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260 Cards in this Set

  • Front
  • Back
dental pulp that is involved in initiation and formation of dentin and formation of enamel is what aspect of pulp function
induction
what induces odontoblast formation
enamel epithelium
what induces enamel formation
dentin and odontoblasts
what synthesizes and secretes inorganic matrix and creates an environment that allows for mineralization of matrix
pulp
what type of dentin is formed prior to root end completion
primary
which dentin formation process is slower that continues over life of tooth and results in gradual decrease in size of pulp chamber
secondary
which odontoblasts produce secondary dentin?
primary dentin
what type of dentin forms in response to irritation or injury?
tertiary dentin
what type of dentin forms after mild irritation such as attrition, early caries, or shallow cavity prep?
reactive dentin
T/F: reactive dentin is continuous with seondary dentin
T
which odontoblasts forms reactive dentin
primary dentin
tertiary dentin formed after a more severe injury i.e. advanced caries, severe attrition, or deep cavity prep is called
reparative dentin
what type of dentin is atubular, poorly organized, and not continuous w/ secondary dentin
reparative dentin
what cells form reparative dentin?
stem cells after primary odontoblasts have been destroyed
T/F: reparative dentin is formed by primary odontoblasts
F
what are the 3 functions of pulp?
1. nutrition 2. defense 3. sensory
how is dentin formed when it's continuity is lost by events such as pulp exposure?
through induction, differentiation, and migration of stem cells to exposure site
T/F: pulp can ID foreign substances/toxins from bacteria in caries and cause an immune response
T
T/F: there are proprioceptors in the pulp
F
what is sensed when there is physiological stimulation in the tooth?
pain
fast/sharp pulp sensation through dentin and enamel is carried by what type of fibers?
alpha (delta) myelinated fibers
which nerve fibers are assoc w/ deep dull ache of chronic inflammation?
unmyelinated C fibers
what substances do odontoblasts secrete?
collagen (mostly type I) an phosphophoryn
what substances are involved in mineralization of dentin?
phosphophoryn and hydroxyapatite
what substance is unique in dentin?
phosphophoryn
where are stem cells densest in the pulp?
core
what is the most common type of cell in pulp?
fibroblasts
where are fibroblasts found in greatest numbers in the pulp?
in the coronal pulp
what are the functions of fibroblasts in the pulp/
maintain collagen and ground substances (give shape and form)
what are the immune cells of the pulp/
dendritic cells and macrophage
what is the most prominent immune cell in the pulp?
dendritic cell
where are dendritic cells most dense?
in odontoblastic layer and around blood vessels
function of dendritic cells
recognize variety of antigens and initiates immune response
what are fixed macrophages called
histiocytes
when do histiocytes become mobile?
during inflammation
what are the functions of macrophages?
scavengers to remove dead cells and foreign bodies, and to process and present antigens to T memory cells
largest vessels to enter apical foramen
arterioles
where does the exchange of nutrients and waste products take place?
capillaries
when do the extensive shunts b/w arterioles and venules become active?
after pulp injury and during repair
where do the venules drain after they exit the apical foramen?
posteriorly to the max vein through pterygoid plexus or anteriorly to the facial vein
what are the small, thin walled vessels that are in the periphery of the pulp?
lymphatic
where do the lymphatics drain?
into regional lymph glands (submental, subman, or cervical) and empty into subclavian and int jugular
T/F: capillary blood in the radicular portion of the tooth is 2x that of the coronal portion
F: coronal is 2x radicular
what allows for sizeable increases in local blood flow in cases of injury?
the fact that only part of the vascular bed is perfuce at any one time
what are the 2 phases of immune response in pulpal injury?
1st - non-specific response which is rapid occurring w/in mins or hours, 2nd - slower more specific that includes prod of specific antibodies
what do mast cells in pulp do during inflammation?
release histamin - cause vasodilation
during inflammation, what is responsible for most of the vascular changes
local nerves
pathologic changes can occur in periradicular tissues as a consequence of what?
pulpal inflammation and necrosis
3 advantages the periradicular tissues have over pulp tissue
1. more stem cells to participate in flammatory response and tissue repair 2. richer blood supply 3. more sophisticated lymph drainage system
response to inflammation is regulated by what?
1. nonspecific mediators of inflammation (neuropeptides, kinins, cytokines, etc) 2. specific immune responses (presence of IgE and mast cells)
what is a "true" periapical lesion?
osseous lesion secondary to pulpal inflammation
what are the 2 reasons that true PA lesions heal after therapy
1. bacterial irritant is removed 2. defense environment is changed from pulpal space to PA tissues
acute suppurative apical periodontitis
pheonix abscess
T/F: an acute apical abscess can spontaneously drain and become chronic
T
examples of acute periapical pathology
1. acute apical periodontitis 2. acute apical abscess (PA abscess) 3. phoenis abscess
5 examples of chronic PA pathology
1. chronic apical periodontitis 2. suppurative apical periodontitis 3. apical cyst 4. apical scar 5. condensing osteitis
tender to percussion, palpation, or chewing are symptoms of what, with radiographic findings of no pathosis to a def lesion
apical periodontitis
T/F: apical periodontitis involves nonvital pulp
F: vital and NV
classic "swollen jaw" toothache is found in what?
periapical abscess
T/F: periapical abscess has slow onset
F: sudden
what is it if pt has pus, swelling, tender, mobile, fever w/ no radiographic pathosis or widened PDL
periapical abscess
what is an acute exacerbation of a chronic lesion?
phoenix abscess
cause of phoenix abscess
virulent microorganisms
if pt has pus, swelling, pain, tender, mobility, fever, w/ RL lesion, what is it?
phoenix abscess
cause o suppurative apical periodontitis
virulent microorganisms
if pt is asymptomatic, as sinus tract, and no response to EPT or thermal test w/ an apical RL, what is it?
suppurative apical periodontits
T/F: suppurative apical periodontitis is always a pulpal prob
F: can be caused by base of periodontal pocket
how does apical cyst form?
inflammation stimulates epithelial proliferation and forms cyst
sources of epi for apical cyst:
rests of mallassez, periodontal defects, sinus tracts, epithelium from max sinus
if pt is asymptomatic, is non-responsive to pulp tests and has lesion w/ well demarcated borders, what is it?
apical cyst
most apical cysts heal w/ what therapy?
RCT
T/F: apical scar is a pathologic lesion
F: NOT a pathologic lesion
what is an apical scar?
healing w/ fibrous tissue instead of bone
when does an apical scar occur?
when lingual and facial cortical plates are violated
low-grade relatively asymptomatic inflammation of periapical tissue
condensing osteitis
where is condensing osteitis often found?
posterior teeth of young people
how does condensing osteitis appear on radiograph
diffuse RO lesion around root apices
establishment of microbes in a host
colonization
degree of pathogenicity caused by microbes is referred to as
virulence
what does the Focal Infection Theory about pulpless and endo treated teeth say?
they leak bacteria into body and cause systemic diseases
how does infection spread
by local extension
antibiotic prophylaxis may prevent damage from a bacteremia at the time of tx is called
bacteremia
what did the kakehashi, stanley study show
w/ pulp exposures, germ free rats showed healing and conventional rats showed necrosis
what keeps pulp and dentin sterile and protected from oral microenvironment
enamel and cementum
what are the 4 main portals of entry for microorganisms?
1. dentinal tubules 2. direct pulpal exposure 3. periodontal disease 4. anachoresis
how do microorganisms enter dentinal tubules?
1. attrition 2. abrasion 3. gaps at CEJ 4. root planing 5. caries
why does dentin become more permeable nearer the pulp?
b/c there is an increase in diameter of tubules
most oral species of bacteria range from what sizes?
.2-.7 microns
when areas of necrotic or inflamed tissue are exposed, what provides nutrition to the rapidly penetrating microbes?
breakdown products of necrotic pulp, serous exudate, and bacterial byproducts
T/F: direct exposure almost invariably causes tissue to undergo inflammation, necrosis, and become infected
T
T/F: microorgs in subging biofilms assoc w/ periodontal disease reach the pulp very differently than the way that intracanal microorgs reach periodontium
F: they're the same
when does pulp necrosis as a result of periodontal disease occur?
only if the pocket reaches the apical foramen, leading to irreversible damage to bv's entering foramen
what is it called when microorgs are transported in blood or lymph to an area of tissue damage and establish an infection
anachoresis
what is the most accurrate method to to detect and ID microorgs?
polymerase chain reaction
T/F: endodontic infections are polymicrobial
T
T/F: population of organisms in contaminated root canals becomes increasingly aerobic over time
F: anaerobic
what type of microbes predominate in the initial phase of pulpal infection?
facultative anaerobes
what type of microbes predominate over time in pulpal infection?
obligate anaerobes
what are the percentages of types of microbes in teeth w/ carious exposure and PA lesions?
68% strict anaerobes 26% facultative anaerobes 6% aerobes
what are the most common microorganisms in primary endodontic infections
G- bacteria
what are some genera of G- bacteria that have been consistently found in primary infections
1. dialister 2. treponema 3. fusobacterium 4. porphyromonas 5. prevotella
T/F: G+ bacteria are never found in primary endodontic infections
F
what are some genera of G+ bacteria consistently found in primary infections
1. micromonas 2. peptostreptococcus 3. streptococcus 4. actinomyces
T/F: Eukaryotic organisms are commonly found in primary endodontic infectinos
F: rarely
inanimate particles that have no metabolism on their own
viruses
why can't viruses survive in a root canal w/ necrotic pulp
b/c thy require a viable host to infect and replicate
viruses have been found in non-inflamed vital pulps of patients w/ which virus
HIV
where have cytomegalovirus and epstein-barr been found?
apical periodontitis lesions
other than the presence of particular species of orgs, what factors influence the development of symptoms?
1. virulence among strains of same species 2. # of diff species 3. syergetic interactions among species 4. # of bacteria 5. host resistance
what G+ bact if frequently found in RCT teeth w/ prevalence of 30-90% of cases/
E. faecalis
what type of teeth are 9x more likely to harbor E. faecalis?
root canal treated teeth are 9x more likely than those w/ primary infections
are candida species more common in primary infection or persistent/secondary infection
only sporadically in primary, but found 3-18% of cases in persistent/secondary
which orgs have attributes that may allow them to survive in root canal treated teeth?
E. faecalis and C. albicans
what attributes help E. faecalis and C. albicans survive in RCT'd teeth
1. resistance to intra-canal medicaments 2. ability to form biofilms 3. ability to invade dentinal tubules 4. can endure long periods of nutrient deprivation
what are 4 bacterial virulence factors?
1. bacterial products 2. capsules and fimbre 3. cell wall components 4. host response
what bacterial virulence factor is in G- cell wall?
endotoxin
what bacterial virulence factors are in G+ cell wall?
peptidoglycans and lipoteichoic acid
how can an intracanal infection cause apical periodontitis?
bacteria can escape through lateral and apical foramina and cause inflammatory changes to take place
goal of endodontic therapy
prevent development of apical periodontitis or create conditions for periapical healing
T/F: rubber dam is strongly suggested
F: rubber dam is mandatory
T/F: NaOCl full strength is bactericidal and breaks down tissue
T
what irrigant can be somewhat effective in killing bacteria but does not dissolve oraganic tissue
chlorohexidine
what irrigant does not dissolve tissue or kill bacteria
sterile water or saline
what irrigants are effective in dissolving inorganic material and can be used to remove smear layer after cleaning and shaping is complete
chelating solutions (EDTA, citric acid)
what irrigants ahve questionable clinical value, resistance to tetracycline is not uncommon in bacteria isolated from root canals
antibiotic solutions
what is the primary and most reliable method to sterilize instruments
autoclave
what type of instruments will corrode
carbon steel
what component of ZOE based sealers ahve antimicrobial properties
eugenol
when is metronidazole used as antibiotic therapy
if infections goes into fascial plane/bone, it has good antibiotic coverage
odontogenic tooth-aches are derived from what 2 sources
pulp-dentin complex and periradicular tissues
what fibers detect pain in pulp
c-fiber nociceptors (no proprioceptive info)
pulp pain is a result of what
damage sensitization and decreased thresholds
which source does poorly localizable, dull, aching, throbbing pain come from
pulp/dentin complex
periradicular tissues have numerous mechanoreceptors that are most dense where?
PDL
which source does pain in graded response and is localizable w/ proportional disconfort come from
periradicular tissues
what is the ONLY reason for atypical sensitivity?
pulpal pathosis
periradicualr pathosis is mostly defined by what?
tenderness
what are some RL benign lesions?
PCD (cementoma), lateral periodontal cyst, traumatic bone cyst, stafne defect
if benign RL lesions are asymptomatic and frequently non-painful, how do they pulp in a pulp test?
vital
which clinical tests do you perform to diagnose pulpal pain?
visual, transillum, biting pressure to assess indiv CUSPS, thermal pulp, EPT, anesthetic
which clinical tests do you perform to diagnose periradicular pain?
visual, probing, mobility, palpation, bitng pressure to assess indiv TEETH, percussion, radiographs
if you find root resorption, what tests do you go to?
vitality (EPT) and thermal
which lesions are part of the RL odontogenic path lesions DD?
1. ameloblastoma (most common) 2. OKC 3. odontogenic myxoma 4. pindborg tumor 5. adenomatoid odontogenic tumor 6. dentigerous cyst 7. odontogenic origins of necrotic pulp space 8. (peri)radicular cyst large size 9. residual cyst after RCT
DD for non-odontogenic RL path lesions
1. giant cell granuloma 2. osteoblastoma 3. fibro-osseous lesions 4. central hemangioma 5. histiocytosis x 6. malignant neoplasm primary or metastatic
as unpleasnat and emotional experience assoc w/ actual or potential tissue damage
pain
orofacial pain DD if symptoms are acute and non-specific
1. headaches 2. ear aches 3. muscle aching 4. sinusitis
orofacial pain DD if symptoma and chronic and diffuse
Hx Red Flags, pt can't keep on topic, inconsistencies in pain characteristics or location, hx of numerous doctors
if pain is specifically termal induced, what is the only thing that can be responsible
pulp
characteristics of odontogenic dental pain
1. unilat 2. dill, aching, throbbing 3. reduced/elim by local anes 4. sensitivity to temp 5. tenderness to percussion or digital pressure 6. ability to reproduce CC during exam 7. etiologic factors evident
characteristics of non-odontogenic dental pain
1. no apparent etiology 2. bilat pain or mult teeth 3. shooting, stabbing, dull ache 4. no relief by local 5. chronic pain nonresponsive to dental tx 6. increased w/ palpation of trigger points or muscle 7. increased w/ emotional stress, exercise, head position
what explains referred pain w/in different branches of trigeminal nerve
lamination
what is the nucleus for nociceptive (pain) fiber arrangement for CN V
nucleus caudalis
what % of neurons in trigem nucleus caudalis show convergence of sensory input from several structures i.e. pulp and muslce
50%
what would explain referred pain between areas innervated by different nerves
convergence onto same second order neuron
T/F: the PDL is musculoskeletal and typically won't refer pain
T
the pulp is musculoskeletal and won't refer pain
F: pulp is visceral and can refer pain
is it more common to refer pain from or to the teeth?
from
what are some characteristic referral pattern of facial pain from 'deep' structures
1. doesn't cross midline 2. stays w/in same nerve 3. seldom occurs in anterior teeth 4. common in post teeth
T/F: anterior teeth refer to posterior teeth
F
where do anterior teeth refer pain?
frontal area/sinus
which anterior teeth refer pain that crosses midline?
mand incisors b/c mylohyoid and inf alveolar nerves cross midline
where do max canine and 1st PM refer pain?
to teeth in either arch, max 2nd PM or M, mand 1st or 2nd PMs, nasolabial area and lower orbit
where do max 1st M and 2nd PM refer pain?
to opposing teeth (mand 1M and PMs), max sinus, temporalis
where does long-term pain from max 1M and 2PM refer pain?
expand referral area to zygomatic and supraorbital areas
where do max 2 and 3M refer pain?
non-specially to area of opposing teeth, body of mandible, occasionally to ear
where does protracted max 2 and 3M pain go?
zygomatic and temporal areas (side of face)
where do mand PMs refer pain?
more posterior teeth in opposing arch, mental and mid-ramus areas
where does protracted mand PM pain go
spasm of muscles of face, head and neck
where do mand Ms refer pain
teeth in either arch (max 2nd PM and 1M, or forward to mand PMs), EAR, border an angle of mand
where does protracted pain from mand M go
max, headache of lower half of face and masseter stiffness/pain
key to diagnose suspected orofacial referred pain
duplicate pain of CC
T/F: intense non-odontogenic pain has higher probability to refer
T
localized muscle tenderness that is sore to palpation
myalgia
muscular hypersensitive areas w/ 'trigger points' that refer pain to adjacent structures
myofascial ain
what is primary muscle of mastication to refer pain
masseter
where does superficial upper masseter refer pain
max 2PM and Ms, maxilla
where does superficial lower masseter refer pain
mand 2PM and Ms, mand posterior to mental foramen
where does deep masseter refer pain
NO TEETH, orbit and supraorbital, body of mand, diffuse aching to side of face
where does ant part of temporalis refer pain
max inc (centrals and lats), supraorbital
where does middle part of temporalis refer pain
max canine, max 1PM, occipital
where does posterior part of temporalis refer pain
max 2PM, Ms, occipital
where does ant digastric refer pian
mand incisors
what is contraindicated when doing trigger point anesthetic injections for muscle pain therapy?
use of Epi or vasoconstrictors
what is the most common extraoral source of dental pain?
max sinus
where does sphenoid sinus refer pain
hard and soft palate, occipital and mastoid processes
how does max sinusitis pain present?
multiple max teeth involved, usually unilateral, possible season onset
severe shooting, lanciating, burning pain lasts seconds, requiring trigger point activation is ?
trigenimal neuralgia/tic douloureux
how can the trigger zone by activated in trigem neuralgia?
by light pressure, washing, shaving, brushing, chewing, talking, light wind
how does pre-trigem neuralgia present?
dull aching in a quadrant
where has cardiac pain been known to refer pain?
left mandible (10% of the time) or maxilla
examples of atypical pain disorders (neuropathy)
NICO, phantom tooth pain, traumatic/amputation neuroma, sympathetic dystrophy
neuropathies can have pain eliminated by?
local infiltration/anesthesia
which is more common in males, migraines or cluster headaches?
cluster headaches
how are cluster headaches different from migraines in symptoms?
clusters last 15min-2hrs but cluster in 1-8 per day
dull aching pain in jaws, temple and nek worsened by chewing and swallowing would describe symptoms of?
arteritis
female:male ratio for arteritis
4:1
most severe complication for arteritis
transient vision loss as predecessor to blindness
T/F: most orofacial pain is of odontogenic origin
T
guide questions for determining severity
1. prob disturb sleeping/eating/working? 2. how long has this been a problem? 3. have you taken any pain meds? effective?
pain that is referred or provoked by thermal stimuli, and poorly localized is likely to be ?
pulpal
pain that is well localized and occurs or is elevated on mastication or tooth contact is likely to be ?
periradicular
what should you look for on extraoral exam?
tender lymph nodes, swelling, redness, facial asymmetry
what should be the main goal for clinical exam?
replicate stimulus that causes pain
useful pulp tests
cold, heat, electrical, direct dentinal stimulation
useful periradicular tests
palpation, digital pressure, light percussion, selective biting, periodontal probing
what helps differentiate b/w dx that is primarily periodontic or endodontic in nature
perio probing
what is the diff b/w periodontal abscess and endo abscess
perio abscess has vital pulp tissue and will respond to pulp testing
for all cases w/ caries in irreversible pulpitis w/o symptomatic apical periodontitis what must be done first?
complete caries removal to determine restorability
tx for an emergency pt w/ irreversible pulpitis w/o symptomatic apical periodontitis
single rooted tooth-pulpectomy, molar where hemorrhage is controlled-pulpotomy, molar w/ continued bleeding-pulpotomy+pulpectomy in largest root
when doing a pulpotomy, what do you do after temporary is placed and rubber dam is removed
check to see if tooth is out of occlusion
T/F: antibiotics are necessary for pulpotomies
F
what tx is indicated for cases of irreversible pulpitis and tenderness to chewing, percussion
pulpectomy - and reducing occlusion is usually helpful
what would cause pain in cases of pulp necrosis?
periradicular inflammation from irritants coming from necrotic space
why, in some cases, is it hard to obtain profound anesthesia in teeth with necrotic pulp
there may be some residual vital tissue
why would there be pain in a case of pulp necrosis w/o swelling if pt has an abscess?
abscess is confined to bone and fluid pressure in confined space causes pain
tx for pulp necrosis w/o swelling
WL should be determined and complete pulpectomy performed, if GG prep done then put CaOH in enlarged canals
procedure for performing pulpectomy
1. take 25 to patency or estimated WL 2. if time, do GG prep and place CaOH in canals
are antibiotics indicated in teeth w/ pulp necrosis w/o swelling in healthy individuals
no
tx for pulp necrosis w/ localized swelling should focus on what
canal debridement and drainage
what do you do if abscess doesn't communicate w/ apical foramen so drainage cannot be obtained through tooth?
mucosal incision to permit drainage
when would antibiotics not be needed in pt w/ pulp necrosis and localized swelling
w/ good drainage w/o elevated temps or systemic signs
rapidly progressive and spreading swellings are referred to as
cellulitis
when should you prescribe analgesics
1. pt presents w/ severe pain 2. if severe post-op pain is anticipated 3. if pt suffers during procedure 4. if soft tissue involvement (swelling) is present
which analgesic w/o codeine should be prescribed for mild-moderate pain
ibuprofen, ketoprofen, darvocet
which analgesics w/ codeine could be prescribed for mild-moderate pain
tylenol #3 or hydrocodone 5mg
which analgesics should be prescribed for severe pain
tylox or percodan
which antibiotics should be prescribed:
penicillin (1st choice) or clindamycin
what can alter pressure, flow and distribution of blood
sympathetic fibers via precapillary sphincters
sensory fibers release neuropeptides (substance P and CGRP) which do what?
increase blood flow and capillary permeability
process where one branch of a sensory nerve stimulated by injury causes release of peptides by another branch is?
neurogenic inflammation
which nerves provide principal sensory innervation to pulp tissue of max and mand teeth?
V-2 and V-3
where does pulp get sympathetic (motor) innervation?
from T1 and to some extent T2 and C8 via superior cervical gang
T/F: there is parasympathetic innervation of pulp
F
dentin sensitivity is due to what?
sensory nerves w/in dentin tubules
what are the 2 accepted explainations for peripheral dentin sensitivity
1. hydrodynamic theory 2. some substances can diffuse through dentin and act directly on pulp
local anesthetics w/ vasoconstrictor do what to pulpal blood flow
reduce it to less than 1/2 normal rate
what dentin thickness is usually sufficient to shield pulp from most forms of irritation
1mm
T/F: both diameter and density of dentinal tubules increase w/ cavity depth
T
what is the most important characteristic of any restorative material
ability to form a seal
how have restorative resins improved and minimized microleakage?
coefficient of thermal expansion approaches tooth, and more hydrophilic adhesive bonding systems
what is the only restorative material in which marginal seal improves w/ time
amalgam
what is the main source of irritation of dental pulp
microorgs in dental caries
how do microorgs in caries affect pulp
they produce toxins that penetrate tubules and enter pulp ahead of orgs
what mediates the chronic inflammatory cells that respond to toxins that have infiltrated the pulp
odontoblasts and dendritic cells
the formation of tertiary dentin depends on what
aggressiveness of carious lesion
T/F: reactive dentin is similar in morphology to primary dentin
T
T/F: mild caries results in death of odontoblasts
F: causes odontoblasts to lay down reparative dentin
as microorgs approach pulp, existing chronic infection becomes acute characterized by influx of what?
acute inflammatory cells (mast cells and neutrophils)
when does pulpal inflammation become irreversible
when caries reach the reparative dentin
the release of what substances, in response to caries, effect vascular events like vasodilation and increased vasc permeability causing tissue pressure and can cause abscesses
substance P, calcitonin gene related peptides, histamine
factors influencing disease progression in the pulp
1. virulence of bacteria 2. host resistance 3. blood flow 4. lymph drainage
a tooth w/ normal pulp free of clinical symptoms, no rx signs of pathosis, and responds normally to testing is
normal pulp
pulp w/ mild inflammation of pulp tissue, caused by mild or short acting stimuli i.e. incipient caries, cervical erosion, most oper procedures, deep periodontal curettage
reversible pulpitis
tx for reversible pulpitis
removal of irritants and sealing and insulating exposed dentin
severe inflammation, caused by deep caries, extensive oper procedures, impaired blood flow following trauma, can be symptomatic w/ spontaneous and lingering pain or asym w/ no signs or symptoms
irreversible pulpitis
tx for irreversible pulpitis
RCT or extraction
usually asymptomatic but may be assoc w/ episodes of spontaneous pain or pain on pressure, cold, heat, and electric stimuli give no response...condition?
pulp necrosis
tx for pulpal necrosis
RCT
tooth can be symptomatic or asymptomatic depending on ulp and periradicular conditions, has had either partial or complete endo therapy...condition?
previously treated pulp
tx for previously tx pulp
completion of partial RCT or retreat, endo surgery, or extraction