Smoking and Periodontists

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Does Smoking affect periodontal disease?

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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.

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 costs the economy more than $150 billion in annual health-care costs and lost productivity, including $75.5 billion in excess medical expenditures.

These expenditures include dental costs, since smoking increases the disease progression and complicate the treatment of periodontal diseases.

Women between the ages of 20 and 39 who smoke cigarettes have approximately twice the chance of having periodontal disease or becoming edentulous as do nonsmokers.

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 periodontists 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.

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.

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.

It has been hypothesized that smoking may alter the host response in two ways: Smoking could impair the normal functions of the host response in neutralizing infection, and it may alter the host response, resulting in destruction of the surrounding healthy periodontal tissues.

Several studies have shown that the effect of smoking on periodontal tissues may involve both of these processes.

In addition, the host requires functional neutrophils to deal effectively with bacterial infections.

Tobacco smoke has been shown by several studies to have a deleterious effect on various neutrophil functions. For example, smoking has been shown to impair the chemotaxis and phagocytosis of both oral and peripheral neutrophils.

Neutrophils are found in inflammatory lesions, particularly acute lesions, where they concentrate at the site of injury. They are chemically attracted to the site by a process called chemotaxis.

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 non-smokers. 

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.

FIGURE 1a — Apparently healthy gingival tissue in a one-pack-per-day smoker.

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FIGURE 1b — Periodontal pocket probing 10 mm.

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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. ANUG is characterized by punched-out papilla, pronounced gingival erythema, and spontaneous hemorrhage (See Figure 2). Local lymphadenopathy and slight elevation of temperature may also be present.

FIGURE 2 — Acute necrotizing ulcerative gingivitis with severe caries.

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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. 

FIGURE 3 — Nicotinic stomatitis.

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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 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. 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.

A study of porcine bone marrow cells found that nicotine is nontoxic to osteoclasts at clinically relevant levels, and appears to stimulate osteoclast differentiation and the resorption of calcium phosphate, the major inorganic component of bone.

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.


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.

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 patients if dental professionals, made a deliberate effort to promote smoking-cessation programs as well as educate our community on the benefits of not smoking.

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