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Smoking and Periodontal Disease

For many years dentists have intuitively associated smoking with more anxious and less compliant patients, more tooth loss, and poorer responses to treatment. This newsletter reviews smoking and periodontal disease, smoking and periodontal therapy, and summarizes current views on smoking cessation. For those who are interested in assisting patients who choose to quit smoking a free monograph is available designed specifically for dental offices. We would be happy to loan it to you or provide its source to you. Please contact our office should you want more information.

Between 1959 and 1990 twenty-seven controlled studies were published on the incidence of alveolar bone loss and tooth loss in smokers. In a recently completed twelve year longitudinal study of over 1000 women the incidence of tooth loss was 67% higher in smokers. Alveolar bone loss is dose dependent. The greater the cigarette consumption the more bone loss noted. Heavy smokers who cut down on consumption increase the likelihood of retaining their natural teeth. Bergstrom, based on a study of 155 men and women, estimated the risk for developing periodontal disease to be twice as high in smokers as in non-smokers. A second study using a twins registry compared bone loss where smoking exposure varied. In forty of the twin pairs one never smoked and in the balance smoking occurred at different exposures. Bone loss was related directly to the amount of smoking exposure.

In fact there is a growing body of evidence that smoking may cause bone loss unrelated to the level of periodontal inflammation. Several studies have indicated that smoking does not increase the rate of plaque formation. In fact, clinicians often note the scant nature of plaque films supragingivally in patients who smoke. Great care should be exercised in periodontal screening and examination of those who smoke as gingival inflammation and gingival bleeding, two of the cardinal signs of periodontal disease, are often reduced in smokers. Increased keratinization in smokers may be responsible for the less observable inflammation in smokers. This increased keratinization may also account for the fact that smokers have a lower incidence of aphthous ulcers. Smoke’s effect on the surface characteristics of the gingiva may also be represented by increased melanin pigmentation, usually on the attached gingiva of the lower anterior teeth. This occurs in as many as 1 of 3 smokers. While the surface of the tissues may experience these disease masking changes, periodontal pocketing tends to be more severe.

A growing body of information provides some insight on how smoking effects the progression of disease in these diverse ways. At lease three mechanisms by which tobacco influences periodontal destruction have been listed. First, tobacco may suppress the immune response which functions to attack bacteria in the sulcus. Reduced oxygen concentrations as a result of the carbon monoxide in smoke inhibits the movement of white blood cells in the pocket. In addition to a depressed migration these cells lose their capacity to engulf and destroy bacteria. In the case of polymorphonuclear leukocytes (PMN’s) this effect is irreversible and can be noted after a single cigarette.

Second, trace elements within cigarette smoke may add additional stress to the immune response. This second type of challenge on the periodontal tissues is chemical. The products of smoking, including nicotine, and other chemical agents are absorbed on the root surfaces. In bone and soft tissue grafts results become less predictable. P.D. Miller, who has published widely on the coverage of root surfaces using free gingival grafts, cites smoking as a principle reason for failure of soft tissue grafts to cover exposed root surfaces. Multiple studies of smokers and non-smokers show all phases of periodontal therapy, surgical and non-surgical, to be less effective in patients who smoke.

The third way smoking effects the progression of periodontal disease is through the systemic effects of nicotine on cell functions. Nicotine is not absorbed through the intact oral mucosa, but is readily absorbed in the lung tissues. Nicotine produces a peripheral vasoconstriction. In Caucasians smoking is associated with a higher incidence of skin wrinkles around the eyes, called "crow’s feet." Plastic surgery literature reports that smoking increased the likelihood of skin sloughing after face lifts twelve fold. Recent evidence indicates this vasoconstriction may be more pronounced in gingival peripheral circulation than in other tissues. A single cigarette may reduce gingival crest blood flow for 3 hours. Hanes and co-workers have noted fibroblasts absorb nicotine and this results in increased cell metabolism and collagen production, but the secretion of this collagen is reduced. These three mechanisms make nicotine and smoke chemicals significant in the etiology and pathogenesis of periodontal disease.

Prior to discussing how we can help those who would like to improve their periodontal status by reducing or eliminating cigarette consumption, one more observation of the effect of smoking may be clinically useful. It has been reported that smoking triggers the staining reaction which often accompanies the use of chlorhexidine (Peridex). When using Peridex patients will require more frequent prophylaxis if they smoke.

How can the dental profession assist those who currently smoke? Christen lists the following actions. First, recognize that smoking is the strongest of the addictions. It is attached to so many behavioral triggers that relapse after quitting is quite common. Great personal courage is required to overcome the dependency and, as professionals, the dentist and staff must first build trust, offer emotional reinforcement and non-judgmental support.

Second, be aware that almost 70% of those who smoke are either not ready to quit (35%) or plan to quit in the next six months (34%). These have been termed by Ockene the pre-contemplation and contemplation stages. IN a non-judgmental fashion the professional might inquire if the individual is thinking about quitting. For those who are contemplating quitting, this may allow the individual to express and clarify their intentions to move to the 15% who are ready to quit. At that stage, an action plan can be constructed to achieve a process (behavioral change) and an ultimate (health outcome) goal. Quitting is not automatically requested of all individuals as personal commitment is basic to success.

In order to quit, a sense of self-improvement is essential. The dental team should seek to reward and reinforce those 16% of individuals who have recently quit or are off cigarettes. About one third of those who smoke try to quit each year. Seven percent succeed. A programmatic approach with a concerned health professional increases this rate significantly. If we can assist in this expression of concern for patients by providing the monograph mentioned earlier in this update, please contact this office.

We hope this short review of smoking and periodontal disease assists you in identifying periodontal disease in smokers, providing information to those who are at risk and may be contemplating cessation, altering the maintenance requirements for smokers and approaching the smoking patient with a perspective for how difficult an addiction it is to conquer.
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