In 1996, the National Institute for Dental and Craniofacial Research hosted an international conference on microbial ecology. This meeting focused on a new view of plaque as a biofilm. The conference highlighted the importance of this shift in thinking about dental plaque and its role in oral diseases.1 This is not the first time in history dental professionals have shifted their thinking about plaque. Over the past 120 years the view of dental plaque has gone through several changes.
The period from 1880 to 1930 was called the golden age of microbiology (Figure 4).8 During this period, the pathogens that caused many systemic infections of medical importance were identified. Researchers also looked for a single, specific cause of oral diseases. Assuming plaque contained the microorganism that caused periodontal disease, dental scientists studied plaque in search of the causative agent. Using the techniques available at that time (wet mounts or stained smear microscopy), scientists identified four different groups of potential etiologic agents for periodontal diseases. Amoebae, spirochetes, fusiforms and streptococci were isolated from patients with periodontal diseases and, therefore, suggested as possible etiologies. Periodontal treatments of those times varied according to the suspected causative agents and included dyes, systemic administration of arsenic-containing antimicrobial preparations, intramuscular injection of mercury as well as vaccines.9
The 1930s ushered in a different view of the role of plaque and its microorganisms in the etiology of periodontal disease (Figure 5). Dental scientists believed that periodontal disease was linked with some constitutional defect in the individual.9 Mechanical irritants such as calculus and overhanging restorations were also thought to play a major role in the pathogenesis of periodontal disease.10
The belief there was a single microbial agent that caused periodontal disease was replaced by non-specific plaque theories.9 Non-specific plaque hypothesis held that the entire bacterial flora in plaque played a role in periodontal destruction rather than specific bacteria. All plaque was viewed as bad plaque. Furthermore, more plaque meant more disease. Plaque control was viewed as essential to limit the production of gingival irritants that lead to inflammation and periodontal destruction.11 Identification of specific microorganisms was not important. Stringent plaque control was important, and it became the focus of periodontal therapy.
The 1960s marked a return to specific plaque hypotheses (Figure 6). Researchers were successful in showing that periodontal disease could be transmitted between hamsters.12 The electron microscope confirmed spirochetes were in the connective and epithelial tissues of patients with acute necrotizing ulcerative gingivitis in contrast to healthy controls.13 Believing there were differences in plaque brought about by different species, scientists again returned to the search for a specific microbial periodontal pathogen and treatment aimed at the causative agent.9
Newer methods of microbial analysis such as darkfield microscopy, transmission electron microscopy, scanning electron microscopy, DNA probes, BANA hydrolysis and immunoassay aided the search.14
Since that time, scientists have continued to search for the specific etiologic agent with mixed success. Haffajee and Socransky15 have detailed the reasons for the difficulties in pinpointing specific pathologic agents. Some of these difficulties are related to microbial sampling and culturing and include: obtaining a sample from a periodontal pocket, the difficulty cultivating some organisms, and the large number of possible periodontal pathogens that may be found and cultivated from a periodontal pocket. Sampling is further complicated by the fact that periodontal pockets contain not only pathogens, but also opportunistic species. Other difficulties in pinpointing periodontal pathogens are related to the nature of periodontal diseases themselves. First, periodontal disease is not a single disease, but a collection of different diseases. Secondly, these diseases produce periods of disease activity and inactivity and variations in disease activity in different sites within an individual. A final difficulty in identifying specific periodontal pathogens is the variation in individual host response.16
In spite of these challenges, current researchers continue to agree that periodontal diseases are infections caused by specific pathogens. Recently, attention has turned to Tannerella forsythensis (formerly known as Bacteroides forsythus), as well as, Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans as primary pathogens for most periodontal infections with moderate evidence linking another subset of microorganisms (C. rectus, E. nodatum, F. nucleatum, P. intermedia/nigrescens, P. micros, S. intermedium, and T. denticola) as possible pathogens.14,17 Researchers are working to develop diagnostic tests for detection and treatments designed to target periodontic pathogens. Systemic antibiotics such as amoxicillin, metronidazole, tetracycline, doxycycline, and Augmentin have been proposed.15 Local delivery of antimicrobials (tetracycline fibers, metronidazole and minocycline gels, chlorhexidine chips, and doxycycline polymer) have also been introduced.18 While these approaches have enhanced our ability to manage periodontal diseases, they have still failed to provide uniform success. Viewing plaque as a biofilm promises to aid in the effort to effectively manage periodontal disease.