4. Periapical Pathology Flashcards
• PS
○ Other inflam mediators that are involved in increasing pain sens in a patient when undergoing inflam [???]
○ Other peptides that are responsible for inc pain
§ Inflam mediators > chagne pain perception and inc the pain: PG, BD, hist, ST, nerve cofactors
§ If upregulated > multiple effects > inc patient’s pain perception > ____ sensitization
○ Not happening within the brain (that’s central)
§ Happening in the area where things are ataking ____
○ Inc in other inflam mediators besides the NP > causes increase in pain (not in every single situation, but some of the prolonged/longer standing inflammation
• CS ○ Inflam in one part of body for a \_\_\_\_ period of time ○ Signaling come from the \_\_\_\_ itself ○ Lowering of \_\_\_\_ > some of the pain we receive from nociceptors in area where inflam is taking place > perceived at a higher magnitude bc of central regualtion in the brain ○ Component of perception that's not coming from periphery, or local inflammation > coming from the brain! § Higher pain perception if this is occurring
peripheral
place
long
brain
pain threshold
Nociceptive Mechanism - Pulp Responses Clinical Summary
Healthy Pulp: hot, cold, or osmotic stimuli will elicit a mildly painful response when applied to exposed dentin (positive response; “+”, ”WNL”-within normal limits).
Inflamed Pulp: hot, cold, or osmotic stimuli, will evoke pain from the tooth when applied to exposed dentin even at levels ____ elsewhere. Stronger pain is thought to indicate a greater degree of ____ (positive response;“++”, “+++” -painful, very painful response).
Electrical (non- physiological) stimuli directly activate the ____.
innocuous
inflammation
nerve fibers
• Pain perceiption depending on normal pulp and pulpal diseases
• Changes in pulp based on the inflam > mediated by caries/bacteria/microbes (fungi, viruses, etc.)
• Difference bt healthy and inflamed
○ Healthy > cold response from adelta > normal ____ response
§ Brief and sharp response
§ Can also come from hot (very hot w/ a quick change in temp), or osm stimulus (dentin exposed in grinders), sweet, sour although the pulp is healthy
○ Inflamed
§ Reversible inflam (pulpitis)
□ Clinical test: response form the ____ fibers (reaction to cold, unless quick temp change with heat)
® Cold > painful response, but it’s more intense and ____ then the reaction to a normal pulp
◊ How to know > whether response is not normal > testing ____ teeth (maintain a baseline); if tooth next to it has RCT > pitfalls
◊ Would also last a little bit ____ (a second)
□ No ____/asympatomatic reversible pulpitis exists
® Would always experience ____
Exists in axium > it’s wrong
pain adelta sharper multiple longer symptomatic pain
§ Irreversible inflam (pulpitis)
□ ____ cannot tell when this happens!
® ____ pain, waking up in the middle of the night
□ Research > inflam only goes so deep inside a pulpal tissue > no means to show at what level inflam is in the pulp
® If we knew > drill and remove inflam portions
□ Clinical test: inc pain to the cold, and expect it to last ____ than a reversible pulpitis (“lingering pain”)
® Period of time can be different from one ____ to another
® Level of inflammation is ____ into the pulp
◊ Testing device for heat > ____ (sticks)
◊ Devices w a heat tip > defined temp
◊ Most accurate way: patient is not anesthetized > take a rubber dam > ____ one tooth and use hot water over the tooth
} Not a standard test > used in sit when not 100% sure which tooth is causing the pain
} Sometimes > difficult to get a response from a regular clinical test
– A lot of ____ (PFMs) > not sure which tooth is causing the pain
} ____ fibers are involved
® Patient can have a ____ response > first adelta in the periphery, then transmitted to central location where c fibers are firing
◊ Confusion > may not have biphasic response, and cold may alleviate the patient’s pain > diff scenarios depending on the ____, and where the inflam is located
® If pain on tooth > symptomatic irreversible pulpitis
◊ Or an asymptomatic irreversible pulpitis > massive decay on the tooth > pulp is open like size of PA
} Inflam in pulp based on decay that was there, even if patient didn’t feel it, and irreversible bc knowing that by taking out the decay and can’t do anything else but cleaning it out
clinically spontaneous longer patient deeper white gutta percha isolate crown C biphasic pain threshold
• Why does patient have more pain?
○ Healthy pulp rxn > not every patient has the same pain perception (pain thresholds vary)
§ May be next to the one that’s in more pain/lingering pain
• Cannot quantify pain to a certain degree
○ Personal opinions and subjective
• When pulp is not alive > ____ for EPT
○ Didn’t feel anything from that machine
○ If number is below the end number > patient ____ it and there’s innervation in the tooth
• Based on pain and lingering > asymptomatic irreversible pulpitis
○ Patient had no hx of pain thereby it’s asymptomatic
64/64
feels
“Is pulpitis always painful?”
Results:
(1) incidence of “painless pulpitis” about ____%.
(2) incidence is higher with greater ____.
Conclusion: Many teeth seem to progress to necrosis without ____.
Problem: current diagnostics is sometimes unpredictable when it comes to diagnosis of ____ teeth! - low grade pulpal inflammation
- caries pulp exposure
• [???] • If patient comes w/o symptoms/pain > doesn't mean that everything is \_\_\_\_ ○ Can suffer from pulpitis or necrosis • [???]
40 age pain asymptomatic okay
• Pain varies from patient to patient > cannot make a conclusion on where you label pulpal dx as reversible or irreversible based on ____ intensity, test results or a patient’s ____
○ Can show a few things:
§ Only impt sign of pulp inflam is previous ____ of pain > indicator that something was happening regarding pulpal inflam
□ Cannot tell whether it’s rev or irrev
§ History of night pain
□ May not have any clinical value
□ Say that spon pain is indication that something is irrev
® Regular physio conditions can create painful conditions in an irrev situation
• Last point
• Transition stage where pulp dies off > portions of pulp that are dead, and other portions that are only inflamed
○ Status of partial pulp/nec > only thing you can say that when a patient has had in course o fpulpal dx > if had pain > strongest pain they had was at the stage of ____
§ Pt comes to you and sits in chair > what’s my dental hx?
□ Tried to see a dentist (pain started on Friday, but couldn’t see over weekend)
□ Pain stopped on Monday
□ Strongest pain happened when pulp was partially ____, and then eventually > becomes completely necrotic > pain stops from that tooth
□ Dx may progressive
pain
history
history
partial pulp/necrosis
inflamed
The inflammatory process leading to necrosis occurs by compartments and it gradually migrates in the apical direction
• Pulpal dx happens in \_\_\_\_; starts coronally (closest to the irritation) and then it will move its way down the entire RC system of the pulp ○ Closest to the decay > inflam in the pulp, and if you go deeper > the pulp may be healthy ○ Initial stages of pulpal dx ○ W/ decay like this > can continue for a while § One area inflamed, other area healthy § Immune response is fighting the decay; and only at one point will bac overcome the immune response > faster when it enters the \_\_\_\_ > becomes necrotic and dies □ Following local inflammation > \_\_\_\_ (microabscesses in that compartment) > bac move in > pulp is dead > bac is inside the pulp and causing new inflam in an area adjacent to where they moved into the pulp
compartments
pulp space
abscess
The inflammatory process leading to necrosis occurs by compartments and it gradually migrates in the apical direction
• May be difficult to figure out at what point of pulpal disease we're at • Don't know where the \_\_\_\_ is bt rev and irrev pulpitis ○ \_\_\_\_ based on patients history of pain, dental hx, clinical tests and radiographs • After inflam is moving > pulp is becoming partially necrotic and inflamed > degenerative pulp > starting to die off and necrosis ○ Don't know to what level there is necrosis and to what level there is \_\_\_\_ • Will never be an situation where the entire pulpal tissues are the same \_\_\_\_ from coronal to apical ○ Can be degenerating from inflam to total pulp necorsis in a short time, or it may take a little bit longer ○ No \_\_\_\_ exists! § Depends on the \_\_\_\_ of bac, \_\_\_\_ bac and how strong your \_\_\_\_ is
cut-off educated inflammation situation timeline amount aggressive immune system
Endo disease - apical periodontitis
• [???] • Apical disease doesn't mean there is infection ○ Disease comes from infection inside the tooth ○ In the beginning > have dx start around the root tip > have \_\_\_\_ ○ Diff stages of PA disease § \_\_\_\_ only (no bacteria), to flow blown infection when the patient has an abscess (pus, necrosis, bacteria)
inflammation
inflam
Radiographic DD
Odonto vs. non-odonto origin
• Radiolucent lesions in the jaw ○ Odontogenic and non-odontogenic origins of lesions in the jaw ○ Not everything that's radiolucent in an arae of a root tip has to come from a \_\_\_\_ ○ Different things may happen
tooth
radiographic DD
\_\_\_\_ \_\_\_\_ \_\_\_\_ Apical Scar Surgical Defect Periodontal Disease Chronic suppurative osteomyelitis Periapical cemental dysplasia (osteolytic stage) Cementoblastoma (osteolytic stage) Cementifying and ossifying fibromas Odontogenic and nonodontogenic cysts Odontogenic and nonodontogenic tumors Malignant tumor
granuloma
radicular cyst
abscess
Jaw lesions
Twenty year study of Radiolucent Jaw Lesions N = 4,983 (met criteria) of 17,038 specimens
• 5000 out of 17000 histologic specimen was submitted to the pathologist ○ Recapping % for the grouping • \_\_\_\_% of what was found were tumors • ~75% of radiolucent lesions are \_\_\_\_ lesions
3
inflammatory
Non-odonto jaw tumors
____%
Odontogenic jaw tumors
____%
Non-neoplastic
____%
- 8
- 4
- 3
Non-neoplastic bone lesions
Central Giant Cell Granuloma: ____ and root resorbing lesion composed of ____ cells
Fibrous Dysplasia: normal bone and marrow replaced with ____ tissue = resulting weak bone prone to ____
Periapical Cemento- Osseoua Dysplasia: bone
replacement by ____ from fibroblast from ____
• Easy to mistake CGCG with an apical periodontitis ○ First step to say this may not be a regular AP > take x-ray, and take a \_\_\_\_ test (would expect it to be normal), and there wouldn't be a reason why there's a negative cold test (no decay, etc.) • Fibrous dysplasia ○ Signs in the patient's face • Osseous dysplasia ○ Middle aged AA women ○ Typical to see radiolucencies on >\_\_\_\_ tooth ○ Particularly \_\_\_\_ ○ Patient would feel a \_\_\_\_ response (not a change in the pulp, but it's more cementum produced from fibroblasts)
expanding
multi-nucleated
fibrous
expansion
cementum
PDL
cold
>1
mandibular incisors
cold
Developmental odonto cysts
____%
Inflammatory lesions
____%
• Most inflam lesions: \_\_\_\_, \_\_\_\_, \_\_\_\_
21.8
72.8
PA granuloma
radicular cyst
PA abscess
Pulpal necrosis - strangulation theory (NOT!)
• The pulp doesn't \_\_\_\_ all of a sudden • Used to believe that inflam in the pulp; bc it's enclosed > inflam means swelling, and that the pulp swells and cuts off its own \_\_\_\_ ○ Is not true!
die
blood supply
Pulpal necrosis - compartment theory
Progressive Breakdown
Inflammation -> microbial invasion in tissue compartment (infection) -> ____ -> local tissue necrosis -> inflammation starting in adjacent compartment…= vicious circle
* Carious-related necrosis * Decay, bacteria superficial > begin the inflammation * After a while > organisms overcome pulpal defense > vicious circle of \_\_\_\_ infection, superficiail inflam, now the bac will overcome the pulpal defense > move into one area of pulp after making \_\_\_\_ > necrotic > bacteir amoves in > new inflam next to the compartment where they killed the pulp locally > continues on until necrosis takes over the entire pulp
micro-abscess
superficial
micro-abscess
Pulpal Pathology - Pulpitis > Necrosis
strong inflam rxn + bacteria > microabscess > ____
confluent
Pulpal pathology
Vital Teeth
Pulpal Space Without ____ (sometimes superficially in ____)
Aim for Success: Keep ____
Necrotic Teeth (Pulp) Pulpal Space With \_\_\_\_ Aim for Success: \_\_\_\_
bacteria
pulp
sterility
bacteria
disinfect
Pulpal pathology
• IMPORTANT • Looking at difference at pulp that is "only inflamed" and is vital, and compared where the pulpal tissues are necrotic and dead • Infection is superficial where the decay is and inflam in the pulpal tissues ○ When have inflam disease in the pulp > and treating a patient for irrev pulpitis and the tx is to take the pulp out (pulpectomy) and place a filling int eh RC > when this is done in a patient w an irrev pulpitiis > bacteria are not really in the root canal at this point ○ The RCs are free of bacteria (there may be inflammation) § Most important thing to understand is that must prevent getting any \_\_\_\_ into the RC system while it's just inflammatory § Where might bac come from > from the \_\_\_\_ > make sure all the decay is taken out before working in the RC; it may also come from your RC \_\_\_\_ and placed into the patient's mouth following removal of decay § Must make sure that when treating a patient > make sure not picking up an infection, and in an irrev pulp > must work w aseptic conditions to not infect the RC Key to success to treat a patient w an irrev pulp: sterility of workplace, and do not introduce microbes into the RC that didn't have any before
bacteria
decay
instrument
Pulpal pathology
• Bacteria working way down in the RC when th epulp is dying > int stage of partial pulpitis or necrosis > bacteria is inside the pulp > up until point of total necrosis > when have total necrosis > negating trauma of blood supply, etc. > bacteria have infected the whole root canal system ○ Premise has changed > rather than to only work aseptically, when have pulp necrosis > infections are everywhere (bc bacteri ahave moved down into the root canal system and will enter the tubules and layers of biofilms within the RC walls) > must now \_\_\_\_ rather than to only work aseptically
disinfect
Pulpal pathology - periapex
- inflam mediators, immune cells w/ antigens, waste products
- endotoxins, bacteria
• Irrev pulpitis ○ \_\_\_\_ response ○ \_\_\_\_ and inflam mediators going into lymph drainage ○ Nothing massive - \_\_\_\_ only • Necoriss ○ \_\_\_\_ is being taken over ○ Infection - bacteria ○ Move down and kill the point
immune
endotoxins
inflam
pulp
Pulpal pathology - periapex
• At one point bac reaches the apex > tries to get out into the \_\_\_\_ tissues > what will happen > inflammation in the PDL > pulp necrosis (everything has died) > no \_\_\_\_ defense coming from inside the pulp > [???] • At first > not infeciton in the periradiuclar tissues in the same that dx would have to work its way in the pulp from superficial inflammation to pulp necrosis ○ Will try to do same thing in periradicualr tissues ○ Difference in the pulp being encased in the dentin, no other means of \_\_\_\_ supply and \_\_\_\_ defense ○ In periradiuclar tissues >w ill always have a blood supply where \_\_\_\_ repsonse is occurring • [???]
periradicular immune blood immune immune
Apical pathology
• Adaptive and innate immune response taking place in this area • B cells stim by IL > plasma cell > IgG; and IFNgamma > macrophages (first step of immune response) > IL1, 8 TNF > ICAM1, and PMN > LTB4/PG work on the macrophages • IMPORTANT: ○ Release of \_\_\_\_ and \_\_\_\_ § Responsible to trigger bone \_\_\_\_ in the periradiulcar areas
IL1b
TNFn
resorption
Inhibiting ____ and TNFβ “primary importance in mediating the resorptive activity in chronic human periapical lesions”
“…expression of pro-inflammatory cytokines IL-1α, IL-1β, and TNFα, with the capacity to induce ____…”
“Their coadministration had a ____ effect on RANKL expression…” (osteoblast inhibition)
IL1b
RANKL
RANKL
Bone resorption
• Macrophages > \_\_\_\_ • T cells > \_\_\_\_ • Activate pre-osteoclasts to mature \_\_\_\_ (ruffled borders) > bone resporption ○ What is seen on radiograph > radiolucent area > typical sign of an apical periodontitis
IL1B
TNFb
osteoclasts
Microbes cause apical periodontitis
Kakehashi 1965: Germ-free animals exhibited no PA destruction
Sundqvist 1976: confirmed the cause-and- effect relationship (>90% Anaerobes)
Möller 1981: only devitalized pulp that were infected could induced periradicular lesion
• People didn't know what the cause was, unless various researchers have proved that bac are truly responsible for causing the AP periodontitis • Kakeshashi ○ If have bacteria exposed to a vital pulp > will kill it and work its way \_\_\_\_ into the RCS causing inflam at the end of the root tip
down
• Sterile rats (notobiotic) > no infection, fed sterile food
• Had conventional rats (w bacteria, etc)
• Pulp exposures in both types of rats
• As soon as pulp exposure in a normal rat w bacteria in the mouth > pulp will become ____ > pulpitis and undergoes all stages > pulp ____ and apical periodontitis
• Drilled open the pulps of the germ-free rats > only thing seen was minimal ____ from the drilling, and after a period of time the OB created a ____ over the exposed pulp
○ No inflammation other than minimal from trauma
○ No necrosis/AP periodontitis
• 32 days after opening up
• Conventional > ____ and AP abscess
inflamed
necrosis
inflammation
dentinal bridge
necrosis
Significance for clinical treatment
• 60 single rooted teeth > took x-rays and can see there was apical perio on those rx • When apical perio > endodontic origin > clinical conclusion is that bc we see the apical perio > must've been pulp necrosis > infection of root canal system based on the studies we have seen • What happens when clean out root canal system that's infected > paper point in the tooth > bacterial growth on agar plate and can see its all infected • Treat the pt > clean out the root canal system ○ Just before they closed the roots, and placed the root filling > did another bacterial sample > ignored whatever the sample was giving them; right before they filled those root canals and sealed the tooth > and checkign if there was still inflam on the radiograph, or if AP perio has healed ○ Goal: when pt presents with apical perio > want to see resolve and normal bone fill in w a normal PDL § Can recover after successful endo therapy • Wanted to know > that infection causes the apical perio > wanted to see if you disinfect it will the apical perio go away > tested, and wrote if they still found infection and if none > 5 year recall: ○ Negative culture, they couldn't get bacteria anymore after the cleaning protocol; 94% of cases where negative culture before they filled, the apical perio had healed ○ On the other hand, when had a positive culture > 68% of those teeth showed no apical periodontitis ○ Try to disinfect RC system based on these statistics ○ [???] ○ Even with a negative culture > some still didn't heal § Why don't see 100%? And why when leaving bacteria > 2/3 still healed? WHY? □ When the body can cope with the \_\_\_\_ that's left there and it's not massive > it can heal the \_\_\_\_ ® Same concept as Wolf > can leave some bac behind when you seal a little bit of bacteria after a coronal filling □ Dealing with a certain microbial load > want to get below a \_\_\_\_ where the body can heal the irritation ○ [???] • Endodontic goal for a tooth with a pulpitis (pulp is vital, no AP perio): \_\_\_\_ that the patient develops an apical perio
bacterial
apical periodontitis
threshold
prevent
What is Apical Periodontitis?
Apical Periodontitis represents a local immune response to ____
infection
Apical periodontitis
Abscess - ____%
Granuloma - ____%
True cyst - ____%
Pocket (bay) cyst - ____%
• Have abscesses, granulomas and cysts • Usually AP perio is a \_\_\_\_ ○ A lot of \_\_\_\_ • Can develop into an abscess > bacteria get into the tissues (not only inflam) ○ Acute or chronic • Cysts ○ Differentiate cysts bt a pocket and true
12 73 9 6 granuloma bleeding
Periapical Granuloma
Most endodontic periapical lesions are ____ and not of ____ origin. This is supported by clinical studies, which have found that ca. 80% endodontic periradicular lesions ____ satisfactorily after proper root canal therapy.
inflammatory
infectious
heat
Granuloma versus Cyst
Lesions cannot be differentially diagnosed as either radicular cysts or apical granulomas based on ____ evidence alone.
A trend exists towards increased incidence of ____ among larger lesions.
* Cyst may have an \_\_\_\_ lining, empty space, \_\_\_\_ crystals inside a cyst * Larger apical perio > higher the likelihood it's a \_\_\_\_
radiographic cyst epithelial cholesterol cyst
Periapical cyst - development
ERM = Epithelial Remnants of ____
Cyst: a real or imagined lumen was lined with____
• Eptiehlail remantns of malesthais > starts to proliferate > gives \_\_\_\_ lining of cystic cavity
malassez
stratified squamous epithelium
epithelial
Cyst Formation Theories
Nutritional Deficiency Theory: Epithelial proliferation results in a mass that is too ____ for nutrients to reach its core, resulting in ____ necrosis ____.
Abscess Theory: Assumes ____ necrosis occurs first, and ____ is stimulated to encapsulate the infection.
Merging Epithelial Strands: As ____ strands continue to grow, they merge to form a three-dimensional ball mass, thereby trapping ____ tissue inside which degenerates and forms a cyst.
• NDT ○ The central portion of mass dies and becomes necrotic ○ Lined with epithelium • AT ○ Stims epithleium to encapsulate the infection ○ Doesn't start with epi • MES ○ Epi strands may grow and connect > 3D bone mass > traps CT inside > closes and forms a cyst
large
liquefaction
centrally
liquefaction
epithelium
epithelial
connective
Periapical cyst
True cyst
The cystic cavity is not attached to the ____.
Pocket/bay cyst
The cystic cavity is connected to the ____ and the ____.
Both cysts cannot be diagnosed ____.
• True cysts vs pocket/bay cyst ○ These are both radicular cysts > at the root of the tooth ○ Difference bt the two: § For the pocket/bay cyst: has been shown that these cysts have a connection to the root canal system inside the tooth □ (B) is still connected to the root canal system □ [???] □ AS long as you have a conenction of the cyst with the root canal system > the cyst is caused bc of something coming out of the \_\_\_\_ system; if being pushed out further into the area, or irritation happens somewhere else > if you clean the root canal base and the pocket/bay cyst may heal, a \_\_\_\_ is completely ignoring this (whatever stim'd it to become a cyst is untouched when you do the endo therapy) ® Explanation why some cases with an apical perio > achieve good disinfection > lower \_\_\_\_ inside RCS > you do not get rid of it > and \_\_\_\_ in healing the apical perio • Patient has no swelling or sinus tract (it's not a fistula) > \_\_\_\_, and depnding on the presence of pain > sympto or asympto apical perio ○ If patient shows signs of swlling and pus > not simply an inflma in this area anymore > \_\_\_\_ ○ If the patient has these and pain > \_\_\_\_
root apex
root apex
root canal
clinically
root canal true cyst microbial load fail apical perio abscess acute apical acbscess
ncidence of periapical cysts among all inflammatory periapical lesions
____ are approximately 15-20% of all endodontic periapical lesions.
• 15-20% are cysts ○ [???]
periapical cysts
Acute apical abscess
____, pus, ____, redness
____ !!!!!
____ may be necessary !!!
swelling
tenderness
symptomatic
incision and drainage
Chronic apical abscess
____
mostly ____
Tracing of sinus tract with ____ to localize origin of tract.
* If patient has a sinus tract > place gutta percha > trace the sinus tract to know where it's coming from > patient will also have an abscess, but these are non-symptomatic > bc of \_\_\_\_ occurring over the sinus tract * Infection in this area > that once caused pain, swelling, etc > but bc of the sinus tract > pain is released
sinus tract
asymptomatic
gutta-percha
drainage
