3 - Etiology of Pulpal Disease Flashcards
what are pulpal irritants
living and non-living
examples of living pulapl irritatngs
bacteria, fungii, viruses
examples of non-living pulpal irritants
mechanical, thermal, and chemical
what are bacterial toxins
- endotoxin
- LPS
- exotoxin
what is an endotoxint
bacterial toxin part of bacteria
what is an exotoxin
bacterial toxin excreted by microorganism
are bacterial toxins very potent and cause cell damage
YES
what are microbial irritants
- bacterial proper
- microbial toxins (endo and exotoxins)
is direct pulp exposure a prerequisite for pulapl resonse and inflammation
NO
what are factors affecting pulapl response
- Virulence of bacteria
- Ability to release inflammatory fluids
- Host resistance
- Amount of circulation
- Lymph drainage
If bacterial invasion of pulp is severe sooner or later what happens
damage will become extensive and
spread throughout the pulp
___ can lead to an interruption of blood flow to the pulp
Inflammation
Inflammation can lead to an interruption of blood flow to the pulp, THE PULP THEN WILL BECOME
___
NECROTIC
one the pulp becomes necrotic, what is it colonized by ___
bacteria
Eventually bacterial byproducts and other irritants from necrotic tissue will diffuse from the ___ into the ___causing destruction of these tissues
canal; periapical tissues
what is the Kakehashi Study
- pulp exposure in conventional and germ free rats
- conventional rats developed pulpal and periradicular lesions
- germ free rats did not develop lesions
what is considered the most important study in endodontics
Kakehashi
what are mechanical irritants to the pulp
- operative procedures
- trauma
- ortho
- periodontal scaling
what removes cementum therefore exposing dentinal tubules resulting mechanical irritation to the pulp
periodontal scaling
what are chemical irritants to the pulp
- antibacterial agents
- acids
- acidic liners and bases
- temporary and permanent filling materials
what are steps lesion progression
- release of inflammatory mediators
- increased vascular permeability
- exudate formation
- increase in intrapulpal pressure
where does pressure increase occur? does it progress fast or slowly?
occurs in small compartmentalized regions
progresses slowly
does pain associated w/ inflammatory mediators lower the sensory nerve threshold
YES
T/F: pain associated w/ inflammation mediators effects vascular permeability resulting in DECREASED tissue pressure
FALSE! ELEVATED tissue pressure
does pressure associated w/ inflammatory mediators act directly on sensory nerve receptors
YES
describe the special environment of the pulp
- poor collateral circualtion
- pulp surrounded by hard unyielding walls
- area of terminal circulation
Among the various forms of dental treatment, ___ are the most common cause
of pulpal injury
restorative procedures
what are sources of bacteria in leaky restorations
- ingrowth from surface (open margins)
- bacteria in smear layer
- bacteria in deep dentin
Diameter and density of dentinal tubules [increases, decreases] in direct proportion to the depth of the cavity preparation
INCREASES
Usually ___mm of dentin thickness is needed to protect the pulp from most irritants
2
what is frictional heat
drastic increase in temp severely damages pulp
can frictional heat initiate inflammatory response
yes
can frictional heat desiccate dentinal tubules
yes
preps without coolant can reduce what
pulpal blood flow
how to prevent heat
- use high speed with EFFICIENT water coolant
- light pressure (use new burs so less pressure needed)
- intermittent cutting
what speed to use high speed at
100,000 - 250,000 RPM
preps without coolant can markedly reduce pulapl blood flow. why wouldn’t we want that
reduction of blood flow makes tooth necrotic
Use of rubber points at high-speed can increase pulp temperature by ___ degrees Celsius enough to cause pulpal damage
16
what is an outward movement of dentinal fluid if back pressure can dispace odontoblasts?
dentin dessication
prolonged air drying should be avoided to avoid what
dentin desiccation
Impressions or cementation of restorations can produce an outward movement of dentinal fluid. This is what type of force?
hydraulic forces
Research indicates ___ of
materials to be more important than their
___
physical properties; chemical composition
Evidence is that pulpal injury after restorations is
mainly caused by ___
bacterial microleakage
Bacteria will grow underneath a restoration only a in the presence of ___
microleakage
what are factors that affect microleakage
- Marginal adaptation of the material
- Shrinkage
- Contraction gaps
- Elastic deformation of tooth structure
T/F: In and of itself acid etchants DO appear to produce injury to the pulp
FALSE! it does NOT
how do acid etchants cause pulpal injury
- Buffering effect of dentin neutralizes acid
- Greatly increases dentin permeability
in tooth sensitivity after restoration placement, is discomfort usually a short or long duration?
SHORT
what to do to avoid sensitivity after restoration placement
check occlusion
persistent and increasing discomfort after restoration placement might be indicative of what? especially when?
indicative of irreversible pulp damage especially if there is spontaneous pain
spread of canal inflammation and/or infection occurs thru what
- apical foramen
- lateral canals
- dentinal tubules
periradicular pathosis can range from ___ to ___
slight inflammation to extensive tissue destruction
cellular damage occurs thru what
- release of non-specific inflammatory mediators
- specific immunologic mediators
in periradicular lesions, products released from ___ contribute to inflammatory process and cause swelling, pain, and tissue destruction
activated systems
what are inflammatory mediators found in PA lesions
- vasoactive amines
- bradykinin
- lysosomal enzymes
- complement fragments
- leukotrienes
- PROSTAGLANDINS
- CYTOKINES
what are vasoactive amines
hismatine, serotonin, etc.
what inflammatory mediators are shown to play important role on bone resorption
cytokines and prostaglandins
what are arachidonic acid metabolites
phospholipase A2
phosphalipase A2 results from what
- cycooxigenase
- lipooxygenase
cyclooxigenase results from what
- prostablandins
- prostacyclin
- thromboxane A2
lipooxygenase results from what
leukotrienes
arachidonic acid ->/<- phospholipase A2 pathway is inhibited by what
corticosteroids inhibit both pathways
what medication affects cyclooxigenase and inhibits prostaglandin, prostacyclin, and thromboxane A2?
Aspirin and NSAIDS
what medication inhibits prostaglandins
COX-2 inhibitors: clebrex
what medication inhibits leukotrienes
- some asthma meds
- some asthritis meds
what is an intense pain and/or swelling after a root canal procedure
flare up
pushing canal contents into periradicular lesions can create a type ___ reaction that could result in severe flare up
TYPE I
what are mechanical and chemical irritants
- over-instrumentation
- overfills gutta-percha and/or sealer
- irrigants
- medications
what results in endo damage
- severance of BV
- activation of coagulation pathways contribute to inflammation
- activation of kinin system and complement cascade
- vasoactive amines
- foreign body reactions
what causes endo damange
- endo irrigating solutions NaOCl (chlorox)
- intracanal medications
what are specific mediators
antigen/antibody
T/F: root canals are a pathway for sensitization
TRUE
what are immunologic responses
- antigen (bacteria and their products)
- B and lympohcytes and plasma cells
- antibodies and T lymphocytes
are are antigens of immunologic responses
- microorganisms
- microbial toxins
- altered pulp tissue
what are specific antibodies of immunologic responses
- immunoglobulins
- immunocompetent cells
- IgE and Mast cells
IgE and Mast Cells in PA lesions suggest what
type I immunologic response may occur
what are the elements needed for reactions to be present in human periradicular lesions
- antigens
- immuno-competent cells
- specific antibodies (immuno-globulins)
T/F: vaious types of immunologic reactions can start, amplify and perpetuate lesions
TRUE
how to prevent periradicular inflammation
- avoid pushing debris thru apex
- do not over-instrument
- do not overmedicate
- avoid pushing NaOCl thru apex
do periradicular lesions persist until causing agent is removed (bacteria in canals)
YES
how should canals be sealed to avoid recurrence of pariradicular lesions
hermetically sealed
if defense mechanisms are compromised, infection can spread where
spread into adjacent tissues
if defense mechanisms are compromised, is it potentiall grave and result in fatal consequences
yes
you should worry about the host response for what type of patients
immunocompromised patients
it is important to distinguish infection from what
inflammatory conditions
T/F: medications you give to the patient is more important that the local treatment done to patient
FALSE! what you do for the patient (local treatment) is more important than any medications you give the patient
is it possible for periraduclar tissues that have been destroyed to regenerate with original tissue after endo therapy? why?
YES! because irritating stimulus has been removed
what periradicular tissues that have been destroyed can be regenerated
- alveolar bone
- cementum
- periodontal ligament
can dentin regenerate? why?
NO! because odontoblasts originate in pulp
etiology of endodontic lesions is from what
microbes, microbial toxins and/or inflammatory mediators within root canal system
what is the first tissue to be destroyed by endo disease
PDL of periapical tissues
what is the last tissue to fully regenerate
PDL of periapical tissues
T/F: after successful RCT, all tissue CANNOT be restored to their original state except dentin
FALSE!
after sucessful RCT, all tissues CAN be restored to their original state except dentin
