1: Pulpal and Periradicular Pathology Flashcards
(59 cards)
1
Q
tertiary dentine: each type formed by what kind of cells?
A
reactive: formed by pre-existing odontoblasts
reparative: formed by newly differentiated odontoblast like cells
2
Q
what are the 4 layers of the pulp? what do the inner 2 layers contain?
A
- odontoblast layer
- cell free zone (of weil)
- cell rich zone: fibroblasts, immune cells, undifferentiated mesenchymal cells
- pulp core: CT, blood vessels, nerve fibres, fibroblasts
3
Q
what are the cells of the pulp and what do they do?
A
progenitor cells: ability to form formative or defensive cells
formative cells: odontoblasts and fibroblasts
defensive cells: macrophages, lymphocytes, eosinophils, mast cells, plasma cells
4
Q
innervation of the pulp - sensory nerve supply: which nerve to which type of tooth?
A
general innervation: CN V
maxilla: all CN V2
mandible: CN V3
- premolars: mylohyoid nerve of CN V3
- molars: C2 and C3
5
Q
sensory nerves:
- myelinated a-delta and a-beta axons - stimulated by? result?
- unmyelinated c-axons: what type of pain results?
A
- stimulated by movement of dentinal fluid, resulting in a sharp pain
- dull, throbbing pain
6
Q
motor nerve supply to the pulp:
- activation results in?
- sympathetic motor nerve supply by what nerve?
A
- activation results in vasoconstriction, reduced pulpal blood flow
- superior cervical ganglion: T1, C8, T2
7
Q
what are the 3 causes of pulpal inflammation?
A
- micro-organisms: bacteria, viruses
- mechanical causes
- chemical causes
8
Q
microorganisms: what are the microbial irritants they produce?
pulp is infiltrated at the base of carious tubules by?
A
- toxins and by-products
- chronic inflammatory cells, macrophages, lymphocytes, plasma cells
9
Q
once pulp is exposed, it becomes infiltrated by ____ to form an _________ at the site of exposure.
A
- PMN (polymorphonuclear lymphocytes)
- area of liquefaction necrosis
10
Q
what are the two possibilities when pulp tissue is exposed?
A
- remain inflamed for a long time
- undergo necrosis slowly or rapidly
11
Q
pulp tissue inflammation/necrosis: depends on what factors? x5
A
- bacterial virulence
- inflammatory response
- host resistance
- amount of circulation
- lymphatic drainage
12
Q
mechanical factors of pulp damage: 3 main examples?
A
- traumatic accident
- iatrogenic damage during dental procedure: tooth prep, excessive orthodontics, sub-gingival scaling
- attrition/abrasion
13
Q
trauma to crown: 2 causes
A
- impact injury
- fracture of crown
- can result in pulpal exposure
14
Q
how does impact injury result in pulpal exposure?
A
- crown remains intact
- microcracks in enamel allow bacteria to reach pulp
- blood flow damaged
15
Q
chemical factors of pulp damage: examples?
A
- chemical erosion
- inappropriate use of acidic materials
16
Q
irritation of pulp results in?
what are the mediators?
A
- inflammatory response
- inflammatory mediators: histamine, bradykinin, arachidonic acid, neuropeptides (CGRP)
17
Q
immunological response: what are the immunocompetent cells and potential antigens?
A
immunocompetent cells:
- T & B lymphocytes
- macrophages
- dentritic cells (antigen presenting cells)
potential antigens:
- bacterial toxins
18
Q
lesion progression: how does it occur?
A
- increased tissue pressure
inability of pulp to expand
lack of collateral circulation - pulpal necrosis
- periradicular pathology
19
Q
what is the term referring to the inflammation of the pulp
A
pulpitis
20
Q
response of the pulp depends on? elaborate.
A
severity of the insult
- mild: reversible pulpitis
- severe/persistent: irreversible pulpitis
21
Q
classification of the status of the pulp: what are the 7 classifications?
A
- clinically normal pulp
- reversible pulpitis
- symptomatic irreversible pulpitis
- asymptomatic irreversible pulpitis
- necrosis
- previously treated
- previously initiated therapy
22
Q
normal pulp: how does it appear?
A
- symptom free
- responds to sensibility testing: response subsides when stimulus is removed
- histologically: no inflammatory change
23
Q
dentine sensitivity:
- pain occurs with? associated with?
- what kind of pain?
- what is the diagnosis when sensitivity is caused by a specific factor? what could the specific factors be?
A
- thermal, chemical, tactile or osmotic stimuli, associated with exposed dentine
- severe and sharp pain, does not linger when stimulus is removed
- reversible pulpitis. specific factors can be caries, fractures, recent restorations etc.
24
Q
reversible pulpitis:
symptoms?
causes?
A
- pain: short and sharp, not spontaneous
- stimulus: cold, sweet, sometimes hot
- no significant radiographic changes apically
- caries into dentine, fractures, restorative procedures, trauma
25
reversible pulpitis: treatment?
- conservative pulp therapy + removal of the cause and pathway of irritation
- consider diagnosis as provisional, review in 3 months
26
irreversible pulpitis
- occurs if?
- what kind of pain?
- sensibility tests?
- occurs if inflammatory process continues
- spontaneous pain, response to hot/cold lingers after stimulus is removed
- sensibility tests responsive
27
why is irreversible pulpitis difficult to diagnose?
- may confuse whether pain is from maxillary or mandibular arches at early stages
- tooth will not be TTP until periapical tissues are involved
- no periapical changes radiographically
28
irrerversible pulpitis: treatment?
- once pain is located to the correct tooth,
1. RCT: if tooth is restorable
2. extraction
29
advanced symptomatic irreversible pulpitis: symptoms and treatment?
symptoms:
- excrutiating pain
- moemntarily relieved by cold: pulp allodynia and hyperalgesic
- tooth often TTP
- reacts violently to heat
treatment:
- RCT
- pulpotomy
- extraction
30
odontopaste: what is it? what does it contain? what are its purposes?
- antibiotic: clindamycin hydrochloride
- anti-inflammatory: triamcinolone
- relieves pain until definitive root canal therapy can be carried out
31
pulp canal classification:
occurs in response to?
leads to?
RCT not necessary unless ___?
- trauma, irritants
- eventual obliteration of pulp space
- clinical signs of pulpal necrosis
32
internal resorption: inflammatory
- occurs at which point of pulp chamber?
- activation of what cells?
- symptoms? pulp becomes?
- perforation will show on?
- treatment?
- occurs at any point within pulp chamber or root canal
- activation of dentinoclasts within inflamed pulp tissue in contact with necrotic, infected coronal pulp tissue
- asymptomatic, pulp will become necrotic
- CBCT: cone beam computed tomography
- RCT, depending on extent
33
internal resorption: replacement
- how common?
- how does replacement occur?
- not due to ____?
- symptoms? what changes DO NOT usually occur?
- uncommon
- dentine is resorbed, replaced with bone-like hard tissue
- not due to presence of bacteria in pulp
- (asymptomatic), periapical changes do not occur
34
pulpal necrosis:
- breakdown of ___ which allows ____ to _____?
- caused by?
- pulpal tissue, bacteria, colonize root canal system
| - direct exposure, dentinal tubules, cracks in dentine/enamel
35
pulpal necrosis
- no collateral circulation results in?
- irrerversible pulpitis leads to?
- traumatic injury causes? why?
- collapse of venules and lymphatics under increased tissue pressure
- liquefaction necrosis
- ischaemic necrosis, due to the disruption of blood supply
36
pulpal necrosis: symptoms?
- usually asymptomatic, unless inflammation has progressed to periapical tissues
- no response to sensibility testing
37
previously treated: a clinical diagnostic category indicating what?
- indicates that the tooth has been endodontically treated and the canals obturated with root canal filling material
38
previously initiated therapy: indicates what?
tooth has been previously treated by partial endodontic therapy
- pulpotomy, pulpectomy
39
periradicular/periapical conditions - occur when? what is the inflammatory/immunological response?
- when microbes and by-products reach the peridradicular tissues
- resorption of surrounding bone, epithelial cells proliferate to form granuloma or cyst
40
normal periradicular tissue: how will they appear? (clinically and radiographically)
- non-sensitive to percussion and palpation testing
| - radiographically: tissues normal, lamina dura intact, uniform PDL space
41
symptomatic peri-apical periodontitis - causes?
inflammation of periradicular tissues
- bacterial toxis
- chemicals
- occlusal trauma
- RCT over instrumentation
- RCF beyond apex
42
what is the pulpal status for symptomatic perirapical periodontitis?
irreversibly inflamed
| necrotic
43
symptomatic periapical periodontitis: signs and symptoms?
- discomfort to biting/chewing
- sensitivity to percussion
- palpation may or may not produce a sensitive result
- sensibility testing will depend on whether pulp is irreversibly inflamed or necrotic
44
symptomatic periapical periodontitis: radiographically?
PDL appearance?
lamina dura?
PDL may appear normal
| lamina dura either intact, widened, or have a distinct radiolucency
45
symptomatic periapical periodontitis - treatment?
adjustment of occlusion
| removal of canal irritants and necrotic pulp
46
acute periapical abscess: causes?
bacteria progression into periradicular tissues, patient's immune response cannot defend against invasion
47
acute periapical abscess: signs and symptoms
- rapid onset
- PAIN: exquisitely tender to tooth
- pus formation
- mobility of tooth
- systemic involvement
- swelling: depending on location of apices and muscle attachments, can be localized or diffused
48
acute periapical abscess: radiographically?
PDL space may be normal, slightly widened, or demonstrate distinct radiolucency
49
acute periapical abscess: treatment?
drainage
RCT
extraction
50
asymptomatic periapical periodontitis
- occurs when?
- clinically?
- radiographically?
- occurs when bacterial products from necrotic or pulpless tooth slowly ingress the periradicular tissues
- mostly asymptomatic, percussion and palpation test produce non-sensitive response
- radiolucency around apex of tooth
51
chronic periapical abscess:
inflammatory reaction to?
characterized by?
- to pulpal infection and necrosis
| - characterized by gradual onset, little/no discomfort, intermittent discharge through an associated sinus tract
52
chronic periapical abscess:
clinically?
radiographically?
clinically: usually asymptomatic, percussion and palpation tests produce non-sensitive result
sensibility tests are non-responsive
radiographically: radiolucent area on bone
53
focal sclerosing osteomyelitis
- associated with what condition?
- tooth will have aetiological factor for?
- symptoms depend on?
- condensing osteitis: periapical inflammatory disease, resulting in more bone production than bone destruction in affected area
- low-grade, chronic inflammation such as necrotic pulp, extensive restoration or crack
- symptoms depend on whether or not pulp is inflamed or necrotic
54
condensing osteitis:
radiographically?
treatment?
- increased radiodenstiy and opacity in one or more roots
| - RCT
55
focal osteoporosis:
- not a ____?
- symptoms?
- usually affects what kind of tooth?
- radiographically?
- treatment?
- LEO: lesion of endodontic origin
- asymptomatic
- virgin tooth/normal pulp
- increased radiodensity and opacity around one or more roots
- no treatment necessary
56
periradicular cyst:
- mostly affects where?
- patients usually how old?
- which gender?
- maxillary or mandibular teeth?
- mostly human jaws
- pts in third decade
- affects men more than women
- maxillary teeth more than mandibular
57
periradicular cyst:
- ____ cyst? of what origin?
- arises from?
- what bacteria commonly isolated?
- odontogenic cyst, inflammatory origin
- epithelial cells rests of Malassez in PDL
- actinomyces
58
histopathological features of radicular cysts:
epithelial lining?
cholesterol clefts - formed by?
what else is found?
- usually stratified squamous epithelium
- formed by degradation of inflammatory cells
- fibrous capsule of collagen fibres
- inflammatory cells
59
periodontal abscess
- symptoms?
- pocket?
- sensibility testing?
- rapid onset, spontaneous pain, TTP, pus formation, swelling
- deep periodontal pocket
- sensibility testing normal response
