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(Theilade et al, 1965), in which all oral hygiene is withdrawn over a period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 ginffivitis occurs more frequently in smokers. Possible mechanisms
for this increased susceptibili b ty 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.
References:
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.
TO
TOP |