Endodontic microbiology and dressing strategy Flashcards

1
Q

How are infections caused?

A

bacteria penetrate or infiltrate skin or mucosa

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2
Q

3 ways bacteria can infiltrate a tooth

A
  1. exposition of pulp via trauma or attrition
  2. caries
  3. gingivitis/periodontitis
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3
Q

Characteristics of bacteria in oral cavity (3)

A
  • highly variable mixture of facultative anaerobe and true anaerobe species
  • either gram + or -
  • in special biotopes, a well organised commensal spectrum of bacteria will develop
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4
Q

Why do bacteria produce biofilms?

A

protection

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5
Q

How does the biofilm change as it develops?

A

the spectrum of species changes from aerobe to anaerobe

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6
Q

How does cariogenic bacteria progress into dentine? (4)

A

using dentinal tubules for invasion

dentinal tubules (1-2um) 
bacteria (0.1um) 

5-20 bacteria can fit in a tubule

propagation happens by adhesion and multiplication

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7
Q

What kind of bacteria are found in deep dentine lesions and why?

A

facultative and strict anaerobe species: streptococci, lactobacilli

they have passed a process of selection (the deeper, the more difficult to get nutrients and oxygen)

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8
Q

How do streptococci vs lactobacilli produce energy?

A

streptococci: mostly facultative anaerobes, some strict anaerobes
lactobacilli: facultative anerobes or microaerophillic

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9
Q

What is the signficance of lactobacilli if found in salivary cultures?

A

indicate presence of active dentine lesions

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10
Q

What happens when bacteria arrives in the pulp?

A

face a functioning system of defence, so a more or less balances state between attack and defence will be created

mechanism responsible for that is -> inflammation

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11
Q

Describe the progression of pulpal inflammation. (6 steps)

A
  1. Formation of secondary dentine (prior to bacteria entering the pulp)
  2. Hyperaemia: blood vessels widen and fill w erythrocytes
  3. Acute pulpitis
  4. Necrobiosis: pulpal invasion (some pulp vital, some dead)
  5. Necrosis: complete destruction of pulpal tissue, biofilms develop in the canal walls
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12
Q

Describe how acute pulpitis progresses (3)

A
  1. spaces between cells are filled with serum
  2. then blood vessels become permeable for leukocytes
  3. micro-abscesses form as it nears necrosis and bacteria enters the pulp
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13
Q

What microroganisms/cells are present in necrobiosis

A

masses of invading microorganisms

inflammatory cells

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14
Q

What is gangrene?

A

means necrosis with superimposed infection but most people just call it necrosis

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15
Q

What types of bacteria can be seen in a pulpal biofilm? (3) How do yeasts appear under microscope? (1)

A

spirochettes, filaments with or without gram negative bacterial wall

yeasts are circular, appear larger than bacteria

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16
Q

How do bacteria in pulpal biofilms survive without nutrients from the oral cavity such as carbohydrates? (2)

A

commensal symbiosis created by interspecies ecology of biofilms

species feed on metabolic products of other species, creating a network of interactions → helping them survive dire conditions of the pulp and host defences

17
Q

What is internal infection? Why is this clinically signficant?

A

infection of tubuli from inside

we must file the canals and remove enough dentine as bacteria can exist within canal walls and in dentine

18
Q

Different pathways to apical perio (flowchart)

A
19
Q

What is apical periodontitis?

A

After invading the whole pulp, bacteria meet a second line of defence at the apical foramen → triggers inflammation in PA tissues

(now faces full power of human’s immune defence)

20
Q

How does the balance between virulence of bacteria and immune defece cause either acute or chronic apical perio? (seesaw problem)

A

low virulence, good defence → chronic apical periodontitis

high virulence, low defence → acute apical periodontitis/abscess

21
Q

When does acute apical perio happen and what are some forms?

A

balance of virulence and defence in favour of attacker

primary acute apical perio, secondary acute apical perio, periapical abscess

22
Q

When does chronic apical periodontitis happen? What is the result (which cells are present)?

A

balance of virulence and defence in favour of defence

granuloma with lymphocytes, plasma cells, monocytes and macrophages (immune cells)

23
Q

When does chronic apical abscess happen?

A

equilibrium of virulence and defence

24
Q

T/F We can identify all root canal bacterial species using cultures***

A

No, only 10% can be cultured with conventional bacteriological methods

there is HIGH VARIABILITY in the species present in a sample and therefore you cannot determine the exact spectrum of bacteria causing endo disease

nowadays we use molecular biology and genetic screening

25
Q

How many species can be identified in the initial colonisation of the pulp?

A

mixed flora of only a few species (2-8) can be identified, mostly streptococci and obligate anaerobes

CANNOT only be only one as they need commensal symbiosis

26
Q

Which species are most common in problem cases? Why do they cause an issue?***

A

enterococcus faecalis

candida albicans

  1. resistant against CaOH2
  2. high penetration into tubuli
  3. forms biofilms