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
