The study of bacteria in plaque shifts to interaction of oral flora with tissue

Bacterial plaque seems to be the domain of the dental hygienist. Our efforts are directed toward either its removal or prevention of its formation or effects, whether it be in an early soft state or later as calculus. Dental plaque is considered a biofilm. It`s made up of numerous bacteria and is similar to other microbial biofilms in nature and within the body. We spend our day dealing with this fascinating and frustrating biofilm.

Trisha E. O`Hehir, RDH, BS

Bacterial plaque seems to be the domain of the dental hygienist. Our efforts are directed toward either its removal or prevention of its formation or effects, whether it be in an early soft state or later as calculus. Dental plaque is considered a biofilm. It`s made up of numerous bacteria and is similar to other microbial biofilms in nature and within the body. We spend our day dealing with this fascinating and frustrating biofilm.

Despite efforts to identify a specific pathogen within bacterial plaque responsible for the common, chronic-inflammatory periodontal disease, none has been found. We have a "top ten list" and a favorite few which are receiving a great deal of attention. However, no single bacterial species fulfills Koch`s postulates. To identify a specific pathogen, it must be present in all cases of periodontal disease and when a pure culture is introduced into a pocket, disease must result. So far, no bacterium fulfills these criteria. The bacteria associated with common periodontal disease are also found in the mouths of those with healthy tissues. Identifying specific pathogens within a person`s mouth will not predict periodontal breakdown.

Instead of a specific infection-like diphtheria or tuberculosis, we are dealing with a complicated ecological system further complicated by the human immune response. According to Professor Hubert Newman of the Eastman Dental Institute in London, UK, we are dealing with bacterial shifts in this ecosystem rather than an infectious disease linked to a single infectious agent.

In 1990, Newman published a review article on the ecology of bacterial plaque and its relationship to the periodontium. This was not his first writing on the subject. Since 1972, he has published numerous informational, research, and book chapters on the subject. His basic premise has been that a shift in the normal oral flora, a change in the proportions of bacteria one to another, leads to periodontal pathogenesis. Rather than looking for a single, specific pathogen, we must understand the mixed flora and ecology of dental plaque.

Normal oral flora actually provides natural resistance to disease, both by the presence of certain bacteria and the byproducts they produce. Streptococcus species, for example, are capable of inhibiting several other pathogenic disease arousing bacterial species. With this in mind, it is clear that complete plaque removal may not be the best approach. There is a balance to be reached where the normal oral flora and the periodontal tissues exist in harmony.

That harmony is disrupted when plaque accumulation exceeds the balance. Stagnation of bacteria within the interdental areas leads to disease and should be our primary concern. Changes in diet over the centuries are the chief reasons for increased stagnation. Highly fibrous diets in the past required prolonged chewing, increasing salivary flow, and thus reduced the likelihood of plaque accumulation and stagnation. The fluid flow of both saliva and gingival crevicular fluid are important in the ecology of plaque as they remove or neutralize the bacteria and their byproducts. Prolonged chewing of highly fibrous foods produced frictional removal of plaque and greater salivary flow than we see with our current softer diet.

Diets high in carbohydrates, specifically sucrose, lead to selective colonization of bacteria capable of living in thicker plaque layers and producing polysaccharides. With stagnation comes a shift in the proportions of bacterial species living within the biofilm. An increase in anaerobes occurs, leading to what is termed a "mixed anaerobe" infection.

Cariogenic organisms may actually be responsible for the onset of gingivitis as Streptococcus mutans can induce gingivitis and gingival bleeding. What was supragingival plaque may actually become subgingival plaque when covered by swollen gingiva.

No single species or strain is exclusively responsible for the shift from health to advanced disease. On the contrary, proportional shifts are evident with no one specific pathogen identified. Pocket environment is a major factor in the growth of suspected pathogens.

To achieve an ecological balance within the mouth, variability of the host response and shifts in bacterial micro-flora must be considered.

References:

- Newman, H.: Plaque and Chronic Inflammatory Periodontal Disease. J of Clinical Periodontology 17: 533, 1990.

Trisha E. O`Hehir, RDH, BS, is a senior consulting editor of RDH. She also is editor of Perio Reports, a newsletter for dental professionals that addresses periodontics.The Web site for Perio Reports is www.perioreports.com. Her e-mail address is trisha @perioreports.com.

Top Ten Bacteria

(1) Aa - Actinobacillus actinomycetemcomitans

(2) Pg - Porphyromonas gingivalis

(3) Pi - Prevotella intermedia

(4) Bacteroides forsythus

(5) Eikenella corrodens

(6) Campylobacter rectus

(7) Fusobacterium nucleatum

(8) Bacteroides denticola

(9) Actinomyces naeslundii

(10) Treponema denticola

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