Endo - Etiology And Pathogenesis

Front 1

2 main types of pulp necrosis?

Back 1

Sterile
Infected

Front 2

What is a radicular cyst?

Back 2

= apical periodontitis + cyst

Front 3

Types of resorption

Back 3

- cervical
- internal inflammatory root res.
- surface
- external inflammatory root res.
- replacement res.

Front 4

Necrosis of pulp usually occurs as result of ______________.

Back 4

Trauma

Front 5

T/F: 80-90% of cases of necrosis are symptom free

Back 5

TRUE

Front 6

T/F: Bad quality of endo tx will always lead to a lesion.

Back 6

False - will only lead to a lesion if bacteria are present.

Front 7

Diisease progression of PA region is always (ahead/behind) of the pulp.

Back 7

Diisease progression of PA region is always ahead of the pulp.

Front 8

What are possible pathways into the pulp for bacteria? (know this well!!)

Back 8

- caries
- enamel caries
- leakage
- hair fracture
- lateral canal
- dentinal tubules
- deep pockets
- bacterimia
- trauma exposed pulp

Front 9

Which restorative materials allows the a tight seal?

Back 9

ZOE

Front 10

Pulp reacts to bacteria even when it is not close to the pulp. Why?

Back 10

fine structure of the tooth, dentinal tubules allow antigens to move from bacterial/infection location to pulp

Front 11

Endodontic bacterial ecology is mainy affected by (3things)

Back 11

1. Nutrients
2. Redox particles (oxygen availibility)
3. Competition

Front 12

What flora is predominant in apical peridontitis in primary treatment and post-treatment?

Back 12

- in primary treatment: anaerobes dominate (yeasts/enteric absent)
- In post-treatment:; Enterococcus faecalis (35-70%), yeasts (5-20%)

Front 13

Pathogenesis and spead of apical periodontitis?

Back 13

o Periodontitis occurs due to osteoclast activation – removing bone ahead of the bacterial infection prevents a bone infection (difficult to tx)
o Infection may spread
• Dentinal canals
• Lateral canals
• Periapical area (generally, host defenses will take care of the periapical area – disinfection removes the infection from the pulp)

Front 14

Is bacteria responsible to resorption?

Back 14

NO, the host responses are!
But.. Trauma, Bacteria and necrosis may act as stimulating factors.

Front 15

T/F: once lesion is visible on radiograph, the bacteria has arrived there.

Back 15

FALSE. Inflammatory rxn is 1 step ahead of bacteria and usually when the lesion is seen on the radiograph early on, bacteria have not yet arrived there - good prognosis!

Front 16

Why do abscesses occur?

Back 16

too much bacteria and host defenses not strong enough to overcome --> destruction, swelling and pus

- endo tx can push bacteria out of canal and cause absess

Front 17

Bacterial flora in AP resembles that in __________

Back 17

pocket flora

Front 18

How does bone defend itself from infection? Is it effective?

Back 18

Not effective. Defense mechanism is to remove bone by osteoclasts. Why? because bone cannot defend itself properly.
- bone is replaced by highly vascularized tissue --> increased ability to defend itself

Front 19

If bone does get infected, what is the consequence?

Back 19

osetomyelitis

Front 20

A patient has a PA lesoin, but it has not grown in a while despite the lack of treatment - why may this be?

Back 20

remodelling has occured and body has striked a balance bw infection and defenses. treatment is still necessary!

Front 21

Describe the features of cervical resportion

Back 21

- starts apically at junctional epithelium
- pulp is vital and healthy
- no caries or bacteria in lesion
- resorbing human cells osteoclasts are present

Front 22

Describe the features of internal inflammatory root resorption

Back 22

- starts from inside the pulp
- bacteria ARE involved

Front 23

Describe the features of external inflammatory root resorption

Back 23

- can be very agressive and cause resorption very quickly
- trauma related

Front 24

Describe the features of replacement resorption (tooth:anylosis)

Back 24

- slow resorption
- often there is hx of trauma --> leads to replacement resorption

Front 25

Define Reversible pulpitis

Back 25

inflammation should resolve and the pulp return to normal

Front 26

Define Symptomatic Irreversible Pulpitis

Back 26

- vital inflamed pulp is incapable of healing.
- Additional descriptors: Lingering thermal pain, spontaneous pain, referred pain.

Front 27

Define Asymptomatic Irreversible Pulpitis

Back 27

- vital inflamed pulp is incapable of healing.
- Additional descriptors: No clinical symptoms but inflammation produced by caries, caries excavation, trauma, etc.

Front 28

Define pulp necrosis

Back 28

= death of the dental pulp.
- The pulp is usually nonresponsive to pulp testing.

Front 29

Define: normal apical tissue

Back 29

Teeth with normal periradicular tissues that are not sensitive to percussion or palpation testing. The lamina dura surrounding the root is intact and the periodontal ligament space is uniform.

Front 30

Define: symptomatic apical periodontitis

Back 30

- Inflammation, usually of the apical periodontium,
- clinical symptoms including a painful response to biting and/or percussion or palpation.
- It may or may not be associated with an apical radiolucent area.

Front 31

Define: Asymptomatic apical periodontitis

Back 31

- Inflammation and destruction of apical periodontium that is of pulpal origin,
- appears as an apical radiolucent area,
- does not produce clinical symptoms.

Front 32

Define: Acute apical abscess

Back 32

An inflammatory reaction to pulpal infection and necrosis characterized by rapid onset, spontaneous pain, tenderness of the tooth to pressure, pus formation and swelling of associated tissues.

Front 33

Define: Chronic apical abscess

Back 33

An inflammatory reaction to pulpal infection and necrosis characterized by gradual onset, little or no discomfort, and the intermittent discharge of pus through an associated sinus tract.

Front 34

Define: Condensing osteitis

Back 34

Diffuse radiopaque lesion representing a localized bony reaction to a low-grade inflammatory stimulus, usually seen at apex of tooth.