Secondhand smoke and risk for Periodontitis.
As dental hygienists, we need no one to tell us how debilitating periodontal disease can be for our patients. The attachment loss, tooth loss and infection can be a threat to their oral health along with the problems of diminished confidence, quality of life and self-image. Our magazines and scientific journals are full of articles regarding products to treat periodontal diseases, or instruments to help us provide more effective therapy, or research and continuing education courses to aid in our constant pursuit of optimal oral health. This article is an update on what we know and what we need to know regarding Periodontitis and the impact of a significant lifestyle factor: cigarette smoke. (1)
The Impact on Periodontitis by Smoking
Thirty percent of Americans reportedly have moderate to severe periodontitis; (2) this represents approximately 93 million people. (3) In addition, the institutions that we trust to keep our statistics up to date (Centers for Disease Control and Prevention and Centers for Health Statistics) have warned that our current estimates underrepresent the number of actual cases of periodontitis by as much as 50 percent. (3) Suddenly, it seems that periodontitis is even more prevalent than we once thought.
If so many people have periodontitis, what are its causes? From what historical and current literature tells us, we know that periodontal diseases are multifactorial and can be impacted by systemic disease, medication, personal oral hygiene and genetics, but the greatest single modifiable behavior associated with the disease is smoking. At least 20 percent of periodontitis cases are attributed to smoking. (2)
It is common knowledge that smoking is a vasodilator, but less well known is that smoking heavily influences the immune response, in more ways than decreased blood flow. For instance, nicotine and carbon monoxide found in cigarette smoke negatively influence wound healing. In fact, patients who smoke are expected to respond less favorably, or unfavorably to periodontal treatment. (4) Bergstrom et al. went so far as to say that "no other known factor can match the strength of smoking in causing harm to the periodontium. "(4) Specifically, smoking impacts neutrophils by encouraging their destructive activities. Fibroblasts are also affected with consequences for connective tissue, and smoking encourages the proliferation of inflammatory mediators. Smoking has even been associated with an increased prevalence of potential periodontal pathogens. (5-7) Protective antibodies are reduced in smokers, specifically immunoglobulin G to A. actinomycetemcomitans, (8) a pathogen known for its association with localized aggressive periodontitis.
Since the most recent update by the American Academy of Periodontology (AAP) to the Periodontal Classification System in 1999, the Surgeon General has made statements recognizing the dangers of cigarette smoke, and has linked smoking to causation of periodontal disease. (4), (9), (10) So while no formal name exists for smoking-induced periodontitis, we do know that smoking causes periodontitis in a dose-dependent relaationship. (11), (12)
Social and Political Acceptance of Smoking
The health consequences of smoking are part of the reason that America has seen a progression in social reaction to smoking. The changing health knowledge and governmental stance on smoking can be tracked by reading statements from the U.S. Surgeon General to the public. For instance, in 1964, Surgeon General Luther Terry spoke out against smoking, linking it to pulmonary disease. (13) Since that time, more than 20 reports published by the U.S. Surgeon Generals have highlighted the hazards of smoking.
In dentistry, we have seen the change from "have you thought about quitting?" to "you should quit." With the assistance of the "5 As": ask, advise, assess, assist and arrange a follow-up, dental hygienists can now play a large role in helping patients quit smoking. We have many resources available to us, from quitlines to pharma-cotherapeutics, and we are also seeing several insurance companies covering the costs of smoking cessation tools. Many clinicians use some sort of smoking cessation program, thanks in part to increased education for dentists and dental hygienists about smoking. (14) According to the Clinical Practice Guidelines of the U.S. Public Health Service, smokers who are approached at the right time may be in the frame of mind to attempt and have success at quitting. (15) Estimates show that nearly 70 percent of smokers see a clinician and report a desire to quit. (15) This means that we as clinicians have a real opportunity to impact the health of our patients. You may be thinking that your patients do not want to hear about quitting smoking. However, studies show that patients are actually responsive to dialogue about smoking in the dental office, (16) especially if the clinician can relate smoking to more than a habit. For example, linking smoking to a patient's existing intraoral complaints or a perceived health risk may be effective. (17) Researchers have actually gone so far as to call the time shared by dental hygienists and their patients "teachable moments," where instruction can lead to meaningful change. (16)
So how successful are programs designed to help patients quit? It has been reported that there are more former smokers than there are active smokers. (18)
What about Secondhand Smoke?
In 1972, the Surgeon General characterized involuntary smoking (secondhand smoke) as hazardous. (19) Involuntary smoking continued to surface in 1986, (20) 1994, (21) 2004 (9) and 2006. (22) These reports gave evidence of the changing social perception of smoking; initially, smoking was known as a common habit, fashion trend or rite of passage. It then became known as a dangerous health risk, and was later found to be dangerous whether voluntary or involuntary. Along with the evidence came decreased social acceptance. The 2004 report of the Surgeon General included 960 pages addressing health consequences of smoking. (9) The 2006 report drew major conclusions about tobacco smoke, with Surgeon General Richard Carmona, MO, stating, "There is no risk-free level of exposure to secondhand smoke." (22)
As of 2007, environmental tobacco smoke (ETS) exposure was one of the top three causes of preventable death in the United States. (23) Cigarette smoke is known to contain harmful substances, such as carbon monoxide, formaldehyde, cyanide, ammonia and nicotine, (22) among others to which one might not suspect even casual exposure. Cigarette smoke also contains more than 50 known carcinogens, (23) to the degree that it is categorized as a Class A carcinogen by the Environmental Protection Agency (EPA). (24) As such, it costs the United States roughly $10 million annually in non-smoker health care costs to treat smoking-related illness. (25) As with many diseases, social gradients exist in smoke exposure: minority races, those with the least education, and individuals at low income levels are more exposed. (26) Children from smoking households are particularly at risk for exposure since smoke-free law coverage does not limit smoking within personal residences. (26), (27) Research on smoking continues, with an increasing number of published papers addressing the dangers of secondhand smoke. In fact, recent research has focused on the reasons why secondhand smoke is dangerous, revealing that it poses many of the same dangers as firsthand smoke, (23), (28-30) with significant alteration to the immune response. What does that mean for us?
How Does Secondhand Smoke Relate to Periodontitis?
Passive (involuntary) smoking, like active smoking, impacts the immune response, namely polymorphonuclear leukocyte (PMN) function such as phagocytosis, chemotaxis and oxidative burst. (28) As reported by Numabe et al. in 1998, phagocytic activities of PMNs intensify after both smoking and passive smoking. (28) Additionally, the results suggested that certain substances in smoke overstimulate the host response in the oral cavity, (28) making the exposed more likely to experience attachment loss and tooth loss. (31) But what about secondhand smoke's effect on periodontitis?
According to Arbes et al., periodontal disease was 1.6 times more likely among nonsmokers with self-reported exposure to ETS (32) than those not exposed. In 2006, Nishida et al. attempted to determine just what passive smoke does in periodontitis. (33) Results revealed an elevated concentration of interleukin-1[beta], albumin and aspartate aminotransferase (AST), in those exposed to passive smoke (33)--all of which are markers associated with inflammation. Further, Nishida et al. determined that the evidence regarding the long-term influence of involuntary smoking on periodontitis progression was insufficient, so they conducted a study of Japanese employees during annual health checkups from 2003 to 2005. (34) Their study concluded that the risk for periodontitis progression was greater for those exposed to involuntary smoke, afong with increased inflammatory response intraorally. (34) Shizukuishi et al. added to Nishida's work, concluding that by stimulating inflammatory responses in periodontal tissues, "passive smoking exposure may be a risk factor of periodontal disease." (35) All of these scientific studies laid the foundation for emerging research further linking periodontitis to secondhand smoke.
Making It Current
For my thesis project at the University of North Carolina, I investigated environmental tobacco smoke and its association with periodontitis in nonsmokers. We found that among nonsmoking Americans participating in the NHANES survey from 1999 to 2004, nearly half had been exposed to cigarette smoke at a detectable level. Of those exposed, nearly 3 percent had moderate to severe periodontitis, not including gingivitis. Interestingly, if the new reports of under-representation of periodontitis are taken into account, many more Americans in the NHANES survey could have had moderate to severe periodontitis. After statistical analyses and adjustment, this finding had important implications: adults with high levels (> 1.5ng/mL) of measurable nicotine exposure had 89 percent higher odds of periodontitis. So as serum cotinine--isolated from nicotine--increases, so does the risk of periodontitis. This finding has relevance for preventive counseling and patient education. Casual exposure to ETS is something people don't think much about, but they should. Tobacco control policy has endeavored to limit public exposure to cigarette smoke, but health care providers are in a position to motivate patients to make protective decisions about voluntary exposure. We can inform parents about the risk of secondhand smoke to children to encourage less exposure at home. Additionally, informing patients who spend time in high-smoke environments about the potential risk to their health is our duty. By spreading knowledge and awareness, we will be empowering our patients to know the evidence and understand the risks, thereby helping prevent smoking-related disease.
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(33.) Nishida N, Yamamoto Y, Tanaka M, et al. Association between passive smoking and salivary markers related to periodontitis. J Clin Periodontol. 2006; 33(10): 717-23.
(34.) Nishida N, Yamamoto Y, Tanaka M, et al. Association between involuntary smoking and salivary markers related to periodontitis: a 2 year longiraiainal study. J Periodontol. 2008; 79(12): 2233-40.
(35.) Shizukuishi S. Smoking and periodontal disease. Clin Calcium 2007;17(2):226-32.
Julie Sutton, RDH, MS, graduated from the University of North Carolina-Chapel Hill School of Dentistry with a master's degree in dental hygiene education in May, 2011. She presented a poster on her research at the 2011 International Association of Dental Research meeting in San Diego, Calif. She also won an award from the UNC School of Dentistry for her poster presentation at the annual Dental Research and Review Day in February. She will present the poster at the ADHA Center for Lifelong Learning in Nashville, Tenn. in June, 2011. She is currently pursuing an academic career in dental hygiene education.
Sutton's thesis committee for the project included Anne Sanders, MSocSc, PhD, MHEc; Leah M. Ranney, PhD; and Rebecca S. Wilder, RDH, MS.
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|Date:||May 1, 2011|
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