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Bacterial population
Host defense
The
After
After
the age of 2, human microflora is established which generally lives in harmony with the body (commensal or beneficial)
After
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
Therefore,
These
microorganisms, mainly bacteria, populates the oral cavity in biofilms called: Dental Plaque circumstances permit, disease occur state Vs disease
When
Health
state
Materia Alba:
Soft deposits Lacks organization Easily removed by water spray
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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
Supragingival:
Coronal related to calculus and caries Marginal related to gingivitis
Subgingival related to
periodontitis: Tooth-attached Unattached Tissue-attached
Biofilms
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
Organic
Inorganic
Occurs in stages:
The All
surfaces of the oral cavity are coated with a glycoprotein pellicle pellicle comes from saliva, GCF, bacterial, and host tissue cell products & debries
The
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
Within
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
Initially,
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
Streptococcus
species are the most predominant pellicle colonizers and provide an array of adhesins after attachment
Fusobacterium
species coaggregate with all other oral bacteria are therefore proposed to play a major role in biofilm formation
They
Agonistic Interactions
Antagonistic Interactions
Providing Providing
Cooperation
proteins
Inhibition of growth:
Certain bacteria such as S. sangius, S. uberis, A. viscosus produce factors that are inhibitory to the growth of A. actinomycetemcomitans
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:
The
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
Only The
A.A.
periodontitis
Disease
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
Environmental
In
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
It