Smoking is a Major Risk Factor for Periodontal Disease

In the United States there are an estimated 50 million smokers, and another unknown number of individuals exposed to secondhand smoke. It is well recognized that smoking is the cause of many systemic pathologies, of which lung cancercardiac disease, and stroke are best known and most feared. Unfortunately, lethal tobacco products—cigarette and use of smokeless (“spit”) tobacco—have gone unnoticed as causal agents for disabling and disfiguring oral and pharyngeal cancer. There have also been many articles published over the past five decades pointing out that tobacco is a causal agent for periodontal disease, an oral disease that affects millions. The enormity of this relationship is found in a statement that smoking accounts for one-half of all periodontal cases and three-fourths of oral cancer cases in the United States.

Men who used chewing tobacco were four times more likely than those who had never used tobacco, to have one or more decayed or filled root surfaces. It is now beginning to emerge that probably one of the most important questions that can be asked on the patient’s dental and medical history form is, “Do you smoke or live with someone who smokes, and/or do you use smokeless tobacco?”  Smoking is a high-risk habit and constitutes a major periodontal problem.  The litany of tobacco-associated lesions found in the mouth include squamous-cell carcinoma, gingivitis and periodontitis, burns and keratosis patches, black hairy tongue, palate erosions, leukoplakia and epithelial dysplasia, and tooth staining.

The use of tobacco products has an adverse effect of the onset, prevention, prognosis, treatment and maintenance phases of periodontitis. Part of this negative outlook is because smoking also causes adverse changes in the body’s immune response system that present major barriers to successful periodontal treatment.

  • Smoking is associated with alveolar bone loss, with epithelial attachment loss, gingival recession, and with periodontal pocket development.
  • Tobacco users are 2.5 to 6 times more likely to develop periodontal disease than nonsmokers. A patient’s smoking history is a useful clinical indicator of future periodontal disease activity.
  • There appears to be a relationship between the number of cigarettes smoked and the risk of developing periodontal diseases.  As the number of cigarettes smoked increases, so does the severity of the periodontal disease.
  • More smokers than nonsmokers are classified as having severe adult periodontitis and severe early-onset generalized periodontitis.
  • Almost 100% of 30- to 40-year-old heavy smokers have periodontitis;the response of these patients to therapy is not as favorable as for nonsmokers.
  • Approximately 86 to 90% of refractory periodontitis (not responsive to treatment) patients are current smokers.
  • There is a strong association between smoking and alveolar bone and tooth loss.
  • Smoking is associated with adverse changes in the body’s immune system.
  • The gingival fibroblastic repair function is altered, resulting in a thickened fibrotic gingiva.
  • Following treatment, the improvements in probing depths and epithelial attachments are still more favorable for the nonsmoker.
  • There is more pocketing of the anterior segments of teeth for smokers than nonsmokers.

Smoking Cessation and Recovery

Smoking cessation is an essential component for the successful treatment of periodontal disease—there is little rationale for treating periodontitis without eliminating one of the major causes of the disease.  Thus, there is also the question of whether periodontal surgical treatment is indicated without a commitment by the patient to quit smoking.  As with other smoking diseases, cessation is only the first step of a long healing process where the smoker often does not approach the lower risk of the nonsmoker for 10 to 20 years.  Krall and coworkers estimated that the risk of tooth loss 12 years after smoking cessation was reduced by 20%. However, the fact that the rate of tooth loss of ex-smokers falls between the data for current smokers and those who never smoked indicates that recovery is taking place. The periodontal status and bone loss of ex-smokers also appears to be intermediate between current smokers and those who never smoked.
Gingival improvement is more rapid following smoking cessation although a bit quixotic. Usually a smoker’s gingiva has a glazed fibrotic appearance with rolled edges after years of smoking. Bleeding is minimal on brushing. It is believed that this is due to the local effect of the tobacco smoke possibly suppressing the inflammatory reaction. This local and direct effect of components in the cigarette smoke are believed to also account for a greater amount of pocketing that occurs in the anterior teeth. However, about 10 to 12 weeks after quitting smoking, there is an increase in bleeding, possibly caused by a recovery of the inflammatory response. About a year after cessation, the fibrotic, thickened anatomy of the gingiva begins to assume a more normal appearance and the periodontitis appears to stabilize. For the majority of patients, attachment loss ceases or dramatically slows.

The present methods for prevention and treatment of gingivitis and periodontal disease emphasize the need for meticulous day-to-day oral hygiene procedures. Even so these preventive actions are not intended to, nor are they adequate to continuously replace a compromised portion of the immune system brought on by smoking. Where smoking occurs, the chemical and manual methods of plaque control still help to reduce the bacterial challenge. However, with round-the-clock impaired humoral and cellular body defenses, and with an impaired gingival fibroblastic repair capability, the entire defense and recovery process is jeopardized.