Dental Plaque

Term plaque was first used in dental context by G.V Black in 1898. 

Definition of dental plaque: (WHO-1978)

Dental Plaque is defined as a specific but highly variable structural entity resulting from sequential colonization and growth of micro organisms on the surfaces of teeth and restoration consisting of micro organisms of various strains and species are embedded in the extra cellular matrix, composed of bacterial metabolic products and substance from serum, saliva and blood.

Features:

Plaque is white, grayish or yellowish in color with globular appearance. It is non-calcified and soft and may be readily visualized on teeth with no hygiene measures for 1 to 2 days. It is mainly present on gingival 3rd of tooth surface, proximal areas, pits, fissures, cracks, beneath overhanging restorations and around malaligned teeth. 

Composition:

Plaque consists of about 80% of water and 20% solids (micro-organisms and inter-cellular matrix).

1) Micro-organisms:

  • Bacteria: Bacteria are the main constituents of plaque. More than 325 bacterial species have been found in plaque. 1 gm of plaque contains about 2 x 1011  bacteria.
  • Mycoplasma species.
  • Protozoa.
  • Yeast.
  • Viruses.

2) Inter-cellular matrix:

It forms about 20 to 30% of the plaque mass.

Constituents of inter-cellular matrix are:

  • Organic materials: polysaccharides (mainly dextran) , glycoproteins, proteins and lipids.
  • Inorganic materials: calcium and phosphorus are the main inorganic constituents of plaque. Other minerals like sodium, potassium and fluoride are also found in traces.

The main sources from where inter-cellular substances of plaque are derived, are:

  • Saliva: Glycoproteins and inorganic constituents of supra-gingival plaque are derived from saliva.
  • Gingival crevicular fluid: Albumin and inorganic components of sub-gingival plaque are derived from gingival crevicular fluid.
  • Bacterial products: Polysaccharides.
  • Diet and breakdown products of cell wall: Lipids.
  • External sources: Fluoride is mainly derived from fluoridated toothpastes and mouth washes.

Classification: 

1) On basis of location of the plaque on tooth surface:

  1. Supra-gingival plaque: Plaque present above or at the level of gingival margin is termed as supragingival plaque. The plaque present in direct contact with the gingival margin is termed as marginal plaque.
  2. Subgingival plaque: Plaque present below the level of gingival margin is termed as subgingival plaque. Subgingival plaque can be:
    • tooth-associated plaque.
    • tissue-associated plaque.

Differences between supra and sub-gingival plaque

Supra-gingival plaque
Sub-gingival plaque
Present above the gingival marginPresent below the gingival margin
Always tooth-associatedMay be tooth-associated or tissue-associated
Primary source of nutrition for bacteria is saliva and ingested foodPrimary source of nutrition for bacteria is gingival crevicular fluid
Mainly responsible for gingivitis (marginal plaque) or calculus formation and dental cariesResponsible for calculus formation and root caries(tooth-associated plaque) and destruction of soft tissue (tissue-associated plaque)

2) On basis of pathogenicity: 

  1. Cariogenic: Generally acidogenic and gram-positive.
  2. Periopathogenic: Mostly basophilic and gram-negative.

Formation of dental plaque:

Plaque formation begins immediately after a tooth surface is cleaned. It takes about 4 to 9 days for the plaque to become fully mature. Microscopically, plaque formation is a highly ordered and predictable process.

Dental plaque formation is broadly divided into following phases:

  • Pellicle formation: During the very initial phase of plaque formation, all the surfaces of oral cavity (tissue surface, teeth, removable and fixed appliances) are coated with dental pellicle made up of glycoprotein. The forces involved in pellicle formation are: van der Waal forces, electrostatic forces and hydrophobic forces. Pellicle present on hard surfaces of oral cavity acts as a substrate for the attachment of bacteria.  
  • Initial colonization: The bacteria progressively get accumulated on pellicle to form dental plaque. Only a few hours after pellicle formation, bacteria can be identified on dental pellicle. Gram-positive facultative micro-organisms are the predominantly found bacteria during the initial phase of bacterial colonization on the dental pellicle. The molecules on the bacterial surface by which these bacteria adhere to the pellicle are known as ‘adhesins’. The pellicle has receptors to which these adhesins.
  • Secondary colonization: It occurs by the colonization of the additional bacterial species that do not adhere to the clean tooth surface, instead they adhere to the other bacteria which are already present in the initially colonized plaque mass. These bacteria are thus known as secondary colonizers.  This process of adhering of micro-organisms to one another is known as ‘co-aggregation’. Secondary colonizers include: prevotella intermedia, capnocytophaga species, porphyromonas gingivalis, fusobacterium nucleatum etc.
  • Plaque maturation: The maturation of plaque mass takes place by the growth of bacterial species attached to it, as well as by the colonization and growth of new species of bacteria in it. During this process, there occurs a change from initial aerobic environment (characterized by presence of gram-positive facultative bacterial species) to a highly anaerobic environment (characterized by gram-negative anaerobic microorganisms). 

Bacterial co-aggregation during plaque maturation

Bacterial co-aggregation

Macroscopic Structure of plaque:

The inter-cellular matrix forms a hydrated gel (a feature of all bio-films). This bio-film acts as a barrier, so that the bacterial products are retained and concentrated within it and also the bacteria get protected from the external harmful substances like antimicrobial agents. In this way this hydrated gel helps the bacteria in it to proliferate and colonize.

Microscopic Structure of plaque:

Several methods have been used to view the micro-structure of the plaque. These methods include: light microscopy, transmission electron microscopy, scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM).

Ultrastructurally, the inner layer of plaque (attached to tooth surface), mainly consists of densely packed coccoid and rod shaped bacteria and the outer layer in addition has filamentous bacteria. Usually, the plaque represents corn-cob appearance. Corn-cob formation is seen between rod shaped bacterial cells forming the inner core of the structure and the coccal cells that attach along the surface of these rod shaped cells. The term corn-cob for this structure of plaque was coined by Jones (1971). Tissue adhered subgingival plaque contains many motile, gram negative rods and spirochetes.

Methods of detection of plaque:

Direct vision:

Plaque is whitish-yellow. Identification of the dental plaque is difficult because of the color similarity between the tooth surface and dental plaque. But it can be readily seen by on teeth after 1 to 2 days of uninterrupted plaque formation with no oral hygiene measures. 

By instrumentation:

Plaque on the teeth can also be detected by using an explorer or a periodontal probe. This can be done by running the explorer or probe along the gingival 3rd of the tooth. This method can also detect small amounts of plaque that is not visible to the naked eye. 

Disclosing agents:

Dental plaque has the ability to retain a large number of dye substances because of the polarity difference between the components of the plaque and the dyes. These dyes can be used as disclosing agents for the plaque. Disclosing dyes work by changing the color of dental plaque so that it contrasts with the tooth surface. The first chemical reported to stain plaque was iodine but now a days many dyes have been used as disclosing agents for the plaque, they include:

  • Fuchsine
  • Erythrosine
  • Methylene blue
  • Merbromin
  • Fluorescein
  • Brilliant blue
  • Crystal violet
  • Gentian violet

So far, the use of disclosing agents is the easiest, fastest and the most reliable method of plaque detection. This method also helps us to educate and motivate the patient to maintain oral hygiene.

Various plaque hypothesis:

1) Specific plaque hypothesis:

The period from 1880 to 1930 was called the golden age of microbiology. During this period, the pathogens that caused many systemic infections of medical importance were identified. 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.

2) Non-specific plaque hypothesis:

This was given by Walter loesche in 1976. This hypothesis suggests that the noxious substance produced by the entire plaque flora is responsible for the periodontal diseases. So, according to this, small amount of plaque produces lesser amount of noxious substance and large amount of plaque produces more noxious substances. Thus more plaque meant more disease. But this hypothesis fails to explain that why some people undergo more periodontal destruction, inspite of the presence of very less amount of plaque in them while others with enormous amount of plaque do not show that much of destruction.

3) Specific plaque hypothesis:

This hypothesis was also given by Walter loesche. This hypothesis suggests that only certain plaque is pathogenic and its pathogenicity depends on the increase in some specific microorganisms in the plaque. This hypothesis was well accepted in 1960’s as studies with electron microscope confirmed that spirochetes were in the connective and epithelial tissues of patients with acute necrotizing ulcerative gingivitis while they are absent in the controls with healthy periodontium. The scientists were working on identifying the specific pathogens responsible the periodontal diseases and also aiming the treatment at the eradication of the causative pathogens.

Haffajee and Socransky have enumerated the reasons for the difficulties in pinpointing specific periodontal pathogens:

Difficulties related to microbial sampling and culturing:

  • Obtaining a sample from a periodontal pocket
  • Some organisms are difficult to cultivate
  • Periodontal pocket contains a large number of pathogens
  • Opportunistic species are also present in the periodontal pockets along with the pathogens.

Difficulties related to the nature of periodontal diseases themselves:

  • periodontal disease is a collection of different diseases and is not just a single disease.
  • Periodontal diseases have periods of disease activity and inactivity .
  • Variation in disease activity in different sites within an individual.
  • Variation in individual host response.

 This hypothesis also fails to explain that why in some cases the disease is present even in the absence of the putative pathogen while in others the disease is absent insipite of the presence of the pathogen.

4) Ecological plaque hypothesis:

This hypothesis was given by P.D Marsh. According to this, changes in the environmental conditions leads to ecological shift. This ecological shift favors the growth of pathogenic bacteria or expression of pathogenic traits. So, according to this hypothesis, disease can be prevented not only by targeting the putative pathogen directly, but also by interfering with the selection pressures responsible for their enrichment.

Ecological plaque hypothesis

Plaque as biofilm:

The life cycle of a biofilm is characterized by attachment of planktonic bacteria to a surface or by migration or division of sessile cells to cover an empty region of the surface, production of extracellular polymeric substances (EPS) to adhere cells irreversibly to the substrate, and then by additional EPS production, cellular motility and reproduction, and phenotypic differentiation to produce a mature, thick and spatially structured biofilm.

Dental plaque forms via an ordered sequence of events, resulting in a structurally- and functionally-organized structure. Distinct stages in plaque biofilm formation start with acquired pellicle formation. These are,

  1. Reversible adhesion involving weak long-range physicochemical interactions between the cell surface and the pellicle, which can lead to stronger adhesin-receptor mediated attachment
  2. Colonization
  3. Co-adhesion resulting in attachment of secondary colonizers to already attached cells19
  4. Multiplication and biofilm formation (including the synthesis of exopolysaccharides) and,
  5.  On occasion, detachment and re-colonization.

Diagrammatic representation of Biofilm development

Plaque as biofilm

Methods of tooth and tissue destruction by plaque:

By enzymes:

Enzymes produced by the microorganisms in the plaque are mainly responsible for the periodontal tissue destruction. Hyaluronidase and proteases have been demonstrated in plaque. They may cause breakdown of mucopolysaccharides and proteins present in the inter-cellular substance of junctional epithelium.

Endotoxins:

Endotoxin is a lipopolysaccharide complex and is a constituent of the cell wall of all gram–ve bacteria. Endotoxin has a chemotectic effect, so it induces phagocytosis by neutrophillic granulocytes. Endotoxins injected into the oral mucosa of experimental animals may cause inflammation and resorption of adjacent bone. Free endotoxin is present in dental plaque and it contributes to inflammatory process.

Metabolites:

Microorganisms in the plaque leads to the accumulation of various metabolites due to their action on carbohydrates and proteins. Hydrogen sulfide and ammonia are two such metabolites produced by the plaque microorganisms. These are cytotoxic products. Also, organic acids produced by the metabolization of carbohydrates plays a vital role in caries development. But the effect of these acids on gingiva is still unknown.

Bacterial antigens:

This is an indirect way of causing periodontal inflammation produced by the immune-pathological processes that set in action by the penetration of microbial agents into the tissue.

Other agents:

Sometimes agents other than bacteria may be responsible for the periodontal problems. These agents include:

  • Viruses: Herpes virus is an etiological agent for herpatic gingivastomatitis and fever blisters.
  • Protozoa: Protozoa like Entamoeba gingivalis and Tricomonas are also found in oral cavity.
  • Yeasts: Among yeasts candida albicans is most frequently found in oral cavity. Infections with candida albicans is more commonly seen in patients of AIDS and patients on long term antibiotic therapy.

Factors affecting plaque formation:

  • Age
  • Diet
  • Salivary flow
  • Oral hygiene
  • Alignment of teeth
  • Systemic conditions

Peri-implant plaque:

Bio-films that form on natural teeth, do not spare the artificial surfaces (exposed to the oral environment) also. No studies have been done to document the structure of peri-implant plaque. But it is clear from many cross-sectional and longitudinal studies that there are many similarities between the microbiota of peri-implant(submucosal) and subgingival plaque.

References:

Please contact author for references

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