Definition:
Plaque is a tenacious adherent deposit that forms on tooth surface. It consist of an organic matrix containing a dense concentration of bacteria.Dental plaque is a whitish soft accumulation of bacteria and their substrate which deposit on the teeth when not cleaned adequately.
Types:
Based on it's relation to the gingival margin plaque is of two types-
1. Supragingival Plaque:
(a) Coronal - Contact with only tooth surface.
(b) Marginal - Associated with the tooth surface at gingival margin.
2.Sub-gingival Plaque.
1.SUPRAGINGIVAL PLAQUE:
Morphology:
* Amount: Can't be detected until reached a certain thickness and small amount cannot be visible until they are disclosed by pigments from within the oral cavity, or stained by disclosing solution or wafers.
* Color: Gray to yellowish gray to yellow.
Site:
Gingival third of teeth with predilection for surfaces, cracks, pits, fissures of occlusal surface, overhanging margin and so forth; mainly in sites protected from the normal mechanical cleansing action of the tongue, the cheeks lips. Other hard surfaces are restorations, or artificial crowns, orthodontic band dental implants, removable orthodontic appliance and denture.
Duration:
May formed within 1 hour after cleaning the teeth, with maximum accumulation occurring in about 30 days or less.
Rate: Very individual to individual teeth and influenced by diet, age, salivary factors, oral hygiene, tooth alignment, systemic diseases and host factors.
Composition:
Dental plaque consists of primarily of proliferating micro-organism along with a scattering of epithelial cells leukocytes, and macrophages in adherent intercellular matrix. It is consists of two portions:
1. Bacterial portion: 70-80% of the total plaque volume 1cc. weighting about 1mg.,contain more then 108 bacteria. There may be as 200-400 different species of micro-organisms. The organism includes-
* Bacteria, mostly.
* Mycoplasma.
* Protozoa
* Virus.
2. Interbacterial matrix: 20-30% of plaque volume. It again consists of two portion,
(a) Organic portion: Consist of mainly-
* Polysaccharide protein complex (Protein-30%, Polysacc. 30%)
* Lipid-15%.
* Remainder portion is-
-Extracellular products of plaque bacteria.
-Food debris
-Derivatives of salivary glyco-proteins.
(b) Inorganic portion:
* Ca, P—mostly
* Mg, K, Na, F-small amount.
Inorganic components are bound to the organic contents by different chemical bonds.
PLAQUE FORMATION:
There is no difference between the plaque formed on the tooth surface or artificial surface except the first layer.
The process of plaque formation involves-
Step-1:Organic pellicle formation.
Step-2:Transition from pellicle to dental plaque colonizing by bacteria.
Pellicle formation:
The first stage in pellicle formation involves adsorption of salivary proteins to apatite surface. This is due to electrostatic ion interaction of calcium and phosphate groups in the enamel surface with oppositely charged groups in the enamel and in the salivary macromolecule. That is why it's chemical composition consists mainly of
(a)glycoproteins,
(b) immunoglobulin,
(c) And different carbohydrates.
Formation of plaque:
It involves two processes-
1. Initial adherence of salivary organisms to the acquired pellicle.
2. The proliferation of attached bacteria to already attached cells
1. Bacterial adherence:
In dental plaque development, two adhesive process are required-
1st. Bacteria must adhere to pellicle surface and become sufficiently attached to withstand the oral cleansing factor.
2nd.-They must grow and adhere to each other to allow plaque accumulation.
Oral bacteria very markedly in their ability to attach to different oral surfaces. For example:
-Strepto. mutans, S. sanguis, Lactobacillus species, Actinomyces viscosus have been found in enamel.
-Strepto. salivaris, Actinomyces naeslundii populute the doresum of the tongue.
-Bacteroids, Spirochetes are found in the gingival crevice and periodontal pocket.
This ability is due to interaction between specific bacteria and pellicle. Different physical and chemical mechanisms have been proposed to explain these interactions.
i. Electrostatic forces: In which negatively charged components of the bacterial cells surfaces and negatively charged tooth surface constituents (an ionic residues of the surface glycoprotein’s of pellicle) become linked via cations such as calcium.
ii. Organic solutes: Salivary proteins may either inhibit or promote adhesion, depending on the bacterial species.
iii. Hydrophobic interaction: This association is based on the close structural fit between molecules.
Different binding sites or chemical bonds are identified within bacteria and pellicle, e. g. adhesion (a specific receptor on bacterial surface) can recognize the carbohydrate molecule of pellicle. Multiple binding sites, involving interaction with salivary glycoprotein’s, extracellular polysaccharides and directs cell to cell adhesion are necessary for the survival of the organisms.
2. Bacterial growth and proliferation:
After pellicle had been saturated with bacterial binding sites, subsequent growth leads to bacterial accumulation and increase plaque mass. For this accumulation of dental plaque, multiplication and cohesion of bacterial cells is required. This is accomplished by the formation of plaque matrix, which depends on-
i. Bacterial metabolic activities.
ii. Saliva derived (environmental) components.
iii. Host derived components.
Bacterial and environmental factors:
# Dietary carbohydrates—> insoluble extra cellular polysaccharide by the action of microorganism like S. mutans, S. sanguis, S. salivarius, Lactobacillus —>increased bacterial adhesion.
# By S. mutans, insoluble glucans is formed—>non specific entrapment of other microorganism from oral fluid—>promoting accumulation of other bacteria.
# Carbohydrate fermentation—> decrease PH—>acidic environment—> Selective organism survive in this acid media—> forms a carcinogenic supragingival plaque—>responsible for carious lesion.
# High O2 concentration—»Multiply aerobic organisms e.g. Streptococcus and lactobacillus consuming large quantity of O2 —>produces a highly destructive products.
# Low O2 concentration; Mature plaque —>O2 multiply obligate anaerobic organisms.
# Nutrition: In supragingival plaque formation most of the nutrients are supplied from saliva. First colonizer e.g. streptococcus, actinomyces take salivary carbohydrates as their nutrition’s. After their establishment this bacteria produces essential products and nutrition’s for other organisms.
Immune mechanism:
1.Oral cleansing mechanism e.g salivary flow, mastication and movements of the tongue and cheek has important role in controlling the rate of supragingival plaque formation.
2.Saliva supply carbohydrates that are essential nutrients for bacteria.
3.Saliva contains lactoperoxidase, lactoferin, lysosomes etc that prevent establishment of sensitive organisms.
4.Saliva plays an important role in bacterial attachment and accumulation.
5.Host immune response: Saliva contains IgA that prevent bacterial attachment.
Significance of supragingival plaque:
1. Plaque Permit the colonization of oral bacteria on tooth surfaces. If this bacteria’s are prevented from maturation they compete with gingival health.
2. If they are allowed to grow and mature—>development of gingivitis—>permit microenvironment —>development of sub gingival plaque.
Therefore, supragingival plaque strongly influences the growth, accumulation and pathogenic potential of subgingival plaque especially in the early stages of gingivitis and periodontitis.
2.SUBGINGIVAL PLAQUE:
The bacterial content of subgingival plaque differs from that of supragingival plaque. This is due to its less subjection to natural homeostatic cleansing activities of mouth. So, relatively stagnant environment allow to colonized the organisms which cant be readily adhere to hard surfaces. The other components are also same except their proportion.
Types:
Subgingival plaque are of three types:
1.Tooth attached.
2.Unattached.
3.Attached to epithelium.
These 3 types of subgingival plaque are given as chart (follow image)
BACTERIAL INVASION TO PERIODONTIUM:
1. Direct invasion : In acute ulcerative gingivitis.
2. Through the junction of epithelium: Due to widened and ruptured intracelluar space of stratum spinosum /destruction of junctional epithelium due to microbial enzymes.
3. Through perforation of basal lamina (normally its a barrier):
Epithelium—>Basal lamina—Connective tissue.
4.Ulceration or microholes in the periodontal wall creating by transmigrating W.B.C. into connective tissue.
5.Penetrating the junctional epithelium between epithelial cells and epithelium attachment and tooth.
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