Dental Infections

Dental pathogens - odontopathogens

• 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 enamel
pellicle.
• This pellicle, or organic covering, contains
many sulfate and carboxylate groups that
confer a net negative charge to the tooth
surface.
• 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.
 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.
• 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, the acids 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.
• 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.
• When fermentable foods high in sucrose are eaten for
prolonged periods, acid production overwhelms the
repair process and demineralization is greater than
remineralization. This leads to dental decay or caries .
Once the hard enamel has been breached, bacteria can
invade the tooth.

• Prevention include minimal ingestion of sucrose; daily

brushing, mouthwashes; and professional cleaning at
least twice a year to remove plaque.
 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 be

controlled by frequent plaque removal; by brushing, and
mouthwashes; and at times, by oral surgery of the gums and
antibiotics.
 Yersiniosis
Yersinia enterocolitica
Gram negative
Rod shaped
Motile below 30 ̊ C but not at 37 ̊ C.
Temp. range -2 -- 45̊ C
Optimum temperature 25̊ C – 29 ̊ C.
pH range at optimum temperature 4.6 – 9.6.
 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 of E.coli.
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
β-
mercaptoethanol.
Not critical for virulence.
Disease associated with genes inv and ail.