Smoking and Periodontal Disease

Smoking and Periodontal Disease

Philip M. Preshaw, Leandro Chambrone and Karen F. Novak

The Smoking Epidemic

Smoking is highly prevalent and can be considered an epidemic in both developed and developing nations. In the United States in 1993, 25.4% of the population smoked; 27.0% of men smoked, and 24.0% of women smoked.35 By 2010, this had decreased to 19.3% of the total population, with 21.5% of men smoking and 17.3% of women smoking.19 Among dentate individuals during the period from 1988 to 1994, 27.9% of adults were current smokers, and 23.3% were former smokers.2 Smoking was higher in younger age groups (i.e., ≤34 years old) as compared with older age groups (≥55 years old), and it was more common among men (30.9%) as compared with women (25.1%).100 In 2012, roughly 43.4 million Americans were smokers, with 8.6 million people suffering from a severe smoking-related disease and 443,000 deaths (or 1 in 5 deaths) being attributable to smoking and exposure to secondhand smoke each year.I In the European Union in 2012, approximately 32.0% of the population were smokers (41% of men and 22% of women)106; this number ranged from 16% in Sweden to 48% in Greece. Smoking accounts for 650,000 deaths each year (or 1 in 7 deaths) in these countries.4 Overall, around 16% of all deaths in European adults more than 30 old were related to tobacco smoking.106 Furthermore, 79,000 nonsmoking Europeans die each year as a result of passive smoking. Worldwide, it is estimated that approximately 13% of the population 15 years old or older are smokers (i.e., there are >1.3 billion smokers [around 1 billion men and 300 million women]); that tobacco kills up to half of its users; and that more than 80% of smokers live in low- and middle-income countries.107 Globally, smoking accounts for 1 in 5 deaths among men 30 years old and older and 1 in 20 deaths among women 30 years old and older.107

Smoking is harmful to almost every organ in the body, and it is associated with multiple diseases that reduce life expectancy and quality of life. Diseases associated with smoking include lung cancer, heart disease, stroke, emphysema, bronchitis, and cancers of the oral cavity, bladder, kidney, stomach, liver, and cervix. Approximately half of long-term smokers will die early as a result of smoking, and those who die before the age of 70 years will lose an average of 20 years of life.30 Most deaths from smoking are due to lung cancer, chronic obstructive pulmonary disease, and coronary heart disease.

Tobacco smoke contains thousands of noxious chemicals, and it comprises a gaseous phase and a solid (particulate) phase. The gas phase contains carbon monoxide, ammonia, formaldehyde, hydrogen cyanide, and many other toxic and irritant compounds, including more than 60 known carcinogens such as benzo(a)pyrene and dimethylnitrosamine. The particulate phase includes nicotine, “tar” (itself made up of many toxic chemicals), benzene, and benzo(a)pyrene. Tar is inhaled with the smoke. In its condensate form, it is the sticky brown substance that stains fingers and teeth yellow and brown. Nicotine, which is an alkaloid, is found within the tobacco leaf and evaporates when the cigarette is lighted. It is quickly absorbed in the lungs, and it reaches the brain within 10 to 19 seconds. Nicotine is highly addictive. It causes a rise in blood pressure, increased heart and respiratory rates, and peripheral vasoconstriction.

All dental patients must be asked about their smoking status. Current smoking status is the minimal information that must be recorded (e.g., “Patient is currently smoking X cigarettes per day”), but the importance of cumulative exposure to cigarette smoke mandates that it is more appropriate to record pack-years of smoking (Box 10-1). Biochemical tests can also be used to assess smoking status, including exhaled carbon monoxide and the measurement of cotinine (the major metabolite of nicotine) in serum, saliva, or urine. Cotinine is measured in preference to nicotine because the half-life of nicotine is short (≈1 to 2 hours),76 whereas that of cotinine is approximately 20 hours.50 Plasma and saliva cotinine concentrations in smokers are approximately 300 ng/mL and the urine concentration is approximately 1500 ng/mL. Nonsmokers usually have plasma and saliva concentrations of less than 2 ng/mL, unless they are passive smokers.

Box 10-1   The Challenge of Assessing Smoking Status

Current Smokers

Ask about current smoking and past smoking. Many smokers are trying to quit and therefore simply asking how many cigarettes they are smoking today may not give an accurate assessment of their lifetime exposure (e.g., a patient who is currently smoking 5 cigarettes per day may have been smoking 40 cigarettes per day until yesterday, when she decided to cut down). Try to get an indication of their approximate level of smoking (e.g., the average number of cigarettes per day for a certain number of years). It can also be useful to calculate the number of pack-years:

< ?xml:namespace prefix = "mml" />Pack-years=Number of packs smoked per day × Number of years of smoking


In other words, 1 pack-year is the cumulative exposure that corresponds with the smoking of 1 pack of 20 cigarettes per day for 1 year. For example, a smoker who has smoked 20 cigarettes per day for 15 years has 15 pack-years of smoking.

When Is a Smoker not a Smoker?

It must be noted that many periodontal research studies have not used these definitions, and this can sometimes make it difficult to interpret the studies, particularly in the context of what constitutes a former smoker. For example, from an exposure point of view, there is a big difference between someone who smoked 5 cigarettes per day for 10 years and who quit 30 years ago as compared with someone who smoked 40 cigarettes per day for 20 years and quit 6 months ago. It is always best in clinical practice to gather full information about each patient’s smoking history.

Smoking is the major risk factor for periodontitis, and it affects the prevalence, extent, and severity of disease. In addition, smoking has an adverse impact on the clinical outcome of nonsurgical and surgical therapy as well as the long-term success of implant placement. With 41.9% of periodontitis cases in the United States reported as being attributable to smoking,100 it is essential to understand the impact of smoking on the initiation, progression, and management of the disease. This chapter discusses the effects of smoking on the prevalence, severity, etiology, and pathogenesis of periodontal disease as well as its impact on treatment. The reader is referred to several excellent reviews of the topic for detailed results of specific studies.44,1,54,53,69,70,83,101,21,105

Effects of Smoking on the Prevalence and Severity of Periodontal Diseases


Controlled clinical studies have demonstrated that, in human models of experimental gingivitis, the development of inflammation in response to plaque accumulation is reduced in smokers as compared with nonsmokers (Table 10-1).15,26 In addition, cross-sectional studies have consistently demonstrated that smokers present with less gingival inflammation than nonsmokers.13,8,9,78,77 These data suggest that smokers have a decreased expression of clinical inflammation in the presence of plaque accumulation as compared with nonsmokers. The microbiologic, immunologic, and physiologic factors that may account for this observation are discussed in detail later in this chapter.

TABLE 10-1

Effects of Smoking on the Prevalence and Severity of Periodontal Disease

Periodontal Disease Impact of Smoking
Gingivitis ↓ Gingival inflammation and bleeding on probing
Periodontitis ↑ Prevalence and severity of periodontal destruction
  ↑ Pocket depth, attachment loss, and bone loss
  ↑ Rate of periodontal destruction
  ↑ Prevalence of severe periodontitis
  ↑ Tooth loss
  ↑ Prevalence with increased number of cigarettes smoked per day
  ↓ Prevalence and severity with smoking cessation

↓, Decreased; ↑, increased.


Although gingival inflammation in smokers appears to be reduced in response to plaque accumulation as compared with nonsmokers, an overwhelming body of data points to smoking as a major risk factor for increasing the prevalence and severity of periodontal destruction. Multiple cross-sectional and longitudinal studies have demonstrated that pocket depth, attachment loss, and alveolar bone loss are more prevalent and severe in patients who smoke as compared with nonsmokers.54,53,83,101 An assessment of the relationship between cigarette smoking and periodontitis was performed in more than 12,000 dentate individuals who were more than 18 years old as part of the Third National Health and Nutrition Examination Survey.100 Periodontitis was defined as one or more sites with clinical attachment loss of 4 mm or greater and pocket depth of 4 mm or greater. Smoking status was defined with the use of criteria established by the Centers for Disease Control and Prevention (see Box 10-1). Of the more than 12,000 individuals studied, 9.2% had periodontitis; this represented approximately 15 million cases of periodontitis in the United States. On average, smokers were four times as likely to have periodontitis as compared with persons who had never smoked after adjusting for age, gender, race/ethnicity, education, and income/poverty ratio. Former smokers were 1.7 times more likely to have periodontitis than persons who had never smoked. This study also demonstrated a dose–response relationship between cigarettes smoked per day and the odds of having periodontitis. In subjects smoking nine or fewer cigarettes per day, the odds for having periodontitis were 2.8, whereas subjects who smoked 31 or more cigarettes per day were almost six times more likely to have periodontitis. In former smokers, the odds of having periodontitis declined with the number of years since quitting. These data indicated that approximately 42% of periodontitis cases (6.4 million cases) in the US adult population were attributable to current smoking and that approximately 11% (1.7 million cases) were attributable to former smoking. These data highlight the serious threat to dental public health posed by cigarette smoking and raise questions about the best methods for managing periodontitis in patients who smoke (Box 10-2).

Box 10-2   Should We Change How We Manage Periodontal Disease?


These questions are intended to be controversial! It is clear that smoking has a huge deleterious impact on periodontal status, and smoking cessation MUST be a core part of periodontal treatment protocols in patients with periodontitis who smoke. The answer to the first question is almost certainly a resounding “YES,” but this probably will never be able to be tested. The answer to the second question is more difficult. Certainly smokers with periodontitis must be educated about the harm that they are causing to their periodontal tissues, and they must be encouraged and helped to quit smoking. Treatment outcomes are improved among smokers who quit as compared with those who continue to smoke.81

These data are consistent with the findings of other cross-sectional studies performed in the United States and Europe. The odds ratio for periodontitis in current smokers has been estimated to range from as low as 1.5 to as high as 7.3, depending on the observed severity of periodontitis.70 A meta-analysis of data from six such studies involving 2361 subjects indicated that current smokers were almost three times more likely to have severe periodontitis than nonsmokers.69 The detrimental impact of long-term smoking on the periodontal and dental status of older adults has been clearly demonstrated. Older adult smokers are approximately three times more likely to have severe periodontal disease,7,62 and the number of years of tobacco use is a significant factor in tooth loss, coronal root caries, and periodontal disease.51,52

Smoking has also been shown to affect periodontal disease severity in younger individuals. Cigarette smoking is associated with increased severity of generalized aggressive periodontitis in young adults,92 and those who smoke are 3.8 times more likely to have periodontitis as compared with nonsmokers.39 Longitudinal studies have demonstrated that young individuals who smoke more than 15 cigarettes per day showed the highest risk for tooth loss.47 In addition, smokers are more than six times as likely as nonsmokers to demonstrate continued attachment loss.49 Over a 10-year period, bone loss has been reported to be twice as rapid in smokers as in nonsmokers16 and to proceed more rapidly even in the presence of excellent plaque control.10 Less information is available about the effects of cigar and pipe smoking, but it appears that effects similar to those of cigarette smoking are observed with these forms of tobacco use.3,31,32,60 The prevalence of moderate and severe periodontitis and the percentage of teeth with more than 5 mm of attachment loss were most severe in current cigarette smokers, but cigar and pipe smokers showed a severity of disease that was intermediate between that of current cigarette smokers and nonsmokers.3 Tooth loss is also increased among cigar and pipe smokers as compared with nonsmokers.60

Former smokers have less risk for periodontitis than current smokers but more risk than nonsmokers, and the risk for periodontitis decreases with the increasing number of years since quitting smoking.100 This suggests that the negative effects of smoking on the host are reversible with smoking cessation and therefore that smoking cessation programs must be an integral component of periodontal education and therapy (Box 10-3). Several tobacco intervention approaches can be used when helping the patient deal with the physiologic factors (i.e., nicotine withdrawal symptoms) and the psychologic factors associated with smoking cessation (Box 10-4).71,85

Box 10-3   Helping Your Patients to Quit Smoking

Smoking cessation is a public health priority for governments around the world. Excellent online resources are available to provide information about the harmful effects of smoking and to help people to quit, including the following:

Smoking cessation must be an integral part of the management of dental patients who smoke, and it is the responsibility of all dental care professionals to address this issue with their patients. The dental team is well placed to provide this treatment, because they see patients on a regular basis as part of ongoing routine dental management. Furthermore, interventions to help patients quit smoking in dental practices are effective, with quit rates of 15% to 20% as compared with approximately 5% in control groups.88 The whole dental team should therefore be involved in smoking cessation, but this is not always the case. Why? Some of the barriers to providing smoking cessation counseling in the dental practice are shown in Table 10-2.

Various methods for helping patients to quit smoking in the dental environment have been described, and these are typically referred to as brief intervention programs. One such program8 is known as the “5 A’s” and it laid out as follows:

ASK Ask the patient about his or her smoking status (see Box 10-1).

ADVISE Advise smokers of the associations between oral disease and smoking.

ASSESS Assess the patient’s interest in and readiness to attempt smoking cessation.

ASSIST Assist the patient with his or her quit attempt.

ARRANGE Arrange for a follow-up visit or a referral to professional smoking cessation services.

A simplified version that is particularly useful for the dental team is the AAR program, which is broken down as follows:

Box 10-4   Methods of Smoking Cessation

Brief Intervention Program in Primary Care

Success rate at 12 months is 5% to 10%.85 Brief advice is very important and should always be given at every dental visit. Enhancing the role of specially trained dental hygienists and prevention auxiliaries in giving lifestyle advice is of major benefit. If the dental team gave even brief advice to most of their smoking patients and achieved a low cessation rate of 5% over time, a significant proportion of smokers in the population would be assisted to quit each year.

Nicotine Replacement Therapy

Success rate at 12 months is 10% to 20%. Nicotine replacement therapy (NRT) generally doubles the success rate of smoking cessation. For example, in primary care settings in which brief advice is given, 12-month success rates double from around 5% to around 10% if NRT is also used. In an intensive setting such as a smoker’s clinic, success rates increase from around 10% to up to 20%. NRT is not a magic cure, but it helps with cravings and withdrawal when a person quits smoking. Although NRT products do contain nicotine, they do not contain the toxic products such as tar and carbon monoxide that are found in cigarette smoke. NRT products include the following:

TABLE 10-2

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