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Theories of Oral Infection Cheat Sheet by

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

Exogenous Theory:

Exogenous pathogens and not endogenous microbiota caused disease
Fails to explain:
> Mode of transm­ission
> Acquis­ition
> Means of coloni­zation
> Effect of treatment on indigenous species
- 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

1) Tooth worm:
5000BC, 1803 - Diagrams and 1825- Case histories
2) Humoral Theory:
Blood, phlegm, black bile, yellow bile - Imbalance= disease
3) Chemical Theory:
Fermen­tation of food remains
4) Parasitic Theory:
Decomp­osition resulting from action of organisms in the mouth

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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