Abstract

Subgingival plaque samples were obtained from 162 sites in 27 adult periodontitis patients and 162 sites in 27 healthy patients using a standardized lavage technique. The distribution of 10 different microbial morphotypes was determined by darkfield microscopy. The lavage technique selectively samples the loosely adherent plaque at the base of the periodontal pocket and not the tooth-associated, adherent plaque. This standardized technique permits quantitative comparisons of numerical density of morphotype composition at different sites, in addition to qualitative comparisons or relative proportions. There was a significant positive association between the numerical density of each morphotype within the non-adherent plaque and the number of sites at which the organism was detected in both healthy and diseased subjects. A previously undescribed darkfield morphotype, has been detected with this method. This morphotype, a small motile coccobacillus (S-MO-CB) has been found to be the numerically dominant species in both health and disease. This morphotype has been recovered in pure culture following passage through a 0.4 mu filter and includes organisms of the Wollinella and Campylobacter genus. Non-motile organisms comprised less than 1-2% of the sample from healthy and diseased sites. Motile forms, such as spirochetes, had a high frequency of detection in healthy individuals. Analysis of pooled plaque samples revealed that the prevalence of cocci and fusiforms was significantly elevated in patients with healthy periodontium, as compared to patients with adult periodontitis. In adult periodontitis patients, the frequency of occurrence of medium spirochetes, filaments and small nonmotile rods was significantly elevated in pooled plaque. Analysis of individual sites indicated that the proportion and numerical density of most morphotypes within the non-adherent plaque were not significantly different in disease as compared to health. Disease is characterized by an increased % of small spirochetes and fusiforms at each site. At diseased sites which harbor small spirochetes, the numerical density is elevated four-fold, as compared to healthy sites which have small spirochetes. The numerical density of other morphotypes is not significantly different comparing healthy sites to diseased sites. Thus, the increase in the % of small spirochetes in disease in due to a site-localized four-fold increase in numerical density within the non-adherent plaque.

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