Bacterial plaque

Bacterial plaque

Plan :

1-Introduction

2-History

3-Definition

4-Classification of deposits

4-1-Hard deposits

4-2-Soft deposits

5-Formation of bacterial plaque

5-1-Formation of the acquired film

5-2-Bacterial colonization

5-2-1-Colonization

5-2-2-Bacterial adhesion

5-3-Maturing of the plaque:

6-Plate classification

6-1-Supragingival plaque

6-2-Subgingival plaque

7-factors promoting the accumulation of bacterial plaque

8-Composition of bacterial plaque

8-1-Extracellular matrix:

8-2-Bacteria

9-Pathogenic action of bacterial plaque

10-The future of the plaque

11-Highlighting

11-1-Clinic:

11-2-Laboratory:

17-Conclusion

18- bibliography

1-Introduction: Currently the etiopathogenic role of dental plaque in the appearance of caries and periodontal diseases remains indisputable. Periodontal disease is a problem

Major in modern dental practice and is the leading cause of tooth loss in adults

2- History:

The existence of dental deposits has been known for a long time, and so,

RHAZI: born in 850 writes: “teeth are subject to deposits, blackening and dirt”

ABOU EL KASSIS: 913-1013: he recognized that there was a relationship between tartar and gingivopathies, and he treated periodontopathies by scaling.

It was GREEN-VARDIMAN BLACK in 1898 who had the merit of using the term “microbial plaque” for the first time.

3-Definition:

*-According to LOE: bacterial plaque is a soft, non-calcified bacterial deposit that forms on insufficiently cleaned teeth.

*-ACCORDING TO Frank: it is an extremely polymorphic microbial jungle comprising aerobic and anaerobic bacteria linked by an intermicrobial or intercellular matrix attached to the surface of the enamel by the amorphous PAE A microbial and of salivary origin we also find desquamated epithelial cells and leukocytes.

4-classification of deposits:

4-1- hard deposits:

4-1-1-Tartar:

4-1-1-1-Definition:

Tartar is an adherent, calcified mass that forms on the surface of natural teeth and dentures. Tartar results from the mineralization of bacterial plaque by precipitation of mineral salts from saliva.

4-1-1-2-Different types: tartar is classified according to its relationship to the gingival margin:

Supragingival tartar: above the gingival surface: visible to the naked eye. Its color is usually: white or yellowish white.

Subgingival tartar: It is dense and hard, dark brown or greenish-black in color, with a consistency similar to flint. Can be detected by: probe, air jet, or by transparency (gum).

4-1-2-pigmentations:

4-1-2-1-Definition:

These are colored deposits on the surface of the teeth, are the results of pigmentation by chromogenic bacteria, foods or chemicals, of dental cuticles.

4-2- soft deposits:

4-2-1-The acquired film: it is a translucent film

-Acquired: forms within a few minutes of the tooth eruption.

-Heterogeneous: of salivary origin.

-Amicrobial: does not contain bacteria.

It forms on recently cleaned teeth, containing salivary glycoproteins, certain sugars and lipids.

It plays several roles: -it opposes the decalcification of the tooth.

-It allows the colonization of bacteria.

Bacterial plaque

4-2-2- Matéria alba: it is a soft and sticky deposit, grayish white or yellow in color, whose adhesive quality is a little less than that of the plate, it is visible without the aid of a revealing solution.

It can form within hours on teeth that have just been cleaned.

It can be removed by a jet of water, it consists of a concentration of microorganisms, desquamated epithelial cells, leukocytes, as well as a mixture of salivary proteins and lipids, with little or no food debris.

4-2-3- Food debris: these are meal residues, easily eliminated by rinsing, or by the mechanical action of the tongue, cheeks, lips as well as the shape and alignment of the teeth.

4-2-4- the bacterial biofilm: it is a soft, granular, amorphous deposit which accumulates on the surfaces of the teeth, on dental restorations and on tartar made up of structured bacteria linked by an intercellular matrix including leukocytes, macrophages and epithelial cells.

5-Formation of the bio film:

Dental plaque forms on surfaces previously covered by salivary deposits or acquired films, according to other authors bacterial adhesion can occur directly on the hydroxyapatite crystals. It can also be deposited directly on the surface of the tooth; both situations can occur on adjacent areas of the same mouth

5-1- formation of the acquired film: Figure (1, 2)

Phase 1: after two hours, salivary glycoproteins are deposited on dental surfaces, there will subsequently be selective adsorption of salivary proteins by the hydroxyapatite of the enamel, the proteins would bind firmly to the calcium of the enamel surface.

Phase 2: This is the transition from a water-soluble protein phase to an insoluble phase, resulting in the deposition of successive layers of salivary mucins.

5-2-colonization:

5-2-1-The sequence: At the beginning there is the adhesion of aerobic gram-positive cocci to the acquired film because of their capacity to produce dextran and levan, the bacterial flora at the beginning aerobic transforms into an anaerobic flora

0-2 days: acquired film and aerobic G + cocci and rods: streptococcus mitis, sanguis, mutans.

2-4 days: filaments and fusiforms.

4-9 days: spirillae and spirochetes.

5-2-2-bacterial adhesion: Figure (2,3,4,5)

5-2-2-1-Definition:

“Adhesion is the dynamic process allowing a bacterium to pass from the free state to the fixed state” C.Mouton 1994

5-2-2-2-The surfaces present:

1-Oral surfaces:

Soft tissues: by perpetual renewal and desquamation of superficial cells, bacteria cannot find a stable base to adhere to.

Hard tissues: represented by enamel,

2-bacterial surfaces:

The bacterial surface contains either structural or molecular elements that are the bacterial mediators of adhesion.

*-The Glycocalyx: Figure (2)

It is a hydrated matrix made up of interwoven polysaccharide fibers, solid and adherent to inert and living surfaces.

*-Fimbriae: Figure (3) these are extracellular appendages, responsible for bacterial adhesion, they are made up of polymerized proteins in the form of filaments.

*-Lipoteichoic acid: Figure (5)

It is a linear molecule integrated into the bacterial wall of G+. This molecule is called amphipathic since it is made up of a hydrophilic carbohydrate domain and a hydrophobic lipid domain.

The lipid part is inserted into the cytoplasmic membrane while the carbohydrate part emerges into the wall after crossing it.

Pili: these are extracellular appendages responsible for bacterial conjugation, they are made up of protein: pilin.

5-2-2-3-physicochemical characteristics of bacterial adhesion: Figure (7)

*The concept of repulsive forces:

The phospholipids of enamel and the proteins of the acquired pellicle are rich in negatively charged polar acid groups as is the bacterial surface, these charges – generate electrostatic forces of repulsion.

*Electrodynamic forces:

Attractive or vander waals forces, their range of action is greater than that of repulsive forces so they will promote the removal of bacteria to a well-defined distance

*Electrostatic interactions:

Divalent cations Ca++ bridge the negative charges of both dental and bacterial surfaces

5-3- maturation of the bio film:

It is achieved through bacterial proliferation and the development of its intercellular matrix, a direct consequence of bacterial metabolism.

As the bacterial layers are deposited, the plaque thickens and is considered mature after about 30 layers.

6-classification of bacterial plaque: Figure (8)

6-1-Supragingival plaque:

Develops on the cervical 1/3 of the teeth, its thickness is maximum at the cervical base and decreases towards the line of the greatest contour.

6-2-Subgingival plaque:

This is the part that houses the gingival sulcus and the periodontal pocket; it is continuous with the supragingival plaque.

It is divided into 02 parts:

– Attached part:

In continuity with the supragingival plaque, in contact with the dental surface and it extends to the bottom of the pocket, it is very cariogenic.

-Unattached part:

This is the part that is in contact with the epithelium of the pocket.

6-3-Biofilm of occlusal grooves:

It is a very cariogenic plaque (furrows and pits), we find acidogenic streptococci: lactobacilli which produce acids.

7-Factors promoting the accumulation of biofilm:

See Court No. 1

8-Composition of the bio film:

Bacterial plaque consists of an extracellular matrix and bacteria.

8-1-The extracellular matrix: acellular fraction.

The extracellular matrix: made up of an organic matrix and a mineral matrix and 80% water, 20% mineral and organic.

*-organic matrix:

1-Carbohydrates: 30%, generally of bacterial origin, formed essentially of polysaccharides and enzymes.

Example: dextran: 9.5% +glycosyl transferase: role of bacterial adhesion. Levan 0.4%, galactose 2.6%.

2- proteins: 30% come from the oral environment, they are synthesized by the bacterial cell, the bacteria carry out their synthesis from amino acids coming from the oral environment or from the degradation of cellular and extracellular proteins.

Example: collagenase: destroys collagen, phosphoprotein phosphatases: of the bacterial membrane are capable of cutting the phosphoprotein bond releasing calcium, phosphate, from the phosphoproteins of the matrix.

3-lipids: 15%:

Plaque bacteria ensure the biosynthesis of all categories of lipids (degradation, shortening, desaturation, and saturation).

Example: the degradation of mucopolysaccharides is the result of the action of several enzymes.

Hyaluronidase: which splits hyaluronic acid.

Condroitin sulfatase: ensures the cleavage of condroitin.

Glucuronidase and hexamidase: complete the degradation.

*-inorganic mineral matrix:

It increases when plaque transforms into tartar.

Its constituents include: Ca++, phosphorus, fluorine, and traces of Na and K ions.

Calcium and phosphorus: increasing their concentration promotes the formation of tartar.

Fluoride inhibits bacterial adhesion.

*-Water: 80%.

8-2-Cellular part: bacteria:

-plaque of the furrows: we find lactobacilli bacteria 0.01%, anaerobic streptococci 27%, filamentous bacteria 23% coryne bacteria 18%.

– Supragingival plaque:

Facultative anaerobic streptococci 27%

Facultative anaerobic corynebacteria 23%

Anaerobic corynebacteria 18%

Peptostreptococci 13%

Flora of veillons 6%

Bacteroides 4%

Fusiform 4%

Neisseria 3%

Vibrions 2%

Spirochetes constitute less than 1%

-Subgingival plaque: with a higher percentage of anaerobes and mobile bacteria. We distinguish:

Attached part: rich in facultative anaerobic rods and gram-negative cocci.

Unattached part: we find mobile bacteria especially anaerobic germs and spirochetes.

Gram positive Gram negative

Aerobic cocci + – aerobic and facultative anaerobic cocci 0.4%

Facultative anaerobes anaerobic cocci 10.7%

: 28.5% facultative anaerobic bacilli 1.2%

Anaerobic cocci 7.4% (actinobacillus actinomyceteme comitans

Aerobic bacilli Capnocytophaga

And anaerobes ekenella corrodens)

Optional 15.3% – anaerobic bacilli: 16%

– Spirilla 1-3%

9-pathogenic action of bacterial biofilm:

Bacterial plaque can exert its pathogenic effect through the release of enzymes, toxins, antigens, certain products of its metabolism and the ability of certain germs to invade the tissues of the periodontium.

9-1- Products of bacterial metabolism:

Bacterial plaque follows two metabolic pathways:

Carbohydrate breakdown and protein breakdown.

Acids from Glycocalyx are capable of demineralizing hard tissues which leads to the formation of dental caries.

If proteolytic activity dominates, there is an increase in pH and therefore there will be an accumulation of: ammonia and hydrogen sulfide which are cytotoxic and amines which promote the formation of tartar from salivary salts.

9-2-Enzymes: most authors have highlighted the bacterial production of several enzymes: keratinase-glucuronidase, hyaluronidase, protease, collagenase, phosphatase, chondroitin sulfatase, elastase, etc.

These enzymes are capable of causing an alteration of the epithelial barrier, a degradation and a lysis of the fundamental substance, thus forming an epithelial breach allowing the passage of other enzymes and toxins which will promote the triggering of inflammation.

9-3- Toxins:

Under the action of enzymes, “trimming becomes a passageway” chaput, the enzymes having created a breach in the epithelial barrier, which will allow the penetration of toxins which will cause an inflammatory reaction at the level of the connective tissue

9-4-Antigens:

Most bacterial antigenic substances are found in the lipids forming: the bacterial wall, cytoplasmic membrane, flagella, capsule.

Antigens may not be completely inhibited by immune defense reactions, and a paradoxical effect will then occur: this reaction turns against the attacked organism and lyses the tissues that it should have protected.

9-5-Microbial invasion:

Bacteria enter the tissues through the pocket epithelium, and through the keratinized epithelium, the latter route having been demonstrated in the case of GUN and PJ and in an advanced stage of periodontal disease (AAC, pg, actinomyces, Capnocytophaga).

These bacteria are found in the chorion, often grouped in clusters

11-The future of the biofilm: (transformation into tartar): according to the following steps:

-Calcification of the intermicrobial matrix and bacteria: apposition of deposits of phosphate salts and Ca++

12-Highlighting of bacterial plaque

12-1-Clinic:

12-1-1-The developers:

-Definition :

These are means of controlling oral hygiene , it allows in fact the awareness of the patient and the possibility of control by the patient himself at home.

12-1-2-The clues:

Definition :

The index makes it possible to quantify the state of oral hygiene and to raise patient awareness.

Among these clues:

12-2-In the lab:

12-2-1-under a microscope: it allows obtaining information on microbial germs.

12-2-2-cultures: allow the cultivation of bacteria in a given selective aerobic or anaerobic medium.

12-2-3-enzymatic tests:

12-2-4-immunological tests:

Bacterial plaque

17-The conclusion

Bacterial plaque represents the primary cause of periodontal disease and the main etiology of serious bone destruction. It should be considered as such and its prevention should constitute the major part of our treatment (initial therapy), in order to ensure the sustainability of the dental attachment system.

18-Bibliography:

-B. PELLAT

EMC volume 4 of dentistry

Dental plaque (23-010-A-15)

Pages: 1- 7

-CHRISTIAN MOUTON

-JC ROBERT

Oral bacteriology.

Pages: 1-20

-GLICHMAN

Clinical periodontology

Pages: 316-336