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endo > microbio of RCS > Flashcards

microbio of RCS Flashcards

1
Q

what necrosis occurs in the RCS

A

liquefactive

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2
Q

is there patholgy without bac in the RCS

A

NO

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3
Q

RCS provides? why?

A

The root canal system provides an ideal environment for bacterial colonization
The RCS is warm, moist & nutritious (has lots of substrate) and has a variable but largely anaerobic climate.
This area is now largely protected from the host defenses

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4
Q

bac invasion of pulp initally forms? progresses to?

A

microabscess progressing to necrosis

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5
Q

basic science most closely associated to endo?

A

microbio

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6
Q

remaining bac after RCT can cause?

A

apical periodontitis

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7
Q

first cells to respond to bac at the apex

A

PMN

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8
Q

chronic inflammation of the apical tissues will form?

A

periapical granuloma

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9
Q
A

periapical granuloma formation used to protect bone

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10
Q

what is this? what is happening to the root?

A

periapical granuloma with resorbtion occuring at the apex

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11
Q

how can RCT alleviate periapical lesions?

A

removal of the bacteria allows healing to occur

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12
Q

pus of RCS

A

due to PMN invasion/death, must be drained

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13
Q

most RC infection are caused by?

A

gram -, anaerobic bac

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14
Q

what do the bacteria of endo infections release? can cause what effects?

A

LPS/endotoxins, can cause fever, osteolysis and collegenolysis

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15
Q

spp involved with RC infections, most frequent spp?

A

Gram -, anaerobic
Porphyromonas sp. ( Bacteroides previously)
• Prevotella nigrescens (Bacteroides previously) most frequent in endo infections
• Peptostreptococcus,
• Fusobacterium
• Eubacterium
• Actinomyces

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16
Q

canal walls/ spaces conducive to the formation of?

A

biofilm

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17
Q

formation of biofilm, responsible for what dx?

A

Planktonic “floating bacteria” adhere to surface and begin adhesion to one another
Biofilm is adhered to the root canal walls
Formation of biofilm is responsible for apical periodontitis

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18
Q

can only one organism cause infection?

A

NO, no single spp is repsonsible (polymicrobial dx)

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19
Q

Progression of RC infections

A
  1. Carious Lesion or Trauma opens tubules to bacterial invasion
  2. Bacteria inflame pulp locally
  3. Inflammation may overcome pulpal defenses and localized abscesses may form in coronal
    pulp
  4. Infection increases in pulp and necrosis begins
  5. Necrosis involves entire RC System
  6. Infection uses “portals of exit” (apical foramen and lateral canals) to invade peri-radicular tissues (apical periodontitis)
  7. Periradicular infection occurs beyond apex ( apical abscess )
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20
Q

ludwing angina

A

medical emergency
due to cellulitis which has spread through fascial planes (sublingual/mandibular)
can eventually increase size and obstruct airway leading to suffocation

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21
Q

BIOFILM must accomplish 6 things to cause disease within the RC System

A
  1. MO must adhere to host surfaces
  2. Obtain nutrients from the host
  3. Multiply
  4. Invade tissue
  5. Overcome host defenses
  6. Induce tissue damage
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22
Q

BIOFILM

A

Think complex, variable & constantly changing bacterial infection
BIOFILM may be defined as a multicellular microbial community characterized by cells that are firmly attached to a surface and enmeshed in a self produced matrix of extra cellular polymeric substance (EPS), usually polysaccharide.

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23
Q

_________bacteria appear to be the most common microorganisms in primary
endodontic infections.

A

gram-, anaerobic

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24
Q

common genera of endo infections

A

-Porphyromonas
- Prevotella
- Peptostreptococcus
- Streptococcus
- Actinomyces
- Olsenella
- Propionibacterium

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25
Q

why would anaerobic bac be favored in chronic infections

A

more O2 is used by bacteria as the infection progresses leading to anaerobic environment

26
Q

bac genera that tend to exist together

A

-Porphyromonas
- Prevotella

27
Q

all endo infections are_______

A

polymicrobial

28
Q

what kind of anaerobes can you see in an endo infection?

A

obligate (req no O2) and faculative (can be with O2 or not, O2 can even increase virulence)

29
Q

resulting biofilm when tooth is challenged with? avoidance of this?

A

BIOFILM becomes more varied, complex, and difficult to control when the tooth is further
challenged by salivary contact or operative contamination (New BUGS or altered
environment)

Avoid leakage of rubber dam or temporary Avoid iatrogenic contamination during
treatment (leaky dental dam, etc.)

30
Q

how do we destroy the microbes?

A

OUR MAJOR WEAPONS: CLEANING AND SHAPING with NaOCl (8.3%) and INTRA-CANAL MEDICAMENTS (CaOH)

31
Q

canal anatomy and our instruments

A

Canals have many ramifications, anastomoses, fins & webs and bifurcations which are inaccessible to instrumentation where MO can hide

32
Q

can files reach all of the canal? how can we help with this?

A

NO, diverse shapes are resistant to mechanical shaping; files never reach ALL spaces in the complex pulpal system.

Correct use of NaOCl is extremely important in eliminating micro-organisms in these
spaces*

33
Q

6 FUNCTIONS OF NaOCl in root canal system

A

Disinfects over time
• Dilutes & Inactivates toxins
• Dissolves substrate over time
• Dissolves necrotic tissue over time
• Flushes & Floats out Debris
• Lubricates Canal

34
Q

NaOCl replinishment

A

NaOCl degrades rapidly to NaCl (salt water) in the canal, therefore must be replenished @ 3-5 min.

35
Q

Typical case requires about _____cc. of NaOCl as irrigant per visit*

A

Typical case requires about 10-12
cc. of NaOCl
as irrigant per visit*

36
Q

NaOCl must be in contact with shaped
canal a minimum of _______ after canal enlarged to #30 or larger.*

A

NaOCl must be in contact with shaped canal a minimum of 30 minutes after canal enlarged to #30 or larger.*

37
Q

A canal smaller than #30

A

A canal smaller than #30 will seldom if ever allow any irrigant to reach the apical 1/3
of the canal

38
Q

Intracanal Medications

A

Medications placed within the canal system between appointments. Intended to increase local anti- microbial action and to further decrease the microbial challenge within the RC
system.
we use CaOH

39
Q

previous intracanal meds

A

Historically, many harsh medicaments were used which were
toxic and damaging to healthy tissue. Some are now recognized
as carcinogenic. These formulations are no longer acceptable for
use (e.g. CMCP, Formocresol, Cresatin, Beachwood Creosote, etc.)

40
Q

new intracanal med, benefits?

A

CaOH: near universal acceptance as the intracanal medication of choice (esp. in necrotic cases)
- pH between 11 and 12- Discourages most microbial growth
- Long lasting (effective over extended periods)- No reported allergic responses
- Easy to apply & remove as a paste
- Available in clinic as “Ultracal”

41
Q

Use of antibiotics to
relieve pain:

A

useless

42
Q

SYSTEMIC Antibiotics are USEFUL ONLY IN

A

ACUTE PA INFECTIONS (Swelling & Fever) or for a patient who is immunologically supressed.

43
Q

Healthy patients without systemic signs and symptoms of infection but with symptomatic pulpitis, symptomatic apical periodontitis, a draining sinus tract, or localized swelling do or do not require antibiotics?

A

DO NOT, just creating resistance

44
Q

when to use antibiotics in endo

A

In conjunction with definitive procedures to debride and drain
Persistent or spreading infection
Systemic involvement w temperature of 100+
Medically compromised
Pre-med when indicated

45
Q

would antibiotics be used with cellulitis

A

yes, there is no drainage occuring, generalized swelling

46
Q

infection with sinus tract, antibiotics?

A

no there is a path of drainage

47
Q

• Endodontic infections may be classified according to:

A

• Endodontic infections may be classified according to Location, Symptoms (Acute or Chronic), degree of Virulence or Organization (localized or diffuse & spreading).

48
Q

locations of endo infections

A

• LOCATION:
– Intraradicular – Extraradicular
• Intraradicular is caused by bugs colonizing within the RCS
• Extraradicular infection is usually a sequel to untreated intraradicular infection. Characterized by microbial invasion of the periradicular tissues resulting in inflammation & infection. AAA or CAA

49
Q

Intraradicular Infections: 3 subclasses

A
  1. primary infections: caused by bugs that initially invade and colonize necrotic pulp tissue within the RCS.
  2. secondary infection caused by bugs not present in the primary infection but introduced into the RCS sometime following professional intervention (secondary to professional intervention; iatrogenic by definition)
    Example of a 2ndary infection is when symptoms arise in a previously ASYMPTOMATIC infected tooth if operator allowed R. Dam leakage or placed leaky temporary.
  3. persistent infection caused by bugs that were members of a primary or secondary infection and in some way , resisted intracanal antimicrobial procedures and were able to endure periods of nutrient deprivation within the RCS. (i.e.) FAILURE OF RCT TO HEAL
50
Q

Bacterial Virulence Factors

A

• The ability to form BIO has been regarded as a virulence factor. Neighboring cells of different species can produce enzymes such as: B-Lactamase, Catalase and proteinases that are retained in the biofilm matrix and can protect other bacteria against antibiotics and host defenses

• Gram – anaerobes) can cause direct tissue damage & osseous breakdown by releasing various bacterial products

51
Q

bacterial products contributing to virulence

A

• Gram – anaerobes) can cause direct tissue damage & osseous breakdown by releasing:
– Enzymes (collagenase, chondroitinase and hyaluronidase)
– Endotoxins toxic substances associated with the outer cell walls that are released upon destruction of cell walls and exotoxins
– Lipo polysaccharide (LPS)-an endo toxin in cell wall of G- bugs
– Peptides/amino acids

52
Q

• Staphylococcus Aureus (aka) S. Pyogenes infections, why bad?

A

(Gram +) can cause serious suppurative infections:
– This bug is thought to produce penicillinase, a B lactamase that has the potential to render Penicillin ineffective*
– Rx Augmentin = Amoxicillin + Clavulanic acid (inhibits penicillinase)

53
Q

If bacteria from the infected pulp tissue gain entry into the periradicular tissue and the immune system is unable to suppress the invasion what happens?

A

an otherwise healthy patient eventually shows signs and symptoms of an acute periradicular abscess, cellulitis, or both.
Clinically, the patient experiences swelling, fever and mild to severe pain.

54
Q

what determines the spread of swelling, possible results?

A

Depending on the relationship of the apices of the involved tooth to the muscular attachments, virulence factors and host resistence ,the swelling may be localized to the vestibule or may extend into a fascial space (cellulitis).

55
Q

cellulitis systemic manifestations?
tooth tests?

A

systemic manifestations: fever, chills, lymphadenopathy, headache, and nausea.

Because the reaction to the infection may occur very quickly, the involved tooth may or may not show radiographic evidence of a widened periodontal ligament space.

most cases the tooth elicits a positive response to percussion

periradicular area is tender to palpation. This is a serious (critical Infection) in fascial plane

56
Q

mm attachment relations to lesions?

A

Muscle Attachments are important in relation to where the lesion “points.” If lesion exits coronal to muscle attachment, it is generally on attached gingiva or alveolar mucosa and we have a localized abscess, which is MORE EASILY TREATED (No Systemic Involvement)

57
Q

Development of Critical Infections

A

• Fascial spaces are potential anatomic areas that exist between the fascia and underlying organs and other tissues. During an infection, these spaces are formed as a result of the spread of purulent exudate.

58
Q

what determines the spread of odontogenic infection into fasical spaces

A

The spread of infections of odontogenic origin into the fascial spaces of the head and neck is determined by the location of the root end of the involved tooth in relation to its overlying buccal or lingual cortical plate and the relationship of the apex to the attachment of a muscle.

59
Q

example of fasical spread using a mandibular molar with apices towards lingual plate above the mylohyoid

A

For example, if the source of the infection is a mandibular molar and the apices of the molar lie closer to the lingual cortical plate and above the attachment of the mylohyoid muscle of the floor of the mouth, the purulent exudate breaks through the lingual cortical plate into the sublingual space. If the apices lie below (or apical) to the attachment of the mylohyoid muscle, the infection spreads into the submandibular space.

• These infections have the potential to be lethal if not treated aggressively

60
Q

how should fasical infections (cellulitis) be treated

A

These infections have the potential to be lethal if not treated aggressively with incision and drainage

61
Q

anatomy of fascial spread

A
62
Q

what teeth should we be vigilant with

A

Be especially vigilant with infections of mandibular molars (especially 2nd & 3rd Molars) when cellulitis occurs in the submandibular space with swallowing difficulty

WHY 2nd & 3rd Molars?
Access from S-M space to Sublingual and Submental spaces ; All 3 are called (Ludwig’s Angina) and infection in these spaces can be Life Threatening*

endo (22 decks)

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