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263 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
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induction
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what induces odontoblast formation
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enamel epithelium
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what induces enamel formation
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dentin and odontoblasts
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what synthesizes and secretes inorganic matrix and creates an environment that allows for mineralization of matrix
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pulp
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what type of dentin is formed prior to root end completion
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primary
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which dentin formation process is slower that continues over life of tooth and results in gradual decrease in size of pulp chamber
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secondary
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which odontoblasts produce secondary dentin?
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primary dentin
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what type of dentin forms in response to irritation or injury?
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tertiary dentin
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what type of dentin forms after mild irritation such as attrition, early caries, or shallow cavity prep?
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reactive dentin
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T/F: reactive dentin is continuous with seondary dentin
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T
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which odontoblasts forms reactive dentin
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primary dentin
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tertiary dentin formed after a more severe injury i.e. advanced caries, severe attrition, or deep cavity prep is called
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reparative dentin
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what type of dentin is atubular, poorly organized, and not continuous w/ secondary dentin
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reparative dentin
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what cells form reparative dentin?
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stem cells after primary odontoblasts have been destroyed
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T/F: reparative dentin is formed by primary odontoblasts
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F
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what are the 3 functions of pulp?
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1. nutrition 2. defense 3. sensory
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how is dentin formed when it's continuity is lost by events such as pulp exposure?
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through induction, differentiation, and migration of stem cells to exposure site
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T/F: pulp can ID foreign substances/toxins from bacteria in caries and cause an immune response
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T
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T/F: there are proprioceptors in the pulp
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F
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what is sensed when there is physiological stimulation in the tooth?
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pain
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fast/sharp pulp sensation through dentin and enamel is carried by what type of fibers?
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alpha (delta) myelinated fibers
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which nerve fibers are assoc w/ deep dull ache of chronic inflammation?
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unmyelinated C fibers
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what substances do odontoblasts secrete?
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collagen (mostly type I) an phosphophoryn
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what substances are involved in mineralization of dentin?
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phosphophoryn and hydroxyapatite
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what substance is unique in dentin?
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phosphophoryn
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where are stem cells densest in the pulp?
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core
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what is the most common type of cell in pulp?
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fibroblasts
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where are fibroblasts found in greatest numbers in the pulp?
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in the coronal pulp
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what are the functions of fibroblasts in the pulp/
|
maintain collagen and ground substances (give shape and form)
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what are the immune cells of the pulp/
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dendritic cells and macrophage
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what is the most prominent immune cell in the pulp?
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dendritic cell
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where are dendritic cells most dense?
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in odontoblastic layer and around blood vessels
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function of dendritic cells
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recognize variety of antigens and initiates immune response
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what are fixed macrophages called
|
histiocytes
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when do histiocytes become mobile?
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during inflammation
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what are the functions of macrophages?
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scavengers to remove dead cells and foreign bodies, and to process and present antigens to T memory cells
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largest vessels to enter apical foramen
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arterioles
|
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where does the exchange of nutrients and waste products take place?
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capillaries
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when do the extensive shunts b/w arterioles and venules become active?
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after pulp injury and during repair
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where do the venules drain after they exit the apical foramen?
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posteriorly to the max vein through pterygoid plexus or anteriorly to the facial vein
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what are the small, thin walled vessels that are in the periphery of the pulp?
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lymphatic
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where do the lymphatics drain?
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into regional lymph glands (submental, subman, or cervical) and empty into subclavian and int jugular
|
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T/F: capillary blood in the radicular portion of the tooth is 2x that of the coronal portion
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F: coronal is 2x radicular
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what allows for sizeable increases in local blood flow in cases of injury?
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the fact that only part of the vascular bed is perfuce at any one time
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what are the 2 phases of immune response in pulpal injury?
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1st - non-specific response which is rapid occurring w/in mins or hours
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what do mast cells in pulp do during inflammation?
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release histamin - cause vasodilation
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during inflammation, what is responsible for most of the vascular changes
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local nerves
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pathologic changes can occur in periradicular tissues as a consequence of what?
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pulpal inflammation and necrosis
|
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3 advantages the periradicular tissues have over pulp tissue
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1. more stem cells to participate in flammatory response and tissue repair 2. richer blood supply 3. more sophisticated lymph drainage system
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response to inflammation is regulated by what?
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1. nonspecific mediators of inflammation (neuropeptides, kinins, cytokines, etc) 2. specific immune responses (presence of IgE and mast cells)
|
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what is a "true" periapical lesion?
|
osseous lesion secondary to pulpal inflammation
|
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what are the 2 reasons that true PA lesions heal after therapy
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1. bacterial irritant is removed 2. defense environment is changed from pulpal space to PA tissues
|
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acute suppurative apical periodontitis
|
pheonix abscess
|
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T/F: an acute apical abscess can spontaneously drain and become chronic
|
T
|
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examples of acute periapical pathology
|
1. acute apical periodontitis 2. acute apical abscess (PA abscess) 3. phoenis abscess
|
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5 examples of chronic PA pathology
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1. chronic apical periodontitis 2. suppurative apical periodontitis 3. apical cyst 4. apical scar 5. condensing osteitis
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tender to percussion, palpation, or chewing are symptoms of what, with radiographic findings of no pathosis to a def lesion
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apical periodontitis
|
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T/F: apical periodontitis involves nonvital pulp
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F: vital and NV
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classic "swollen jaw" toothache is found in what?
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periapical abscess
|
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T/F: periapical abscess has slow onset
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F: sudden
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what is it if pt has pus, swelling, tender, mobile, fever w/ no radiographic pathosis or widened PDL
|
periapical abscess
|
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what is an acute exacerbation of a chronic lesion?
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phoenix abscess
|
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cause of phoenix abscess
|
virulent microorganisms
|
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if pt has pus, swelling, pain, tender, mobility, fever, w/ RL lesion, what is it?
|
phoenix abscess
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cause o suppurative apical periodontitis
|
virulent microorganisms
|
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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
|
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T/F: suppurative apical periodontitis is always a pulpal prob
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F: can be caused by base of periodontal pocket
|
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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
|
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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
|
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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
|
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antibiotic prophylaxis may prevent damage from a bacteremia at the time of tx is called
|
bacteremia
|
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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
|
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when areas of necrotic or inflamed tissue are exposed, what provides nutrition to the rapidly penetrating microbes?
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breakdown products of necrotic pulp, serous exudate, and bacterial byproducts
|
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T/F: direct exposure almost invariably causes tissue to undergo inflammation, necrosis, and become infected
|
T
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T/F: microorgs in subging biofilms assoc w/ periodontal disease reach the pulp very differently than the way that intracanal microorgs reach periodontium
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F: they're the same
|
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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
|
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what is it called when microorgs are transported in blood or lymph to an area of tissue damage and establish an infection
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anachoresis
|
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what is the most accurrate method to to detect and ID microorgs?
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polymerase chain reaction
|
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T/F: endodontic infections are polymicrobial
|
T
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T/F: population of organisms in contaminated root canals becomes increasingly aerobic over time
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F: anaerobic
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what type of microbes predominate in the initial phase of pulpal infection?
|
facultative anaerobes
|
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what type of microbes predominate over time in pulpal infection?
|
obligate anaerobes
|
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what are the percentages of types of microbes in teeth w/ carious exposure and PA lesions?
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68% strict anaerobes 26% facultative anaerobes 6% aerobes
|
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what are the most common microorganisms in primary endodontic infections
|
G- bacteria
|
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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
|
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T/F: G+ bacteria are never found in primary endodontic infections
|
F
|
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what are some genera of G+ bacteria consistently found in primary infections
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1. micromonas 2. peptostreptococcus 3. streptococcus 4. actinomyces
|
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T/F: Eukaryotic organisms are commonly found in primary endodontic infectinos
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F: rarely
|
|
inanimate particles that have no metabolism on their own
|
viruses
|
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why can't viruses survive in a root canal w/ necrotic pulp
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b/c thy require a viable host to infect and replicate
|
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viruses have been found in non-inflamed vital pulps of patients w/ which virus
|
HIV
|
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where have cytomegalovirus and epstein-barr been found?
|
apical periodontitis lesions
|
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other than the presence of particular species of orgs, what factors influence the development of symptoms?
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1. virulence among strains of same species 2. # of diff species 3. syergetic interactions among species 4. # of bacteria 5. host resistance
|
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what G+ bact if frequently found in RCT teeth w/ prevalence of 30-90% of cases/
|
E. faecalis
|
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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
|
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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
|
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which orgs have attributes that may allow them to survive in root canal treated teeth?
|
E. faecalis and C. albicans
|
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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?
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1. bacterial products 2. capsules and fimbre 3. cell wall components 4. host response
|
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what bacterial virulence factor is in G- cell wall?
|
endotoxin
|
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what bacterial virulence factors are in G+ cell wall?
|
peptidoglycans and lipoteichoic acid
|
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how can an intracanal infection cause apical periodontitis?
|
bacteria can escape through lateral and apical foramina and cause inflammatory changes to take place
|
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goal of endodontic therapy
|
prevent development of apical periodontitis or create conditions for periapical healing
|
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T/F: rubber dam is strongly suggested
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F: rubber dam is mandatory
|
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T/F: NaOCl full strength is bactericidal and breaks down tissue
|
T
|
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what irrigant can be somewhat effective in killing bacteria but does not dissolve oraganic tissue
|
chlorohexidine
|
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what irrigant does not dissolve tissue or kill bacteria
|
sterile water or saline
|
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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)
|
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what irrigants ahve questionable clinical value, resistance to tetracycline is not uncommon in bacteria isolated from root canals
|
antibiotic solutions
|
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what is the primary and most reliable method to sterilize instruments
|
autoclave
|
|
what type of instruments will corrode
|
carbon steel
|
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what component of ZOE based sealers ahve antimicrobial properties
|
eugenol
|
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when is metronidazole used as antibiotic therapy
|
if infections goes into fascial plane/bone, it has good antibiotic coverage
|
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odontogenic tooth-aches are derived from what 2 sources
|
pulp-dentin complex and periradicular tissues
|
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what fibers detect pain in pulp
|
c-fiber nociceptors (no proprioceptive info)
|
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pulp pain is a result of what
|
damage sensitization and decreased thresholds
|
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which source does poorly localizable, dull, aching, throbbing pain come from
|
pulp/dentin complex
|
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periradicular tissues have numerous mechanoreceptors that are most dense where?
|
PDL
|
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which source does pain in graded response and is localizable w/ proportional disconfort come from
|
periradicular tissues
|
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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
|
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if benign RL lesions are asymptomatic and frequently non-painful, how do they pulp in a pulp test?
|
vital
|
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which clinical tests do you perform to diagnose pulpal pain?
|
visual, transillum, biting pressure to assess indiv CUSPS, thermal pulp, EPT, anesthetic
|
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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
|
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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
|
|
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
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which antibiotics should be prescribed:
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penicillin (1st choice) or clindamycin
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what can alter pressure, flow and distribution of blood
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sympathetic fibers via precapillary sphincters
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sensory fibers release neuropeptides (substance P and CGRP) which do what?
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increase blood flow and capillary permeability
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process where one branch of a sensory nerve stimulated by injury causes release of peptides by another branch is?
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neurogenic inflammation
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which nerves provide principal sensory innervation to pulp tissue of max and mand teeth?
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V-2 and V-3
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where does pulp get sympathetic (motor) innervation?
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from T1 and to some extent T2 and C8 via superior cervical gang
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T/F: there is parasympathetic innervation of pulp
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F
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dentin sensitivity is due to what?
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sensory nerves w/in dentin tubules
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what are the 2 accepted explainations for peripheral dentin sensitivity
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1. hydrodynamic theory 2. some substances can diffuse through dentin and act directly on pulp
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local anesthetics w/ vasoconstrictor do what to pulpal blood flow
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reduce it to less than 1/2 normal rate
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what dentin thickness is usually sufficient to shield pulp from most forms of irritation
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1mm
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T/F: both diameter and density of dentinal tubules increase w/ cavity depth
|
T
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what is the most important characteristic of any restorative material
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ability to form a seal
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how have restorative resins improved and minimized microleakage?
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coefficient of thermal expansion approaches tooth, and more hydrophilic adhesive bonding systems
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what is the only restorative material in which marginal seal improves w/ time
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amalgam
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what is the main source of irritation of dental pulp
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microorgs in dental caries
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how do microorgs in caries affect pulp
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they produce toxins that penetrate tubules and enter pulp ahead of orgs
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what mediates the chronic inflammatory cells that respond to toxins that have infiltrated the pulp
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odontoblasts and dendritic cells
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the formation of tertiary dentin depends on what
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aggressiveness of carious lesion
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T/F: reactive dentin is similar in morphology to primary dentin
|
T
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T/F: mild caries results in death of odontoblasts
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F: causes odontoblasts to lay down reparative dentin
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as microorgs approach pulp, existing chronic infection becomes acute characterized by influx of what?
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acute inflammatory cells (mast cells and neutrophils)
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when does pulpal inflammation become irreversible
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when caries reach the reparative dentin
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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
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substance P, calcitonin gene related peptides, histamine
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factors influencing disease progression in the pulp
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1. virulence of bacteria 2. host resistance 3. blood flow 4. lymph drainage
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a tooth w/ normal pulp free of clinical symptoms, no rx signs of pathosis, and responds normally to testing is
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normal pulp
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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
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reversible pulpitis
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tx for reversible pulpitis
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removal of irritants and sealing and insulating exposed dentin
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severe inflammation, caused by deep caries, extensive oper procedures, impaired blood flow following trauma
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can be symptomatic w/ spontaneous and lingering pain or asym w/ no signs or symptoms
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tx for irreversible pulpitis
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RCT or extraction
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usually asymptomatic but may be assoc w/ episodes of spontaneous pain or pain on pressure
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cold, heat, and electric stimuli give no response...condition?
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tx for pulpal necrosis
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RCT
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tooth can be symptomatic or asymptomatic depending on ulp and periradicular conditions
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has had either partial or complete endo therapy...condition?
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tx for previously tx pulp
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completion of partial RCT or retreat, endo surgery, or extraction
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