Dental Plaque

Dr.Ghada Maghaireh BDS,MS,ABOD

Dental Plaque as a microbial biofilm

Dental plaque is an example of biofilm.

The term biofilm is used to describe communities of microorganisms attached to a surface.

Such organisms are organized into three dimensional structure enclosed in a matrix of extracellular material derived from both the cells themselves and the environment. Bacteria growing into biofilms are more resistant to the effect of host defense mechanisms and antimicrobial agents when compared to the same cells in a liquid suspension. So it is important to mechanically disturb the biofilm when utilizing antimicrobial therapy (Brushing and professional cleaning)

Dental Plaque and Diet

A carbohydrate-rich diet increases the growth rate of many oral bacteria. It has been shown that the accumulation of dental plaque after 4 days is higher when individuals consume a diet supplemented with sucrose compared with a control diet without added sucrose. A sucrose rich diet change the composition of the microflora into a more aciduric species. In addition, sucrose can be converted by bacteria into glucans which can enhance plaque attachment and contribute to the plaque matrix.

Dental Caries & Dental Plaque

Carbohydrates (Sucrose) + Cariogenic bacteria such as S. mutans

Glucans

Acids

Plaque formation

Demineralization

Formation and Structure of Dental Plaque

The development of dental plaque can be divided into different stages: 1. Pellicle formation. 2. Attachment of single bacteria cells. 3. Growth of attached bacteria leading to the formation of distinct microcolonies. 4. Microbial succession and co-aggregation leading to increased species diversity with continued growth of microorganisms. 5. Climax community /mature plaque (2 weeks or older).

Pellicle Formation

Microorganisms do not colonize directly on the mineralized tooth surface. The teeth are always covered by a layer called the pellicle. It is an acellular proteinaceous film that forms on the naked tooth surface within minutes to hours. In uncolonized areas the pellicle reaches a thickness of 0.01-1 m within 24 h. The major constituents of the pellicle are salivary glycoproteins, phosphoproteins, lipids and components from the gingival cervicular fluids.

Microbial Colonization

Microbial colonization of teeth requires that bacteria adhere to the surface. Mechanism involved in the adherence is very complex and not fully understood.

Initial microbial colonization.

Microbial succession.

Initial Microbial Colonization

The tooth surface is initially colonized by a highly selected part of the oral microflora, mainly S.sanguis, S.orals, and S.mitis. Together theses three streptococci accounts for 95% of the streptococci and 56% of the total initial microflora. Bacteria contain a recognition system on their surfaces that enables components of the bacteria surface (adhesins) to bind to complementary molecules (receptors) in the pellicle.

Microbial Succession

As the microbiota ages, a shift occur from a Streptococcusdominated plaque to a plaque dominated by Actinomyces. Such microbial shifts are known as microbial succession.

Pioneer bacteria create an environment that is either more attractive to secondary invaders or unfavorable for themselves because of a lack of nutrients or accumulation of inhibitory metabolic products.

Microbial Succession

As the bacterial deposits become thicker, the oxygen concentration decreased. Progressive shift from aerobic in the early stages to a situation in which anaerobic organisms are predominant after 9 days. After some weeks of undisturbed growth, the microbial community develops into a climax community that harbors a broad range of bacterial species.

Dental Plaque and Caries

Two main school of thought on the role of plaque in the etiology of caries. 1. The specific plaque hypothesis. 2.The non-specific plaque hypothesis.

The ecological plaque hypothesis.

The Specific Plaque Hypothesis

Only a few species of the diverse collection of organisms comprising the plaque microflora are actively involved in the disease. A considerable amount of evidence supports the association between organisms of the Streptococcus mutans group and caries incidence and prevalence. The cariogenic potential of S. mutans is probably due to the unique combination of properties with which this microorganism is capable. The pathogenic potential can be modified by changes in the environment.
Lactobacilli play a major role in the development of a lesion.

The Specific Plaque Hypothesis

The specific plaque hypothesis has important implications because the association between S. mutans, lactobacilli and dental caries can be used in diagnosis, treatment and prevention of the disease in groups of subjects as well as in the individual case. It focused efforts on controlling disease by targeting preventive measures and treatment against a limited number of organisms.

The non-specific plaque hypothesis

For more than 100 years, investigators have tried to identify the bacteria responsible for dental caries formation and to determine whether their role is one of specificity. Frequent association ofStreptococcus mutans Lactobacillus s and with caries activity gave acceptance to their being specific cariogens. However, dental caries occurrence in their absence, and the presence of other bacteria able to produce substantial amounts of acid from fermentable carbohydrate, provided arguments for non-specificity.

The non-specific plaque hypothesis

Disease is the outcome of the overall activity of the total plaque microflora.
A heterogeneous mixture of microorganisms could play role in the disease.

The Ecological Plaque Hypothesis

This hypothesis propose that the organisms associated with disease may also be present at sound sites, but at levels too low to be clinically relevant. Disease is a shift in the balance of the resident microflora driven by a change in local environmental conditions. In case of dental caries, repeated conditions of low pH in plaque following frequent sugar intake will favor the growth of acidogenic and aciduric species, and therefore predispose a site to caries.

The Ecological Plaque Hypothesis

The hypothesis also acknowledge the dynamic relationship that exists between the microflora and the host. So that the impact of alterations in key host factors (such as saliva flow) on plaque composition is also taken into account. The disease can be controlled not only by targeting directly the pathogen (e.g. mutans streptococci), but also by interfering with the factors that are the shift in the balance of microflora (e.g. lowering the acid challenge).

The Ecological Plaque Hypothesis

Excess sugar Neutral pH S.sanguis S.oralis Remineralization

Stress

Environmental Change

Ecological Shift

Disease

Acid production

Low pH

MS Lactobacilli

Demineralization

Midterm Exam
The

First six lectures will be covered with the exam. Monday 2-4-2012 from 3:15-4:15. 10H1,10H2,10H3.