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Dental Infections

Dental pathogens - odontopathogens

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The human tooth has a natural defense

mechanism against bacterial colonization. The hard enamel surface selectively absorbs

acidic glycoproteins from saliva, forming a

membranous layer called the acquired enamelpellicle.

This pellicle, or organic covering, contains

many sulfate and carboxylate groups that

confer a net negative charge to the tooth

surface.

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Most bacteria also have a net negative charge,

there is a natural repulsion between the tooth

surface and bacteria in the oral cavity.

This natural defense mechanism breaks down

when dental plaque formation occurs.

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Dental Plaque

Dental plaque formation begins with the initial

colonization of the pellicle by Streptococcus

gordonii, S. oralis, and S. mitis.

Once the tooth surface is colonized,

subsequent attachment of other bacteria results

from a variety of specific coaggregation (cell-

to-cell recognition between genetically distinct

bacteria) reactions.

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Streptococci produce extracellular enzymes that

polymerize the glucose moiety of sucrose into

glucan and other polysaccharides. They act like

a cement to bind bacterial cells together,

forming a plaque ecosystem.

After the microbial plaque ecosystem develops,bacteria produce lactic and possibly acetic and

formic acids from sucrose and other sugars.

Because plaque is not permeable to saliva, theacids are not diluted or neutralized, and they

demineralize the enamel to produce a lesion on

the tooth. It is this chemical lesion that initiates

dental decay.

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Once these acids move below the enamel

surface, they dissociate and form soluble

calcium and phosphate ions. Between meals and

snacks, the pH returns to neutrality and some

calcium phosphate reenters the lesion and

crystallizes. The result is a demineralization-remineralization cycle.

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When fermentable foods high in sucrose are

eaten for prolonged periods, acid productionoverwhelms the repair process and

demineralization is greater than

remineralization. This leads to dental decay or

caries . Once the hard enamel has beenbreached, bacteria can invade the tooth.

Prevention include minimal ingestion ofsucrose; daily brushing, mouthwashes; and

professional cleaning at least twice a year to

remove plaque.

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Periodontal Disease Disease is initiated by the formation of plaque that forms at

the teeth-gum margin and extends down into the gums.

Colonization by Porphyromonas gingivalis. Disease can becontrolled by frequent plaque removal; by brushing, andmouthwashes; and at times, by oral surgery of the gums andantibiotics.

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Yersiniosis

Yersinia enterocolitica

Gram negative

Rod shapedMotile below 30 C but not at 37 C.

Temp. range -2 -- 45 C

Optimum temperature 25 C 29 C.

pH range at optimum temperature 4.6 9.6.

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Symptoms

Diarrhea

Abdominal pain

Fever and vomiting The illness may mimic appendicitis.

Illness may last from 2 days to several months.

Has ability to grow at refrigeration temperature.

Invasive type of infection, plasmid associated.

Enterotoxin similar to that ofE.coli.

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Destroyed in 1-3 min at 60 C.

D 62.8 C 0.7 17.8 sec.Heat stable enterotoxin; survives 100 C for 20

mins.

Not affected by proteases but activity lost with -

mercaptoethanol.

Not critical for virulence.

Disease associated with genes inv and ail.