W8 - Microbiology of Endo Infections - Rodrigo Flashcards

1
Q

Does dentine exposure always cause potential pulp exposure?

A

Only when thickness is considerably reduced and permeability is increased

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2
Q

How does dentinal tubule size change in the tooth

A

Conical conformation

largest widest diameter near pulp, smallest near the enamel

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3
Q

Microbiological goal of endo tx (2)

A

Eradicate bacterial colonization or

Reduce bacterial load to levels that permit perradicular tissue healing

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4
Q

What percentage of root surface area remains untouched even after instrumentation

A
  1. 6% to 79.9% untouched
    * this is why irrigants are important
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5
Q

Pathogenesis equation

What is the only thing you can change?

A

P = pathogenesis

N = number of bacteria

V = virulence

I = interaction

R = resistance

You can only change the number of bacteria. Not virulence, interaction, etc

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6
Q

Which type of bacteria are associated with more failures of endo (not species)

Why? (3)

A

Gram positive

  • Bc they are more resistant to antimicrobials
  • Can adapt to harsh environmental conditions in medicated canals
  • gram neg are easy to kill
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7
Q

Does pulp only become inflamed once there is exposure from caries?

A

No - bacterial products can move through tubules and cause pulpal inflammation before exposure

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8
Q
A

Irrev pulp

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9
Q

Are bacteria IN the canal or OUT of the canal in apical periodontitis?

A

Inside the canal → the LEO is the consequence of bac in the canal

When bac are OUT of the canal → Abscess

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10
Q

What is in biofilm? Percentage? (2)

A

15% bacterial colony

85% EPS - Extracellular Polymeric Substance

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11
Q

2 types of endodontic infections classified by anatomic location

A

Intraradicular infection (3 types)

Extraradicular infection

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12
Q

3 types of intraradicular infection

A

Primary infection

Secondary infection

Persistent infection

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13
Q

What causes primary infection?

A

Caused by microorganisms that
initially invade and colonize the
necrotic pulp tissue

type of primary intraradicular infection

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14
Q

What causes secondary infection?

A

Caused by microorganisms not present in the primary

  • *infection** but introduced in the root canal at some time after
  • *intervention**
  • type of intraradicular infection*
  • Couldve been introduced by microleakage or touching the file with gloves before treatment
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15
Q

What causes persistent infection

A

caused by microorganisms that were members of primary or secondary infection and resisted intracanal antimicrobial procedures and were able to endure periods of nutrient deprivation in treated canals.

type of intraradicular infection

leftover bacteria in canal

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16
Q

Synonym of persistent infection

A

Late failure

“can even happen 12 years later”

17
Q

12 years later

A

Late failure / persisting infection

18
Q

How does the size of the lesion affect bacteria colony?

A

Larger the lesion = higher bacterial diversity and density

19
Q

What type of bacterial species occupy primary interradicular infection?

A

Mixed species but mostly anaerobic bacteria of gram negative and positive type

20
Q

What is the major cause of post treatment apical periodontitis

A

Intraradicular infection - either persistent or secondary

  • Usually of gram-positive bacteria
21
Q

Examples of Intraradicular vs Extraradicular infection

A

Intraradicular - apical periodontitis → constitutes effective barrier against spread of infection to bone and other sites

Extraradicular - abscess → bacteria have overcome the barrier and are spreading

22
Q

Where is the bacteria / infection in extraradicular infection?

A

Have pushed through apex

23
Q

What is Rodrigo’s only solution for extraradicular infection?

A

Apical surgery

51:45

Ex. apical periodontitis with development of external biofilm

24
Q

3 Examples of extraradicular infections that are dependent on intraradicular infections

A

Acute / chronic apical abscess

“wet canals” - persistent exudation

25
Q

2 examples of scenarios where extraradicular infection is independent of intraradicular infection

A
  • No longer fostered by the intraradicular infection
  • Persistence of extraradicular infection even after successful eradication of intraradicular infection