. Etiology
Nicotine 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.

9. 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.

10. 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.

11. Conclusion
In 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.

12. 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.

13. References
Trends 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
conscripts
Bergstrom J, Eliasson S. Cigarette smoking and alveolar
bone height in subjects with a high standard of oral
hygiene.

14. Thank you