Cigarette smoking is well known to be a major cause of oral disease and over the last few years the dental profession has made good progress towards addressing this problem, with better training at undergraduate level. But there are still major barriers standing in the way of widespread adoption of smoking cessation intervention by members of the general dental team.
Inadequate knowledge of the effects of smoking, lack of training in smoking cessation techniques, shortage of time and a deficiency in financial remuneration appear to be the main obstacles preventing progress. This two-part article will describe the up-to-date theories of the effects of smoking on oral disease and secondly the practical steps that can be taken to reduce the damaging effects of tobacco use.
Smoking is a major cause of periodontitis, second only to bacterial plaque; and the prevalence and severity of the disease is associated with the degree and duration of smoking habit. Tobacco use has been linked to a 2-8 fold increase risk for periodontal attachment loss and a 4 fold increased in the risk of aggressive periodontitis and associated tooth loss. Cotinine, the metabolite of nicotine and the best surrogate measure of nicotine intake, as measured in saliva, has been shown to be correlated with the incidence of caries, probing pocket depths, tooth mobility and the presence of adverse oral mucosal changes (1). The areas of the mouth mostly affected appear to be the mandibular anterior teeth and maxillary lingual sites. Paradoxically, inflammation in the gingivae is noticeably reduced in smokers, with an associated recession, a fibrotic appearance and reduced bleeding. Worryingly, these effects can be seen after a relatively short period of smoking and so often present in young smokers (2).
A range of damaging bacterial species, or periodontal pathogens, is now considered as the major factor in the development of periodontitis. This oral microflora is difficult to study, and the data is equivocal, but results suggest that the bacterial balanced is disturbed by smoking, towards the proliferation of more aggressive forms, which are more difficult to eliminate following scaling and root planning. Smoking appears to create an environment that favours colonisation of pathogens in shallow periodontal pockets, encouraging infection in new sites and the development of periodontitis in otherwise healthy people. However, this problem appears to be partially eliminated by locally delivered antibiotics, such as doxycycline gel.
As well as periodontitis, tobacco use also leads to malignant lesions, increasing the risk by 6-fold for leukoplakia and a 7 to 10-fold increase in oral cancer. In addition, treatment, both surgical and non-surgical is less successful in smokers, largely due to a reduced healing capacity, which is also implicated in the increased failure rate of implants in smokers (3).
Yet, what is it about tobacco that causes these damaging effects? Tobacco smoke contains about 4,500 gaseous and particulate components; including carcinogens, toxins and oxidants, notably arsenic, cyanide, carbon monoxide and nicotine (4). These substances reduce saliva and mucin production, the natural defence mechanisms of the oral cavity. Furthermore, the high temperature of burning tobacco generates very high concentrations of free radicals (or reactive oxygen species), which are highly charged, destructive moieties which have the potential to react with and damage macromolecules such as DNA and lipoproteins, leading to pro-carcinogenic mutations and cell membrane damage. Whilst these free-radicals are normally neutralised by dietary antioxidants, such as vitamins C and E and Selenium, smokers have poorer dietary intake and lower circulating levels potentially leading to cellular damage.
Smoking also impairs the ability of an individual to react to periodontal attack; including derangement of the immune system include alteration in neutrophil function, vascular factors and increased production of specific inflammatory mediators. Whilst previously, nicotine was regarded only as the addictive element of tobacco and having little direct effect on the disease process, recent research has elevated its role in periodontitis. Locally, nicotine concentrates in the gingival crevicular fluid, binding to the root surface and impairing fibroblast function. Reduced collagen production, increasing collagenase activity and the production of growth factors stimulating osteoclastic differentiation have all been demonstrated in vitro. Nicotine also increases the expression of several interleukins, which are directly implicated in periodontal bone destruction. Systemically, nicotine reduces neutrophil activity, thus reducing the ability to fight off infection and causing a shift in activity towards more destructive processes, affecting the gingivae and bone.
Much of these affects of nicotine are mediated through specific nicotine receptors found on the cell membranes of the immune cells, suggesting a direct effect of smoking on cellular physiology. However, recent research suggests that the inflammatory immune response is modulated by the brain and central nervous system through the so called ‘inflammatory reflex’: the brain affects nerves, neurotransmitters and hormones, which act directly on the immune system. The affect is that depression, anxiety and stress reduce the body’s ability to fight infection, and this is seen by increasing the risk of periodontitis (5). Smoking, contrary to widespread belief, increases stress, especially during the period of nicotine withdrawal experienced by every smoker between cigarettes.
The removal of nicotine and other toxins after quitting smoking quickly has an effect. Non-surgical treatment is much more effective, with improved probing depth and attachment loss and other parameters return towards normal over time (6). It has been suggested that smoking cessation is the key in prevention and control of periodontal disease because it affects both the bacterial and host responses.
1) Barnfather K, Cope G, Chapple I. Relationship between salivary cotinine levels, oral health and lifestyle. IADR/AADR/CADR conference proceeding, San Diego 2004.
2) Johnson G, Guthmiller J. The impact of cigarette smoking on periodontal disease and treatment. Periodontology 2000 2007; 44: 178-194.
3) Binnie V. Addressing the topic of smoking cessation in a dental setting. Periodontology 2000 2008; 48: 170-178.
4) Stampfli M, Anderson G. How cigarette smoke skews immune responses to promote infection, lung disease and cancer. Nature Reviews Immunology 2009; 9: 377-384.
5) Breivik T, Gundersen Y, Gjermo P, von Hörsten S, Opstad P. Nicotinic acetylcholine receptor activation mediates nicotine-induced enhancement of experimental periodontitis. J Periodont Res 2009; 44: 297-304
6) Preshaw P, Heasman L, Stacey F, Steen N, McCracken G, Heasman P. The effect of quitting smoking on chronic periodontitis. J Clin Periodontol 2005; 32: 869-879
Dr. Graham Cope is an Honorary Senior Research Fellow at the University of Birmingham and is a clinical chemist by training and has worked on smoking-related research topics, specifically cotinine testing, most of his career. He is now the director of a medical diagnostics company specialising in point-of-care cotinine testing. Contact firstname.lastname@example.org
Anwen Cope is a recent graduate of Cardiff University Dental School and is a Vocational Dental Practitioner in South Wales.