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Etiology of Pulpal Inflammation

60% of the final exam.


Pulpal inflammation: microbial, traumatic, iatrogenic (dentist caused) idiopathic (dont
know why it happened).
Juveniles, teeth develop from outside to inside, start with thin walls and large pulp, no
root tip, then slowly the walls become thicker and the pulp becomes narrower.
Prevention of pulpitis
First stage is reversible pulpitids, pulp can still go to healthy state if you remove caries.
Prophylaxis, hygien, fluoride application. Trauma prophylaxes in sports (mouth guard).
If pulpitis occurs for longer period of time, stimulant is not removed, it becomes
irreversible.
Early stage of irreversible pulptiis, means still vital and sterile tissue in root canal, but
some infection in coronal portion of pulp, in pulp chamber. Strategies to keep tooth vital
is pulpotomy, cutting off healthy tissue at orifice of root canal. Later stage continuously
bacterial front advances into root canals and the only way to treat the tooth is total
pulpectomy.
If no treatment is done, the tooth becomes totally infected and we have apical
radiolucecy, dark area around root tip on radiograph, body has rremoved bone, a
vulnerable tissue, body removes it and replaces bone by granulation tissue. We dont
have a lot of bacteria in apical granuloma, thick wall of immune competent cells that wall
off the body against the exit out of the root canal system.
Different causes for pulpal inflammation.
Microbial causes, mainly caries.
Tiniest gaps between dentin and filling are enough to allow bacteria to infect
Periodontitis, infection of periodontium.
Trauma: parafunction, deep overbite
Iatrogenic, dentist inflicted trauma. During cavity prep, without enough water coolant,
prep too close to pulp etc.
Idiopathic. Resorption, odontoblasts turn into dentinoclasts, eat away the walls of the
tooth, remove dentin and cavity in tooth appears on radiograph. Typically tissue coronal
to resporption is decrotic, and below it is still vital, because vital cells are removing
dentin. External resporption. Differentiate between internal and external resportpion,
can see contour of root canal as opposted to no contour (internal).
Waiting is not an option in internal resorption.
Neurogenic inflammation, initiated by sympathetic nerves. Atrophic effect on immune
cells, attract immune cells. May induce inflammation and pain without other stimulus.
Seemlilyg perfect tooth can still become inflamed. Stimulation of sympathetic nerve,
cuase recruetemtn of polymorphonuclear nucleocytes and dentritic cells, immune
compenetnt cells that are a link between bacteria nad lymph nodes. They are also
phagocytoes, double function in the immune system. Nerve fibers release substance P.

common dental procedures that cause pain cause substance P to be released from nerve
fibers that has important clinical sig, causes pain and inflammation as well.
Pulpal histology
See dentin and light layer is secondary dentin that odontoblasts have put down. Probably
a cavity opposed to inner surface of dentin, and odontoblast are lined on inside of the
tooth. Connective tissue has reticular and collagen fibers. Rest of pulp is gorund
ubsance, hyaluronic acid etc.
Pulp from tooth. Needs nutreitnsa nd oxygen, so there is blood supply. The
microcirculation is that three to four arterioles are right under odontoblasts, run from
apical to coronal direction, and venules are much higher than arterioles, more centrally
located, one main central venule important in inflammation, drains excess fluid and blood
out of the pulp, has protecteive function, same for lymphatic vessesl.
Inflammation. Pain heat redness and loss of function, main signs of inflammation.
Acute and chronic inflammation.
Trauma, an injury to living tissue caused by extrinsic agent. Surgical or caused by
accident.
Bacteria, rod shaped. Dentin wiall if you have infected tooth under fluorescent
microscolpe.
Necrosis. Localized death of living tissue. Pulp necrosis, indicates that dental pulp has
died, doenst react to sensitivity testing. If pus collects then its an abcess. Pulp abcess or
facial abcess in patient.
Perirediculaar space is part of periodontium. In periodontal abcess, through food
impaction, inflamed pocket with abcess. Rapid onset of pain etc. Pulp is vital.
Inflammation doenst have to do with root canal system. Acute periredicualr also rapid
onset but the pulp is pulpitic, already become necrotic. In vital pulp if you put cold stim
on tooth thats vital, cold stim goes away immedittley, with pulpitis, if you do cold
testing, pain will linger, for minutes tooth is still hurting from cold. No reaction, pulp
tissue is dead.
Chronic perirediucalr abcess, four kidns of abcesses. If no treatment is undertaine,
pulptiis exists for longer period of tiem. Situation becomes chornic, reaction to pulp
necrosis. Onset is gradua, in most cases dont know there is a lesion there.
Acute is a state of inflammation. Location of inflammation. Intrareducular, inside root
canal, and extra radicular. Also foreng body reactions like irrigating and rinsing root
canals then drying them with paper points. Paper point through apex, cellulose, in
periapical space will cause foreign body reaction.

Intraredicular infection, bacteria inside the root canal system. Bacteria contamination can
happen, microorganism reaching pulp space through breeches in pulp space. Bone level
has gone down, horizontal bone loss in distal area of tooth, crown margin doenst fit too
well. Interesting, not necessary for bacteria to reach pulp space, before bacteria enter
pulp, severe inflammation, bacteria shed parts of cell wall, lipopolsacc that can reach
pulp through dentinal tubules, initiate inflammation. Main source of contamination is
carious.
Carious is a slow lesion, chronic, takes time to reach the pulp. Protective mechanisms is
that axons of odontoblasts processes shed minerals trying to occlude the tubules, make
htem less permeable for fluids and bacteria. Posisiton of materials is one way to protect
pulp from invading microorganisms.
Longitudinal cross section through the tooth.
Dont obturate the tooth right away, use extra disinfecting agents, to disinfect dentin walls
and that takes some time. Bacteria to depth of 300 microns. Can be through and through
contamination.
Repair. Decreasing residual dentin thickness. Increasing pulp exposure. Point where
dentin becomes so thin, youve exposed the pulp and you can see the pulp tissue. In
shallow cavities, there is still about half a mm of dentin between pulp and the cavity.
Shallow deep and very deep. very deep is less then a quarter mm. tertiary secretion is
minimal in shallow cavities, survival rate is good. Maximum of reactionary dentin,
odontoblast try to produce a lot of tertiary detnin to get rid of the stimulus and to reduce
influx of bacteria or other substances through detnin. There is minimal reactionary dentin
in very deep cavities, only a few odontoblasts survive. On the verge of having an
exposed pulp. No survival of odontoblasts under lesion, no reactionary dentin. If the
pulp survive,s body recruties odontoblast like cells, line up along the dentin abnd become
new odontobpasts. Dentin that they rpoeduce is not as good as the dentin produced by
primary odontoblast, full of holes. Difference between reactionary dentin, still have live
odontoblasts and reparative that comes up after reqruitment of new cells. Reactionary
dentin is formed by surviving odontoblasts.
Cavity cut in cervical area of tooth. See that the odontoblasts have tried to crate thick
layer of tertiary dentin to create thicker dentin wall between the cavity and the
odontoblasts.
Tertiary dentin leads to calcification of the pulp. Cant see any root canal at on on xray.
Histologically still fine thin root canal but you cant treat it anymore. Complete
obliteration of root canals. Also, how long has the pulp been exposed, chance of survival
or if you can initiate root canal treatment. Partially necrotic after 8 days and completely
after 14 days. Size of pulp exposure is important, tiny opening then prognosis is better
than if its a huge opening where margin can be difficult to seal off. Cance of having
leaking spot in filling is much higher. Contamination, has there been saliva or infected
dnetin chips thorugh opening. Was pulp capping agent put without pressure or with.
MTA used mostly, and calcium hydroxide.

Outcome is infleucned by extent or amount of bacteria that have entered the rot canal.
Periapical tissue reflected by size of lesion. In a large lesion, infection has been more
severe.
Theory that hasnt been proven, anachoresis, through the genral blood stream. In sepsis,
bacteria in blood stream can be transprotedi ntoo tooth. some say no such thing.
Host defense. Metarterioles dilate. Because pulp is in hard tissue, no way it can swell. If
pulp is injured, no way it can swell, thats what maeks it so vulnerable.
Proteolytic enzymes cuase liquefied dead tissue causing pus.
When bacterial components enter root canal system first healthy periapex, assoon as there
is contact with pulp dentin interface, endotoxins and exotoxins released (part of cell wall)
secreted by microorganisms. Pulp becomes necrotic.
Diff between reversible and irreversible pulpitis. Important, decision to start treatment or
not. Pulpitis is still reversible if pain stimulus is momentary, as soon as you take the ocld
away and tooth is warm again, no pain. Rarely spontaneous pain and diagnosis is
reverisbile. In irreversible, ingering pain, spontaneous pain. Therapy in reversible is
restorative. Know the difference,s dont treat teeth with reversible pulpitis. Pain duration
is seconds vs minutes. Pulsating pain and irreversible pulpitis. Frequently radiating pain.
Provoked in reversible, spotnaous in irreversible.
Cleaning effect of instruments, remove both soft tissue and a layer of hard tissue of
dentin. Want to get rid of microbiologic, infection control through risning, and machine
root surface so its smooth and clean.
Shaping effect, means we open up the root canal so we can place needle into the canal
and flush out tissue. Shape to obturate

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