Endodontic Infections Flashcards

1
Q

what is inflammation?

A

the cellular and vascular response to tissue injury

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2
Q

what is infection?

A

the invasion and proliferation of pathogenic microorganisms in the tissue

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3
Q

can you have inflammation without infection?

A

yes

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4
Q

what are some of the bacteria that can cause infections to produce inflammation?

A

Pseudoramibacter
Treponema Dialister
Prevotella Porphyromonas
Fusobacterium
Peptostreptococcus Campylobacter

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5
Q

what do bacteria produce that can lead to inflammation and where can they reach?

A

proteolytic enzymes, organic acids and endotoxins that can reach the pulp and periapical area

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6
Q

what is the purpose of inflammation?

A

to start the release of chemical mediators to repair and heal the damaged tissue

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7
Q

what are the 4 ways inflammation can occur?

A

wounds
injured organs
hypersensitivity reactions
chronic diseases

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8
Q

what are the cardinal manifestations of inflammation?

A

swelling
color change
pain

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9
Q

what are the chemical mediators that cause inflammation?

A

histamine
NO
prostaglandins
bradykinin
other cytokines

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10
Q

what does the release of chemical mediators cause in the inflammatory response?

A
  1. changes in vascular flow
  2. structural changes in the microvasculature
  3. migration of PMNs into the site of injury by chemotaxis
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11
Q

what 5 things occur during swelling?

A
  1. changes in vascular flow
  2. changes in vascular permeability
  3. escape of protein rich fluid
  4. increase in osmotic pressure
  5. outflow of fluid
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12
Q

describe what happens during the change in vascular flow?

A

prostaglandins and nitric oxide relax vascular smooth muscle to cause vasodilation and increased blood flow

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13
Q

what happens during the venule events?(increased permeability, exudate, increase in osmotic pressure)

A

blood flow slows down and margination begins

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14
Q

what is margination?

A

displacing of the leukocytes and macrophages towards the wall of the vessel

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15
Q

what is transmigration?

A

occurs during venule event across the endothelium where leukocytes move by extending pseudopods and squeezing through intracellular junctions

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16
Q

an increase in exudate means an increase in?

A

fluid containing fighting cells like neutrophils and macrophages

17
Q

why does color change occur during inflammation?

A
  1. access of fluid
  2. escape of blood and blood cells from the blood vessels into the tissues
18
Q

what are the chemical mediators of the inflammatory response that can cause pain?

A

histamine
serotonins
bradykinins
prostaglandins

19
Q

where is histamine stored?

A

granules of basophils, platelets and mast cells

20
Q

what are the functions of histamine in the inflammatory response?

A
  • cause pain
  • endothelial cell contraction
  • intracellular gaps
  • increased cellular permeability
  • causes sneezing, runny nose, itchy eyes, hives and bronchospasm
21
Q

where is serotonin stored?

A

cellular granules in platelets and the CNS

22
Q

what are the functions of serotinin in the inflammatory response?

A
  • sensitize nerve cells involved in pain
  • can make CNS more sensitive to pain
23
Q

what are the steps for bradykinin activation?

A
  1. factor XII → XIIa triggers cascade
  2. Facter XIIa activcates Prekallikrein → Kallikrein
  3. Kallikrein activates kininogen → bradykinin
24
Q

how is the kinin cascade amplified?

A

kallikrein activates the formation of more Factor XIIa which amplifies the cascade

25
what is the function of bradykinin in the inflammatory response?
lowers the threshold of nerves leading to more pain
26
what are the steps for prostaglandin formation?
1. injury to phospholipid cell membrane 2. release of arachidonic acid by PLA2 3. COX pathway (PGG2 → PGH2 → prostaglandins)
27
where do aspirin, ibuprofen and steroids inhibit the Arachidonic Acid pathway?
- aspirin and ibuprofen inhibit COX - steroids inhibit PLA2
28
what is the function of prostaglandin in the inflammatory response?
causes pain and inflammation
29
what is endodontic infection?
the invasion and proliferation of pathogenetic microorganisms in the pulp and root canals leading to injury and inflammation
30
what are the pathways of pathogens into the dental pulp?
cracked tooth caries trauma
31
what are the bacteria that can cause caries lesions?
Streptococcus mutans Lactobacilli
32
what are the bacteria that are found in root canals?
Streptococcus mutans Lactobacilli Treponema Prevotella Porphyromonas Peptostreptococcus Streptococcus Fusobacterium Propionibacterium
33
what does the invasion of pathogens into the dental pulp and root canal cause?
infection that causes inflammation resulting in pain, pulp tissue necrosis and bone destruction
34
what is the effect on pulp of placing LPS in cavity preparations? what does this tell us?
LPS is a potent endotoxin that leads to localized pulp tissue damage, neutrophil infiltration, vasodilation, and edema - Confirms that bacterial toxins, not just live bacteria, can initiate pulpitis
35
what did the S. Kakehashi study determine?
that pulpal necrosis and periapical disease occur only in the presence of bacteria; germ-free rats had vital pulps with no pathology after pulp exposure, while conventional rats developed necrosis and abscesses
36
how do periapical lesions lead to osteoclast activation?
the infection and necrosis of the dental pulp causes the body’s immune system to release pro-inflammatory cytokines and express RANK-L
37
How do periapical lesions lead to bone resorption?
activated osteoclasts will begin synthesizing bone ECM- digesting enzymes and mineral- dissolving acid which will start to resorb bone