Factors affecting human supragingival biofilm composition. I. Plaque mass

Abstract

Objective-To examine the relationship between total DNA probe counts of supragingival biofilm samples, clinical parameters and supragingival biofilm composition.Methods-Supragingival plaque samples were taken from 187 systemically healthy adult subjects at baseline (N samples = 4,745). All samples were individually analyzed for their content of 40 bacterial species using checkerboard DNA-DNA hybridization. The relationship between total DNA probe counts and microbial composition was examined by sub-setting the data into 10 groups based on 10 percentile increments of the total DNA probe counts. Differences among groups in terms of species counts and proportions were sought as well as relationships of total plaque DNA probe count and clinical parameters.Results-There was a wide distribution in mean total DNA probe counts among the 187 subjects. With increasing total plaque levels there was a change in the proportions of individual species and microbial complexes. "Small plaques" were characterized by high proportions of species in the yellow, orange, purple and "other" complexes; plaques of moderate mass were characterized by high proportions of Actinomyces and purple complex species, while "large plaques" exhibited increased proportions of green and orange complex species. Measures of gingival inflammation, pocket depth and recession were significantly positively associated with total DNA probe counts. Increased plaque numbers were related to increased pocket depth irrespective of presence or absence of gingival inflammation.Conclusion-The proportions of individual species and microbial complexes in supragingival biofilms are influenced by the total numbers of organisms in the biofilm.

The Biofilm Community: Rebels with a Cause

“…This, in turn, is further perpetuated by autogenic microbial succession and regulated microbiota interactions [31]. While dysbiosis has also been used to describe disease state due to a shift in the normal resident microbiota, previous studies have examined the changes in the microbiota from different oral habitat over a time period [37,38,39,40,41,42,43]. These studies have taken into account other environmental factors in microbial succession and facilitated the understanding of the microbial interplay.…”

“…Additionally, it is important to note that the members of Actinomyces and “purple complexes” decreased but the “red complex” species in the supragingival biofilms was not impacted by the biofilm biomass. Gingival crevicular fluid and surface type were found to be major limiting factors for biofilm development and redevelopment [52]. Biofilm redevelopment was more rapid in the natural teeth as compared to dentures [42].…”

“…The development and composition of the supragingival microbiota is influenced by inflammation and depth of periodontal pockets [11]. Other factors include the nature of surfaces, tooth position, and biofilm mass [38]. …”

Microbial Diversity in the Early In Vivo -Formed Dental Biofilm

“…It is well known that biofilm microbes interact with each other and thus show characteristics significantly different from those of their planktonic counterparts (2). While the biofilm contains beneficial, as well as harmful, bacteria, their relative proportions have a tendency to change as the dental plaque matures (3). These changes depend on bacterial interactions, as well as hostderived factors, which are all responsible for the ensuing development and biological effects of the structure (4).…”

Pathogenic Factors of P. gingivalis and the Host Defense Mechanisms

“…Recent studies using DNA-DNA hybridization that permits the examination of large numbers of species in large numbers of plaque samples also indicated the increased prevalence of P. gingivalis as well as other 'red complex species' (P. gingivalis, Treponema denticola and Tannerella forsythensis) in the subjects with chronic periodontitis (Socransky & Haffajee, 2002). However, it is also evident that the colonization of the putative pathogenic bacteria in subgingival plaque is not sufficient for the initiation/onset of periodontitis, since most periodontopathic bacteria including P. gingivalis may also be present at sound sites (Haffajee et al, 2009). Thus, the onset and progress of chronic periodontitis is based on the balance between the pathogenesis of the periodontopathic microorganisms and the host-defense against them (host-parasite relationship).…”