Smoking and Periodontal Disease
Dental plaque is the primary aetiological factor in periodontal diseases.
However, there are many other factors that can modify how an individual's periodontal tissues will respond to the accumulation of dental plaque. Among such risk factors, there is increasing evidence that smoking tobacco products alters the expression and rate of progression of periodontal diseases.
Epidemiological studies have provided evidence that tobacco smokers have poorer oral hygiene than non- smokers, and also have increased quantities of dental calculus. Most of these differences can be attributed to less favourable toothbrushing habits, particularly evident in male smokers. However, smoking is associated with a decreased flow of saliva, which may explain the increased tendency to form dental calculus.
Smoking and gingivitis
Heavy smokers often present with a thickened, fibrotic appearance of their gingival tissues. Studies following the protocol of the experimental gingivitis in man studies (Theilade et al, 1965), in which all oral hygiene is withdrawn over a period of up to four weeks and the development of gingivitis is observed, have found that the development of gingivitis is delayed among smokers. The rate of plaque accumulation is similar in smokers and non-smokers; however, smokers show less gingival inflammatory change, with less gingival bleeding, gingival redness and gingival fluid flow. (Bergstrom and Preber, 1986). Hence, it appears that smoking may suppress the normal immune response to the accumulation of plaque. The major clinical implication of these findings is that the masking of gingival bleeding in smokers may lead to a failure to recognise the presence of periodontal diseases.
Acute necrotizing ulcerative gingivitis occurs more frequently in smokers. Possible mechanisms for this increased susceptibility include vasoconstriction of gingival blood vessels, reduced activity of leukocytes, and proliferation of anaerobic, fuso-spirochaetal micro-organisms, These factors interact with the other factors implicated in the aetiology of ANUG, namely poor oral hygiene and mental stress.
Smoking and periodontitis
Recent studies have revealed an association between smoking and more severe periodontitis. After allowing for the effects of oral hygiene and the patient's age, smoking has been shown to be associated with deeper periodontal pockets and more alveolar bone loss. There is also evidence that the rate of progression of periodontitis is more rapid among smokers.
The effects of smoking on the response of the periodontal tissues to treatment have only recently been explored. Preber and Bergstrom (1985, 1990), have found that smoking has a detrimental effect on the response of the tissues to both surgical and non-surgical periodontal treatments. Smokers exhibit significantly less reductions in probing depths than that observed among non-smokers.
Possible mechanisms through which smoking alters the expression of periodontal diseases include effects on the composition of plaque and effects on the host response. It has been hypothesized that smoking, through altering the oxidation-reduction potential in favour of anaerobic micro-organisms, would favour the formation of a more pathogenic plaque. However, in vive evidence for an altered composition of plaque is weak. Tobacco may alter the immune system's capacity to maintain an ecological balance. Smoking diminishes oral cellular immunity by reducing the chemotactic response and phagocytic capacity ofleukocytes. Smoking causes peripheral vasoconstriction, further limiting the ability of the tissues to effect an immune response.
Advice to patients
In spite of the awareness of the adverse effects of smoking on health, many of your patients will continue to be smokers. Many will not be aware of the effects that tobacco may have on their periodontalhealth. There is ample evidence in the literature to support advising patients to reduce or stop their smoking as part of the periodontal management of patients.
Extra care needs to be taken in the periodontal examination of smokers. It is likely that many of the more visual signs of periodontal diseases will be masked. However, careful periodontal probing and examination of radiographs will reveal the level of attachment loss present.
Smokers need to be informed prior to the commencement of periodontal treatment that the outcome of their treatment may be compromised if they continue to smoke.
It is important to realise that the majority of smokers give up smoking without the aid of structured smoking cessation programs. By simply taking a few minutes to discuss breaking the habit of smoking with a patient may be the prompt that is needed for that patient to reduce or stop smoking. However, some patients will benefit from a more structured approach to quitting smoking. The Anti-Cancer Foundation has available a range of materials for use by health professionals. It is worthwhile having this material available in your surgery for the patient to take with them.
Theilade E, Wright W,Jensen S, Loe H. (1965) Experimental gingivitis in man II. A longitudinal clinical and bacteriological study investigation. J Perio Res 1:1-13.
BergstromJ, Preber H. (1986) The influence of cigarette smoking on the development of experimental gingivitis. J Perio Res 21: 66876.
Preber H, BergstromJ. (3985) The effect of non- surgical treatment on periodontal pockets in smokers and non-smoker patients. Acta Odont Scand 43: 315-20.
Preber H, BergstromJ. (1990) Effect of cigarette smoking on periodontal healing following surgical therapy. J Clin Perio 17: 324-8
MacGregor IDM. Smoking and periodontal disease. In: Seymour RA, Heasman PA. (eds). Drugs, diseases and the periodontium. Oxford University Press, 1992. pp117-134.
This material has been compiled with the assistance of Dr Louise Brown, Lecturer in Periodontics at the University of Melbourne.