Biofilm Formation, Identification, and Removal

Dental caries and periodontal disease are among the most prevalent diseases known to man. Both are associated with the bacteria contained in dental biofilm. Dental biofilm is complex, with a well-organized structure. Up to 500 bacterial species have been identified in dental biofilm. Studies have shown that plaque accumulates rapidly on clinically plaquefree teeth. For oral and systemic health, the development and maturation of dental biofilm should be impeded and the dental biofilm needs to be regularly and meticulously removed. Removal and reduction of biofilm can be by mechanical means or mechanical and chemical means, and disclosing agents enable visual identification of plaque. Current chemotherapeutics in general do not effectively penetrate thick biofilm, underscoring the importance of the identification and rigorous mechanical removal of the dental biofilm. Introduction Dental caries and periodontal disease are the most common intraoral diseases and among the most prevalent disorders known to man. Both are associated with bacteria contained in dental biofilms. Studies, including one that compared sucrose-restricted and sucrose-supplemented diets, have shown that plaque accumulates rapidly on clinically plaquefree teeth. In the absence of any oral hygiene measures, plaque accumulated on 52 percent to 73 percent of surfaces.1 While poor oral hygiene is causally related to the presence of dental biofilm and gingivitis, there is not a strong correlation between poor oral hygiene and severe periodontitis, nor does oral hygiene have significant influence on the subgingival microflora within deep periodontal pockets.2 Plaque removal from subgingival pockets should be accompanied by professional prophylaxis, scaling, and root planing to halt clinical attachment loss. Supragingival microbes are known to migrate subgingivally, and it is also known that microbes will migrate from one periodontal site to another or to an implant site.3 Regular and diligent removal of supragingival dental biofilm is essential to prevent a large microbial load from developing and to prevent the development of subgingival plaque and periodontal pockets. Biofilm Structure and Biochemistry Prior to the development of dental biofilm, the salivary or acquired pellicle forms. This occurs through the adsorption of proteins from saliva onto the clean tooth surface. One study found different patterns in the adsorption of salivary proteins onto various components of orthodontic appliances — modules, brackets, springs, and elastics — and found differing levels of bacterial accumulation.4 Acquired pellicle formation provides oral bacteria with binding sites, resulting in bacterial adhesion,5 the first step in the formation of dental biofilm. Surface modification can inhibit the development of the acquired pellicle and dental biofilm. When ceramic crown surfaces were treated in vivo with hydrophobic coatings, using disclosing agents it was found that almost no plaque formed on the hydrophobic crown surface and there was almost no detectable pellicle, even after seven days.6 The Role of Adhesion Dental biofilms accumulate on hard and soft surfaces in the oral cavity, including nonbiological surfaces such as implant surfaces, orthodontic appliances and amalgams, as well as on other bacteria. Bacterial adherence is essential for formation of dental biofilm. Following adhesion, the bacteria divide, grow, and accumulate. The bacteria contain a factor called an “adhesin” that meets its counterpart receptor at the site of adhesion, resulting in the adhesion of the bacteria to the surface. Different receptors and adhesins are present on different bacteria and surfaces, such as fimbrae that act as receptors on subgingival bacteria, or collagen and residues of sialic acid and galactosyl that serve a similar function on tissue surfaces.7 Adhesion by one species of bacteria may limit the amount of adhesion by another species in the same space. When the adhesion of streptococci is selectively reduced by preventing the build-up of sialic acid, more P. gingivalis and P. intermedia adhere in the space. It is believed that this is due to galactosyl residues acting as receptors for the Porphyromonas species.8 For a subgingival biofilm to exist, the bacteria must be able to adhere to one or more subgingival surfaces. This is enabled by an early inflammatory process that creates a pseudopocket at the gingival margin, allowing for the development of the anaerobic species associated with periodontal disease and the subsequent development of true periodontal pockets, which in turn provide extra space for the anaerobes9 and an oxygenpoor environment. Unfortunately, the presence of subgingival calculus provides an excellent adhesion site for bacteria and for the retention of subgingival plaque. Bacterial adhesion to soft tissue within the periodontal pocket may also play a role in the deeper invasion of periodontal tissues. Adhesion to the basement membrane and collagen has been found to occur.