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Robert Koch's Germ Theory:
All subjects must present with the same symptoms |
Causative organism must be isolated in pure culture |
When inoculated into a 2nd host, it must produce the same symptoms |
Identical pure culture must be obtained from second host |
Modification of Koch’s postulates for oral opportunistic infections:
> Should be present in sufficient numbers to cause disease
> Should have access to the affected tissues
> Should be in an environment that permits its survival and multiplication
> Inhibitory organisms should be absent or not affect it
> The host must be susceptible
Difficulties:Koch's Postulate in Oral Infections:
> No overt pathogen - mostly mixed infections |
> More than 700 identified oral species |
> Not all members of biofilm community are cultivable |
> Presence may be as a result rather than cause of disease |
> Sites don't appear to be actively progressing at all times |
> Different sites in mouth may break down as a result of different species |
> Strains of putative pathogens may vary in virulence |
> Some strains may harbour bateriophages or plasmids that confer virulence properties |
Non-specific Plaque Hypothesis
Overgrowth of indigenous microbiota |
Same organisms observed in health and disease |
Shifts in microbial proportions rather than specific pathogens |
Any plaque biofilm can cause disease |
Problems with NSPH:
- Focus is on quantitative changes only
- Disease in animals not the same as in humans
- Impractical to compare virulence in different host species
- Doesn't explain why individuals with: 1) longstanding plaque don't develop disease and 2) minimal plaque have lower resistance to disease
Specific Plaque Hypothesis
More sophisticated studies demonstrated: |
> Improved cultural and sampling methods |
> Composition of plaque biofilm differs both inter-orally and intra-orally |
> Increase at a sight of infection |
> Decrease in health or following treatment |
> Qualitative changes in plaque biofilm |
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Exogenous Theory:
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Exogenous pathogens and not endogenous microbiota caused disease |
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Fails to explain: > Mode of transmission
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> Acquisition
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> Means of colonization
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> Effect of treatment on indigenous species
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Contraindications:
- Over simplification
- Overlaps often occurred (Negated SPH and NSPH)
- Eradication of exogenous pathogens (Incorporated both SPH and NSPH)
Ecological Plaque Hypothesis:
Opportunistic endogenous infection |
Ecological shift from predominatly G+ cocci to G- rods/cocci-bacilli |
Any bacterial species may be pathogenic |
Ecological changes in environment dictate virulence mechanisms |
Disease prevented by elimination or interruption of ecological succession |
Role of Biofilms in Infection:
Most common: |
1. Dental caries (supragingival plaque) |
2. Periodontal disease (subgingival plaque) |
Dental Caries Theories
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1) Tooth worm: 5000BC, 1803 - Diagrams and 1825- Case histories
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2) Humoral Theory: Blood, phlegm, black bile, yellow bile - Imbalance= disease
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3) Chemical Theory: Fermentation of food remains
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4) Parasitic Theory: Decomposition resulting from action of organisms in the mouth
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Millers (1882) Chemo-parasitic Theory:
2 stage process: |
i) decalcification of enamel resulting in destruction of dentin |
ii) dissolution of softened residue of enamel and dentin |
Dietary carbohydrates -> convert into acid -> calcium and phosphate diffuse out of enamel -> a caries lesion
Proteolytic Theory (Gotliebb 1946)
Invasion of enamel by m/o's -> proteolytic activity -> alteration of pH -> resulting in liquidification of organic matrix of enamel -> inorganic salts dissolved by acidogenic bacteria |
The proteolytic-chelation Theory
Schutz and Martin (1955) |
Simultaneous attack on organic and inorganic compounds of tooth |
Kaeratinolytic bacteria attack enamel ->
Breakdown of protein and other organic components of enamel (keratin) ->
Formation of complexes with calcium from plaque which chelates with mineral component of the tooth ->
Increased solubility, decalcification of enamel ay neutral or alkaline pH
Current Concepts in Caries Etiology
Keyes Triad & Newbeun's Tetrad
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