Pulpal, Periapical, Odontogenic, and Bone Infecitons Flashcards Preview

Oral Microbio > Pulpal, Periapical, Odontogenic, and Bone Infecitons > Flashcards

Flashcards in Pulpal, Periapical, Odontogenic, and Bone Infecitons Deck (50)
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1
Q

What makes the pulp a unique organ?

A

It is enclosed in hard tissue and inflammation can be particularly damaging

2
Q

Why can pulpal inflammation be so damaging?

A

Increased interpulpal pressure can occur because it is surrounded by hard tissue and can’t go anywhere
This compromises blood flow, resulting in tissue damage
Irreversible damage leads to pulpal necrosis

3
Q

What makes the tooth so unique (for the purpose of this lecture)?

A

Roots are enclosed in bone, and the ingress for circulation is tiny and also surrounded by bone

4
Q

What is the most common cause of pulpal inflammation and necrosis?

A

Bacterial infection

5
Q

How can bacteria infect the pulp?

A

Direct pulp exposure
Bacterial penetration through dentinal tubules from caries
Direct access due to traumatic fracture of the tooth
Travel from bloodstream (unlikely)

6
Q

Traumatic fracture can lead to what?

A

Bacteria can easily enter the pulp
Infection happens quickly if pulps are not mechanically sealed
trauma may damage the blood supply or sever the apex resulting in tissue death

7
Q

What occurs is the pulp is non-vital?

A

There is a disruption of positive fluid flow, making the tooth more vulnerable to invasion by microbes
Infection may take a long time depending on bacterial access
There’s no immune response so bacteria can easily grow once they arrive

8
Q

T/F - Bacteria are necessary for pulpal and periapical disease to occure

A

True - that’s why a good seal is critical for the success of pulpal therapy

9
Q

What characteristics do bacterial species involved with pulpal and periapical disease have?

A

Anaerobic
gram-
bacilli
Multiple species are found in infecitons

10
Q

T/F - DNA-based studies show different bacterial profiles of infections than those seen in previous cultivaiton-based studies

A

True

11
Q

What are the most common species of periapical infection based on DNA analysis?

A

Enterococcus faecalis
Burkolderia
Streptococcus

12
Q

What species are the most common based on cultivation studies with periapical abscesses?

A

Prevotella and Porphyomonas

They’re responsible for the foul odor of necrotic pulps

13
Q

T/F - endodontic infections usually only have one species

A

False - they’re mixed bacterial infections

14
Q

How does oxygen concentration vary in the canal of a pulpal infection?

A

There’s a gradient depending on the area of necrosis

Necrotic canals have anaerobic conditions

15
Q

How do nutrients differ in the canal of pulpal infections?

A

Coronally = salivary constituents and ingested food (saccrolytic bacteria found here)
More apically = serum and cellular proteins are more avaliable (proteolytic bacteria found here)

16
Q

Pulpitis

A

Early stage of endodontic infeciton
Pulp is compromised by infection
Can be reversed if treated early
Early symptoms include lowered threshold and prolonged pain response to cold or other stimulus

17
Q

What is the sign of the shift from reversible to irreversible pulpitis and eventually pulpal necrosis?

A

Spontaneous pain signals

-pain can be quite severe (sharp or throbbing)

18
Q

As pulp becomes necrotic, what happens to immune cells?

A

They can’t enter the pulp due to a lack of blood supply, so the response shifts to the periapical region

19
Q

What happens as immune response shifts to periapical tissues?

A

Bone resorption takes place and allows space for a barrier of inflammatory cells to accumulate and prevent spread of infection
Inflammatory response is usually effective and bacteria are confined to periapical tissues (otherwise, orofacial infections occur)

20
Q

How does the bacterial load compare in the periapical tissues v the pulp in periapical lesions?

A

Low in the pulp (because its necrotic)

High in the periapical tissues

21
Q

Why are periapical leisons often asymptomatic?

A

The pulp is necrotic

Usually need a radiograph to detet

22
Q

Most periapical lesions are what?

A

Periapical granulomas

23
Q

Periapical granuloma

A

Asymptomatic inflammatory response
Macrophage dominant, but other inflammatory cells are also present
Often chronic

24
Q

Acute dentoalveolar (periapical) abscess

A

Acute exacerbation of periapical lesion
Purulent bacterial infection combined to bone at the apex
Very painful - aching, throbbing pain - tooth is sensitive to pressure
Drainage of pus may bring relief

25
Q

How can drainage of acute dentoalveolar abscesses occur?

A

Can occur through spontaneously through a fistula to surface or into tissue spaces
Drainage into surrounding tissues is dangerous and can lead to orofacial involvment

26
Q

Palliative treatment

A

Aimed at relieving patient symptoms

27
Q

What are some Palliative treatments of pulpal and periapical diseases?

A

Pharmaologic treatment with analgesiscs and/or long-acting anesthetic agents
Antibiotics are not effective against infections confined to the pulp or apical periodontitis because the blood supply is cut off and they can’t get there

28
Q

Definitive treatment

A

Treatment aimed at riffing the patient of cause of infections

29
Q

What are definitive treatments of pulpal and periapical diseases?

A

Preferred treatment
Extraction of the tooth OR
Root canal

30
Q

Root canal treatment

A

Chemical and mechanical cleaning of the root canal system

Through cleaning and good coronal seal, it prevents access of substrates and re-infections

31
Q

Persistent apical lesion

A

Infections that occur after root canal therapy

32
Q

How can persistent apical lesions occur?

A

Biofilm may be present on the surface of tooth areas
Debris ma remain within inaccessible regions of the apical canals
Foreign body such as infected dentin fragments may have been displaced by over-instrumentation

33
Q

What is the treatment of persistent apical lesions?

A

External biofilms can be removed by conventional endo therapy
Irregularly shaped apical foramina may be difficult or impossible to instrument from a coronal approach
Apical debris cannot be reached by nonsurgical access
Surgical therapy: “endodontic microsurgery” aka “apicoectomy”

34
Q

Odontogenic infections

A

When dental infections spread to surrounding areas, they’re called odontogenic infections
Range from localized to the alveolar area (dentinoalveolar area) to extending to adjacent facial structures or even systemic infections

35
Q

Cellulitis

A

Infection spreads through soft tissue via vascular channels or direct
Tissue is swollen (edema)
Tissue is hard (indurated) to palpaiton and not fluctuant

36
Q

What is the source of upper and lower facial cellulitis?

A
Lower = always dental
Upper = dental about 1/2 the time
37
Q

What is the “2nd phase” that cellulitis may proceed to?

A

Abscess formation

  • fluctuant and errythematous
  • natural drainage may occur, but it will not resolve without drainage
38
Q

Microbiology of Cellulitis and dental abscesses

A

Polymicrobial (4-6 species)
Cellulitis = facultative anaerobes
Abscesses = anaerobic species
Streps, peptostreps, prevotella, and sometimes fusobacterium

39
Q

How do you treat cellulitis?

A

May be temporarily managed with antibiotics
Will resolve more quickly if source of infection is removed
If it is well established, it may require antibiotics even after extraction of the tooth

40
Q

How do you treat abscesses?

A

If extraction or RCT doesn’t provide drainage, surgical incision and drainage is required
Penicillin and Clindamycin are two first line antibiotic chices

41
Q

Alveolar Osteitis

A

aka Dry Socket
Delayed healing of extraciton site - clot doesn’t form properly, exposing bone
Biofilm forms on bone surface

42
Q

Alveolar osteitis symptoms

A

Swelling, redness, exposed bone
Painful - throbing and aching
Mal-odor, bad taste, oozing

43
Q

Alveolar osteitis treatment

A

Gentile debridement and medicated dressing

44
Q

Osteomyelitis of the jaw

A

Spread of odontogenic or periodontal infection to jaw
Seen as a radiolucent area
May be surrounded by incolcrum (radiopaqe walling off)
Usually occurs in immunocompromised patients

45
Q

Osteomyelitis of the jaw symptoms

A

Swelling, pain, errythemia

Fever

46
Q

Osteomyelitis of the jaw treatment

A

Surgical debridement

Longterm antibiotic therapy

47
Q

Medication-induced Osteonecrosis of the jaw (MRONJ)

A

Exposed bone that does not heal
Rare unless patient is in immunosupressive cancer treatment and high dose-IV antiresorptive agent after a dental infection/extraction
Very rare

48
Q

Etiology of MRONJ

A

No osteoclasts, so non-shedding bone acts like a tooth and has reduced vascularity
Biofilms accumulate on the bone

49
Q

Treatment of MRONJ

A

Remove biofilm by debridement
Systemic antibiotics are ineffective
Temporarily stop anti-resorptive drugs

50
Q

How can we prevent MRONJ?

A

Avoid dental extractions in immunocompromised patients with history of bisphosphonate Tx
Maintain good oral health in at-risk patietnts
Conservative surgical approaches
Avoid bone exposure if possible
Antimicrobial mouth rinses after surgery