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Smoking-associated periodontitis is not simply a reflection of oral cleanliness. Smoking extends a favorable habitat for bacteria such as P. gingivalis, P. intermedia, and A. actinomycetemcomitans to shallow sites (< or =5 mm). Molecular byproducts of smoking interfere with mechanisms that normally contain growth of damaging bacteria at the surface of the oral mucosa in gingival crevices. In this way, smoking can promote early development of periodontal lesions.

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National efforts directed toward improving our understanding of the epidemiology of periodontal disease began nearly a half century ago following the development of Russell's periodontal index (PI). United States Public Health Service agencies began national surveillance activities for periodontal disease with the first National Health Examination Survey in 1960 to 1962, and this continued periodically through 2004 in the National Health and Nutrition Examination Survey (NHANES). Periodontal disease status was assessed by using the PI in the earlier national health surveys, but beginning in the 1980s, direct measures for clinical attachment loss were made in national health surveys and continued through 2004 in NHANES. This article provides a general history of the development and implementation of national surveillance efforts for periodontal disease from the mid‐1950s to 2005. It also provides brief background information on the factors that have influenced these national surveillance efforts.

We used an immunoassay to demonstrate marker organisms (Porphyromonas gingivalis, Prevotella intermedia, and Actinobacillus actinomycetemcomitans) in 3 private practice populations (F‐ME periodontist, 55 patients; MHM periodontist, 179 patients; and EWM general dentist, 19 patients). Occurrence of the marker organisms involves the whole oral environment, not just individual sites, as shown by close correlation between presence of the marker organisms in 2 independent sites/samples within a single mouth. Presence of the marker P. gingivalis (and P. intermedia) relates closely to periodontal pocketing while presence of A. actinomycetemcomitans does not have this pocket‐associated characteristic. There was no significant relationship between presence of the marker organisms and the number of teeth in a mouth, and in the periodontal practice patients there was no significant effect of gender on occurrence of the marker organisms. A. actinomycetemcomitans and the other 2 markers were found over the entire age range (12 to 75) of our patients. Regular periodontal treatment reduced occurrence of all marker organisms and increased the frequency of marker‐negative patients and sites. Occurrence of the marker organisms above immunoassay threshold levels appears to represent how receptive a patient is to each individual organism. Most patients appear receptive to the presence of P. intermedia whether treated or not. Significantly fewer patients who underwent regular treatment show the presence of P. gingivalis or A. actinomycetemcomitans when compared to untreated patients. Diagnostic application of microbial markers requires ongoing clinical assessment of patients and careful clinical judgment. J Periodontol 1998;69:1382–1391.