Pulp Micro Flashcards
Primary cause of endo disease.
Bacteria
Primary source of bacteria.
Caries
Dentinal tubule density increases or decreases as you get closer to the pulp?
Increases
Size of the dentinal tubules increase or decrease as you get closer to the pulp?
Increases
These do not have to penetrate the pulp chamber for bacteria to enter.
Caries
Irreversible pulpitis occurred when the bacteria were within how many millimeters of the pulp?
0.5 mm
Little pathosis is seen how many mm from the pulp?
> 1.2
Dentin formed during development and eruption.
Primary
Dentin formed after tooth formation is complete.
Secondary
Formed by external influences, like caries or attrition.
Tertiary/Irritation
A tertiary dentin secreted by odontoblasts and have more regular tubules.
Reactionary
A tertiary dentin secreted by odontoblast-like cells after death of odontoblasts.
Much stronger stimuli than reactionary.
Can be irregular and atubular.
Reparative
Removes the smear layer to expose dentinal tubules.
Acid etch.
Are always colonized by bacterial biofilms.
Cracks
There’s no break in the DEJ yet, but there’s already inflammation occurring in the pulp.
Enamel fissures.
Developmental anomalies that can lead to bacteria getting into the pulp.
Developmental groove
Dens in dente
Dens evaginatus
Periodontal pathogens pass thru lateral canals or the apical foramen to cause pulpitis.
Retrograde pulpitis.
Removal of cementum/dentin, and exposes dentinal tubules and can sever a lateral canal.
Root planing.
Microorganisms in the blood or lymph go to areas of inflammation where they can cause an infection.
Will not cause pulpal necrosis.
Anachoresis
Need this in order to have a LEO.
Pulpal necrosis.
What are the following: Pili Capsules extracellular vesicles Enzymes LPS LTA
Bacterial virulence factors.
Polysaccharide layer outside the cell envelope. Helps avoid phagocytosis.
Capsules
Contain enzymes and toxic chemicals involved in:
Hemagglutination Hemolysis Bacterial adhesion proteolytics activities Neutralizing antibodies.
Bacterial extracellular vesicles.
Virulence factors that neutralize immunoglobulins and complement components.
Proteases
Made by gram (-) bacteria, agonist of TLR4, causes fever, BP changes, and inflammation.
LPS
Components of LPS.
Lipid A core
Core polysaccharide
O-antigen
Virulence factor made by gram (+) bacteria; agonist of TLR2
LTA (Lipotechoic acid)
Bacteria with a thin peptidoglycan wall and stain pink (don’t retain the crystal violet).
Gram Negative
Have more bacteria than secondary endo infections, and are a polymicrobial infection dominated by gram negative, obligate anaerobes
Primary endo infections
This region of the root canal has lower oxygen tension, nutrients from the periapical area, lower bacterial number, and less accessible to treatment.
Apical
These bacteria predominate early in the primary endo infection.
Gram + facultative anaerobes.
What’s the most dominant bacteria in primary infection?
Gram negative obligate anaerobes.
Bacteria in primary endo infections that remain AFTER chemomechanical preparation (Root Canal).
Gram + facultative anaerobes.
Reinfection of a RCT tooth is called this.
Secondary endo infection
Predominant bacteria in secondary endo infections.
Gram + facultative anaerobes.
Most recovered bacterial species in secondary endo infection.
Enterococcus faecalis.
Most common fungus in secondary endo infections.
Candida
Survival methods of this bacterium:
- Invade dentinal tubules
- Resists Ca(OH)2 by using a proton pump.
- Forms biofilms.
- Can enter VIABLE BUT NON-CULTURABLE STATE, so the doctors can’t grow it in the lab.
E. faecalis
Components of biofilm.
1) 15% bacterial cells in microcolonies.
2) 85% Extracellular Polymeric Substance (polysaccharide)
Communication to coordinate gene expression
Quorum sensing.
These are 100-1,000 times more resistant to antibiotics.
Biofilms
What do you put the gutta percha in for 1-2 minutes AFTER cutting it with the gauging cutter?
NaOCl
This antibiotic must be given with another antibiotic.
Metronidazole
Antibiotic of choice for endo infections bc it’s low-spectrum, efficient, low toxicity, and low cost.
Pen VK
Augmentin kills 100% of bacteria. So why not use it for endo infections?
Colitis- will kill all the normal flora in the gut.
Components of the Adaptive/Specific immunity.
B and T cells
Immune cells of the pulp
APC’s
T cells
B cells
Mast cells
Pulp immune cells only present during inflammation.
B cells and Mast cells
APC’s present bacteria that they’ve phagocytosed in the pulp to the T cells via MHC Class I (Killer T cells) and MHC Class II (Helper T cells).
Cytokines are released to cause inflammation and increase vascular permeability
Pulpal Response
Substances released in a pulpal response that cause vasodilation.
CGRP, Substance P, NKA
Increase in interstitial pressure during pulpal inflammation would spread down the canal and “strangle” the entering blood vessels, leading to necrosis.
This DOES NOT occur.
Pulp Strangulation Theory
How is the periapical response different from the pulpal response in an endo infection?
Activation of osteoclasts.
How are osteoclasts activated?
Cytokines are released that cause osteoblasts to make RANKL.
These make RANKL.
Osteoblasts.
Bind RANK to activate osteoclasts.
RANKL.
Binds RANKL to prevent activation.
Osteoprotegrin
Inflammatory cells found in the periapical lesion of an endo infection.
- Macrophages Dominate
- Lymphocytes (T cells > B cells).
- Plasma cells
- Neutrophils
Predominant inflammatory cell found in the periapical lesion.
Macrophages
What do the Zones of Fish describe?
Areas of bone infection in a periapical lesion.
Zones of Fish in order are:
1) Zone of infection
2) Contamination
3) Irritation
4) Stimulation (stimulates osteoblasts to make RANKL).
No bacteria are found in this zone.
Contamination
Where healing STARTS when the nidus of infection is removed.
Zone of stimulation
Most common endo lesion
Granuloma
A ______ is not an area where bacteria live, but in which they’re destroyed.
granuloma
