MS2 - Endodontic Microbiology Flashcards
Are endodontic infections strictly associated with just bacteria?
Bacteria remain the major cause, but other microorganisms have been associated, such a fungi and viruses
Comment on the state of the dentine-pulp complex before and after being exposed to the oral cavity
the dentine-pulp complex is normally sterile and isolated from the oral microbiota, but if these protective layers are lost, the pulp will be exposed to the oral microbiota
Does dentinal exposure of bacteria (dentinal caries) represent a significant route of pulp infection?
as long as the pulp is vital, dentinal exposure does not represent a significant route of pulp infection. except when dentine thickness is considerably reduced and dentine permeability is significantly increased
in what way does the dentine permeability increase?
dentine tubules travel the entire width of dentine and have a conical formation
- smallest diameter near the enamel or cementum (0.9um)
- Largest diameter near the pulp (2.5um)
Does bacterial invasion through dentinal tubules occur more rapidly in a tooth a vital or non-vital pulp?
non-vital pulp
how does the vitality of the pulp affect the rate of caries progression through dentine?
if the vitality of the pulp is compromised, and the defence mechanisms are impaired, even a small number of bacteria may initiate pulpal infection
What are some causes of root canal exposure and/or infection? (4)
- caries (most common)
- dental trauma
- direct pulp exposure
- bacteria associated with perio propagating through dentinal tubules or apical/lateral ramifications
Can periodontal disease lead to an endodontic infection?
Yes
Microorganisms associated with perio can reach the pulp through dentinal tubules or through apical / lateral ramifications
(extra)
What is a Ramification in endodontics?
potential pathway through which bacteria can travel from a necrotic root canal to the PDL and cause disease and vice versa (from PDL to pulp - eg periodontitis)
Can rapid pulpal necrosis occur as a result of periodontal disease?
Only if the periodontal pocket reaches the apical foramen → due to irreversible damage to the main blood vessels that penetrate the apical foramen
What is that main goal of endodontic treatment that will get the best long-term success
Microbial reduction → eradicate bacteria colonisation or reduce the bacterial load to levels that permit periradicular tissue healing
** Bacteria have to reach a quorum of cells sufficient to cause disease (bacterial load) → before that threshold is reached, no signs and symptoms will be present
Approximately how much of a root canal is untouched after completing instrumentation?
A study found that around 60-80% of the total root canal length remained untouched by instrumentation → irrigation is very important
*What is the microbiological rationale of reinfection after endodontic treatment?
* Bacteria have to reach a quorum of cells sufficient to cause disease (bacterial load) → before that threshold is reached, no signs and symptoms will be present
- if the threshold is exceeded, infectious disease is established (apical periodontitis)
- if the treatment does not succeed in reducing bacteria levels below the threshold, the disease will persist
- Successful treatment is not to sterilise the root canal, but to reduce the bacterial populations to subcritical levels compatible with healing
In term of the microbiology in a root canal system, what deems a treatment successful?
Not necessarily making the root canal sterile, but reducing the bacterial populations to subcritical levels compatible with healing
What does the (fake) equation P=N.V.I. / R stand for
+which of these factors can we change?
Pathogenicity = Number of bacteria x Virulence x Interactions / Resistance
- the only factor that we can influence is number of bacteria
Are gram positive or gram negative bacteria more prone to resistance during RCT and what in an example of the bacteria?
Gram positive
E. faecalis
(can persist after rct and dressing)
Which type of bacteria is more prone to resistance during RCT, and what is an example of this type of bacteria?
Gram Positive bacteria
E. faecalis
What are the 4 basic dynamics of of pulp response from caries exposure?
How deep does bacteria travel before the. pulp responds?
the pulp responds by inflammation long before the bacterial products reach the pulp
Can you predict the time it will take a pulp exposed to bacteria to become necrotic?
No, its unpredictable
From the histological point-of-view, what represents the transition from reversible pulpitis to irreversible pulpitis?
The occurrence of focal necrosis (although of limited extension) associated with bacterial colonisation
i.e. small amt of necrosis
No matter what the route of bacterial access to the root canal is, what is a pre-requisite for estabilishing primary endodontic infections
necrosis of pulp tissue
T/F Occurence of apical perio is only dependent on how virulent the bacteria is
F, multifactorial disease that is a result of the interplay of many host and bacterial factors
(Extra)
Can you have periapical inbfection/inflammation without an infection in the pulp?
no
What is the possible cause of this lesion?
no caries or occlusal fracture / pulp exposure
trauma or perio causing bacterial invasion though lateral canals/dentinal tubules, causing pulp necrosis leading to apical periodontitis
(this case was trauma)
What may be the cause of these lesions?
large restorations and caries near the pulp - likely pulp necrosis due to the sequelae of bacterial pulp exposure leading to apical periodontitis
T/F Bacteria exists in periradicular bone (where you see PA RL) with apical perio
F, bacteria is inside the canals, apical perio is inflammation consequent to infection
also in abscess if it was there
Explain the spatial distribution of endodontic microbiota
- planktonic bacterial cells: suspended in fluid and enmeshed in necrotic pulp tissue in the main root canal → just irrigation can remove
- biofilms, only 5-10% of the bacteria (but the problem): sessile, multicellular microbial community (of microcolonies) enmeshed in self-produced matrix of extracellular polymeric substance (EPS - 85% of volume of biofilm), mostly comprised of polysaccharides but also proteins and nucelic acids → matrix protects bacteria. Biofilms can be:
- intracanal/radicular: only way to remove is through files
- extra-radicular
What are Planktonic bacterial cells (in brief) and how can these be removed from the root canal?
bacteria suspended in a fluid phase and enmeshed in necrotic pulp tissue
can be removed with irrigation
Why are biofilms difficult to treat and how should they be removed from the root canal?
They are cells that are enmeshed in a self-produced matrix of extracellular polymeric substance (EPS)
require mechanical and chemical disruption of the biofilm - filing and irrigation
how can endodontic infections be classified according to their anatomic location?
- Intraradicular infection
- Extraradicular infection
what is an intraradicular infection?
Infection caused by microorganisms colonising the root canal system
*What are the 3 categories of intraradicular infections and how are they categorised in this way?
categorised according to the time the microorganisms entered the root canal system
- Primary infection - caused by microorganisms that initially invade and colonise the necrotic pulp tissue (through dentine tubules, ramifications, exposed pulp etc)
- Secondary Infection - caused by microorganisms not present in the primary infection, but i_ntroduced in the root canal_ system some time after intervention (eg. leakage in temporary resto b/w appts, touching the files/gutta percha w gloved fingers)
- Persistent Infection - Caused by microorganisms that were members of the primary and secondary infection and r_esisted intracanal antimicrobia_l procedures and were able to endure periods of nutrient deprivation in treated canals (e.g. E. faecalis)
What is shown in these 2 examples?
e. g 1) persistent intraradicular infection - had apical perio, good tx provided, but no healing due to persistent bacteria
e. g. 2) persistent infection and late failure - bacterial load was reduced and good bone healing occured but bacteria remained (good short term success)
What is shown here?
primary Intraradicular infection
What is shown here?
Secondary intraradicular infection
How does the size of a periapical lesion relate to the diversity and bacterial load in the canal in primary intraadicular infection?
the larger the lesion, the greater diversity and density of bacteria in the canal
(directly proportional)
What type of bacteria are most prevalent in primary intraradicular infections?
Mixed community dominated by anaerobic bacteria, with diverse range of gram +ve and -ve
What bacteria are most commonly responsible for secondary or persistent intraradicular infections and why can they cause issues and which characteristics allow this?
Gram positive bacteria
Bacteria that resist intracanal procedures and are present at the time of obturation can influence the outcome of the endodontic tx - are a major cause of post-tx apical periodontitis
character: can be more resistant to antimicrobial treatment measures and have ability to adapt to harsh environmental conditions in instrumented and medicated root canals
(exceptions include some anaerobic rods - F.nucleatum, Prevotella)
When may effective complete chemo-mechanical preparation (CMP) be ineffective immediately post-op?
when there is extraradicular infection
What causes apical perio lesions vs extraradicular infection (e.g. most common - acute apical abscess)?
apical perio - formed in response to intraradicular infection and constitute an effective barrier (by immune system) against the spread of infection to alveolar bone and other body sites (bacteria NOT in apical perio lesion)
extraradicular infection - in specific circumstances, bacteria can overcome this defence barrier and establish extra-radicular infection
What is the most common form of extraradicular infection?
acute apical abscess
What are the forms of extraradicular infection that are dependant on intraradicular infection?
- acute apical abscess
- chronic apical abscess
- “wet canals” (persistent exudation)
What are the features of an extraradicular infection that is independent of the intraradicular infection and how can they be treated?
-Bacteria are outside the canal and are no longer fostered by the intraradicular infection
→ can persist even after the successful eradication of the intraradicular infection
- the bacteria travel through the dentine / cementum and establish themselves on the outer surface of the root (i.e. there is extra-radicular biofilm)
- the only treatment when this happens in apical surgery
What technology is available to perform a RCT
- EAL
- microscope
- thermoplastic obturation
- CBCT guided endodontics
- digital x-ray
- Sonendo (modern irrigation machine)
In irreversible pulpitis, where in the pulp is the majority of bacteria located? What about necrotic pulp? How does this effect how long the RCT takes?
irreversible pulpitis - pulp chamber or coronal-middle ⅓ of the root → can do single session
necrotic pulp - whole pulp infected
How will you know if extra-radicular infection is present?
if apical perio persists after thorough tx (i.e. when you know intra-rad infection is resolved)
