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Evidence for Active Host Control of the Periodontal Microflora

F.-M. EGGERT*1, M.H. McLEOD1, G. FLOWERDEW2
(1Dept. Oral Health Sciences, U. of Alberta, 2 Clin. Res. Centre, Dalhousie University, Nova Scotia, Canada).

See the Bottom Line for Smoking & Your Gums


Many adults have encountered suspected periodontal pathogens and they have low levels of circulating antibodies as evidence of the encounter. But most of these adults do not have severe periodontal diseases and they do not carry high numbers of these organisms in their mouths. In contrast, most periodontal patients have elevated levels of circulating antibodies to these suspected periodontal pathogens and they carry appreciable numbers of these organisms in their mouths. Our study examined the relationship between infection with specific marker organisms Porphyromonas gingivalis, Actinobacillus (Haemophilus) actinomycetemcomitans and Prevotella intermedia , as detected with the Evalusiteä immunoassay (Kodak Canada Inc.), and smoking versus non-smoking status of patients. With its internal positive controls, the immunoassay provides a reliable measurement of sites negative for all 3 marker organisms at the threshold levels set for the assay. We found a significant difference of infection with the marker organisms, between smokers and non-smokers in patients attending our specialist periodontal practices (F-ME 19 new & 36 recall patients; MHM 100 new & 79 recall patients).

For patients receiving regular periodontal treatment, we found a significant proportion of samples and sites negative for all 3 marker organisms in non-smokers while smokers did not show an equally high proportion of non-infected sites (F-ME & MHM pooled n = 234, c 2, p < 0.001). For patients not receiving regular periodontal treatment we found no difference in negatives sites/samples between smokers and non-smokers. On a whole-mouth basis there was no significant effect of smoking vs non-smoking on whether A. actinomycetemcomitans or P. gingivalis were present (F-ME n=55 c 2 = NS, MHM n=179 c 2 = NS). Smoking was associated with an increased presence of P. intermedia in one series of patients (MHM new: n = 100, c 2 , p < 0.05; MHM recall: n=79,c 2 , p < 0.01), but not in the other (F-ME new & recall).

Immunoassay results identify problems with host defences at 2 different biological levels: 1) Smoking inhibits the ability of a periodontal patient to suppress the 3 marker organisms following conventional periodontal therapy and thereby complicates periodontal treatment through inhibiting its beneficial effects. Smoking interferes with defence mechanisms accessible at or within the mucosal surface. 2) Whether A. actinomycetemcomitans or P. gingivalis are present at periodontal sites is determined by factors that appear to operate at a second level within host defences that is not accessible to the effects of smoking.

The opposing effects of smoking versus periodontal therapy indicate a dynamic balance between host mechanisms that lead to mucosal integrity and factors affecting growth of the mucosal microflora in the periodontal environment.  

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The Bottom Line for Smoking and the Health of Your Gums is:

a) Smokers cannot clear bacteria from their mucosal surfaces to the same extent as non-smokers.

b) Our work shows that the magnitude of this effect is about 5 to 6 times (500 to 600%) worse clearance than non-smokers. The magnitude of the effect we have observed is about equal to that demonstrated by other means in papers such as that of Dr. Walter Loesche (Loesche, W.R. et al,1997, J. Clinical Periodontology 24: 718 - 726).

c) Smoking diminishes the otherwise beneficial effects of conventional non-surgical periodontal therapy. This means you will find it harder to get a good result from periodontal maintenance treatment.

ã1997 Copyright F-Michael Eggert, All rights reserved.  

 

 

 

Presented at:

Periodontal Diseases and Human Health. New Directions in Periodontal Medicine

Sunstar-Chapel Hill Symposium, 1997 Chapel Hill, North Carolina, USA 


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