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DENT 371

Dr. Hisham Al-Shorman

Bacterial population

Host defense

Health is a state of balance


human intrauterine fetus is sterile


birth, colonization of the mouth by bacteria takes place


the age of 2, human microflora is established which generally lives in harmony with the body (commensal or beneficial)


eruption of teeth, the oral microflora (>500 species) is established

Swallowing, mastication and blowing the nose

Flow of different fluids (saliva, nasal, GCF,..)

Tongue and oral hygiene measures

Movement of cilia in nose and sinuses

High turnover of the oral epithelial cells

Old belief

Periodontal diseases are caused by the cumulative accumulation of all types of bacteria on teeth
A small group of bacteria are the initiators for the disease and most of tissue destruction is caused by the host reaction to bacteria The central role of microorganisms has always been, and is still, recognized

Current undedrs -tanding



microorganisms, mainly bacteria, populates the oral cavity in biofilms called: Dental Plaque circumstances permit, disease occur state Vs disease




Materia Alba:
Soft deposits Lacks organization Easily removed by water spray

Dental Plaque Calculus

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A bacterial community (biofilm) adhering to teeth and other oral structures embedded in a matrix of polymers of bacterial and salivary origin

When calcified, it becomes calculus

70% of the plaque is

composed of micro-organisms, mainly bacteria
>500 species Range: 103 in healthy crevice 108 bacteria (in diseased crevice) Non-bacterial species: mycoplasma, yeasts, protozoa and

30% is composed of a few : epithelial cells macrophages leukocytes embedded in a matrix

Coronal related to calculus and caries Marginal related to gingivitis

Subgingival related to
periodontitis: Tooth-attached Unattached Tissue-attached


are: matrix-enclosed bacterial populations adherent to each other and / or to surfaces or interfaces They are ecological communities that evolved to permit survival of the community as a whole Fluid-filled channels Bacterial behavior in biofilms Vs planktonic Resistance to antimicrobials

Secondary Colonization

Intercellular Matrix
20 30 % of the plaque mass Organic and inorganic material from saliva, GCF and bacterial products



Polysaccharides Proteins Glycoproteins Lipid material

Ca & P with traces of Na, K, F Primary source: saliva

Occurs in stages:

1. Formation of the pellicle

2. Initial bacterial adhesion and attachment 3. Secondary Colonization 4. Plaque Maturation

The All

initial phase of plaque formation

surfaces of the oral cavity are coated with a glycoprotein pellicle pellicle comes from saliva, GCF, bacterial, and host tissue cell products & debries


The hydroxyapatite surface: -ve charged phosphate groups

Salivary and crevicular fluid macromolecules components : +ve charged They interact directly or indirectly Mechanisms involved the following forces: Electrostatic Van der Waals Hydrophobic

Functions as a protective barrier Provides lubrication and prevents tissue desiccation Also a substrate to which bacteria can attach and accumulate to form dental plaque


a few hours, bacteria are found on the dental pellicle (primary colonizers) Mechanisms not fully understood Suggested stages:
Transport of bacteria to the surface Initial (reversible) adhesion Attachment Colonization and plaque formation

vicosus, Streptococcus sanguis

Gram positive, e.g. Actinomyces

The primary colonizers are

Aerobic which uses oxygen, therefore reduces the redox potential Gram +ve which use sugars and saliva for nutrition

the end of this stage, a shift takes place!

At the end of initial colonization, a shift occurs to:

Anaerobic environment Gram ve colonizers which do not use sugars for nutrition These bacteria are the pathogenic ones!

Secondary colonizers that do not initially colonize clean tooth surfaces attach to primary colonizers Examples of these secondary colonizers :

Prevotella intermedia, Prevotella loescheii, Capnocytophaga spp., Fusobacterium nucleatum and Porphyromonas gingivalis

F. nucleatum with S. sangius

P. loescheii with A. viscosus

Capnocytophaga ochracea with A. viscosus

F. nucleatum with P. gingivalis F. nucleatum with Treponema denticola


species are the most predominant pellicle colonizers and provide an array of adhesins after attachment


species coaggregate with all other oral bacteria are therefore proposed to play a major role in biofilm formation


Agonistic Interactions

Antagonistic Interactions

Providing Providing

growth factors favorable growth conditions in the metabolism of digested



Inhibition of growth:
Certain bacteria such as S. sangius, S. uberis, A. viscosus produce factors that are inhibitory to the growth of A. actinomycetemcomitans

Inhibition of attachment Competition on nutrients

corncob configurations: growth of cocci on the surface of filamentous microorganisms

test tube brushes are gram negative filamentous bacteria, some of which may be flagellated The axial portion of the test tube brush consists of a single or several long filaments held together by an amorphous extracellular matrix

Subgingival niches:

tooth (or implant) surface The surface of epithelial cells The gingival exudates fluid medium The superficial portion of the pocket epithelium

Subgingival bacteria have the capacity to invade dentinal tubules An alteration in the composition of subgingival plaque occurs during pregnancy.
Gingivitis and bleeding increased without an increase in plaque levels Bacterial anaerobic to aerobic ratios increased in addition to P. intermedia proportions The relative increase of P. intermedia may be a more sensitive indicator of altered systemic hormonal situation than clinical parameters of gingivitis

Plaque as a whole is the important factor! But, it is seen that:

Some individuals with much plaque, calculus and gingivitis do never develope destructive periodontitis Some individuals with periodontitis have affected sites next to unaffected sites

These findings indicate that not all plaque is equally pathogenic

Only The

certain plaque is pathogenic

pathogenicity depends on the presence of or increase in specific microorganisms


link with localized aggressive



can be attributed to changes in the environment which disrupt homeostasis between the plaque microflora and host factors, rather than just bacteria alone, have in relation to periodontal disease



the past, it was thought that plaque grows by apposition of new bacteria at the plaque surface is now clear that plaque grows in thickness primarily through cell division of adherent bacteria


Topography of supragingival plaque

Start from gingival margin and interproximal areas Start from grooves and cracks etc

Tooth surface roughness Individual variables influencing plaque formation

Heavy plaque formers / light formers Salivary composition and flow is the main factor Wettability of tooth surface is another factor

Variation within dentition - more on:

Molars and premolars Buccal surfacaes Mandibular teeth Marginal and proximal areas

Impact of patients age

Spontaneous cleaning not really!