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Pathology > Sequelae of pulpal disease > Flashcards

Sequelae of pulpal disease Flashcards

1
Q

pulpitis? classifications?

A

inflammation of the pulpal tissue
Reversible vs irreversible
Acute vs chronic
Symptomatic vs asymptomatic

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2
Q

Tx planning with pulpitis

A

determine extent with testing and use knowledge/ judgement

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3
Q

MECHANISM OF ACTION:
INFLAMMATION OF THE PULP

A

 Limited blood supply
 No collateral support
 Destructive, small space
 Expansile process due to…
▪ Blood vessel dilation
▪ Leakage of fluid into surrounding tissue
▪ Migration of cells

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4
Q

reversible pulpitis

A

pulp can recover

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5
Q

reversible pulpitis histo

A

vasodialtion with lymphocyte infiltration

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6
Q

irrreversible pulpitis, what is happening?

A

cannot recover, acute inflammation and abcess formation

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7
Q

pulpal necrosis

A

due to untreated pulpitis
tooth killed with blood supply lost, becomes discolored

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8
Q

acute pulpitis
histology similar to?
must be?
what parts of pulp usually affected?
due to?
commonly in what age group?

A

similar histology to an abcess, lots of PMN
must be no possible drainage
usually at one pulp horn or all pulp
due to bacterial invasion thru non-sclerosed dentin tubules, adolescents commonly

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9
Q

chronic pulpitis

A

little to no penentration of virulent bac into the pulp
usually in older teeth with previous restorations, slow caires
dentin tubules have narrowed and reparative dentin formed

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10
Q

is chronic hyperplastic pulpitis symptomatic

A

no, due to decreased nn fibers

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11
Q

CHRONIC HYPERPLASTIC PULPITIS

A

primary molars with rampant caries
forms a pulp pollup due to open foramen and ample blood supply
prolif of pulp and granulation tissue form the pollup

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12
Q
A

CHRONIC HYPERPLASTIC PULPITIS

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13
Q

CHRONIC HYPERPLASTIC PULPITIS histology

A

fibrotic pulp

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14
Q

POTENTIAL SEQUELLAE OF BACTERIAL PULPITIS flow chart

A
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15
Q

4 factors of PERIAPICAL LESIONS development

A

Presence of opened or closed pulpitis
Virulence of involved microorganism
Extent of sclerosis of dentinal tubules
Competency of host immune response

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16
Q

PERIAPICAL GRANULOMA
mass of?
located? what type of teeth?
symptomatic?

A

 mass of chronically inflammed granulation tissue-not true granuloma tissue (granulation tissue)
 apex of non-vital teeth ONLY
 mostly asymptomatic

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17
Q

PERIAPICAL GRANULOMA radiograph

A

radiolucency at apex

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18
Q

PERIAPICAL GRANULOMA may develop as?

A

 May develop as the inital periapical pathosis or arise after an initial periapical abscess

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19
Q

PERIAPICAL GRANULOMA could become?

A

a periapical cyst or abscess

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20
Q

periapical granuloma indication for what Tx?

A

RCT (or extraction if needed)

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21
Q

periapical granulomas and accessory canals

A

mostly occur on apex, can possibly occur laterally due to accessory canals

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22
Q

histology of a periapical granuloma
may be deposits of?

A

granulation tissue present (all inflammatory cells present)
may be cholesterol deposits and RC material

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23
Q

periapical granuloma healing

A

can be healed with good RCT

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24
Q

cyst, components?

A

 Pathologic cavity located in soft tissue or bone lined by
epithelium

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25
Q

RESTS OF MALASSEZ role in cysts

A

will proliferate forming the epithelial lining of the cysts

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26
Q

APICAL PERIODONTAL CYST (PERIAPICAL CYST)
inflammatory?
most common in which arch?
symptomatic?
growth rate?
tooth vital?
root resorption?

A

 An inflammatory cyst, most common in mandible
 Asymptomatic, slow - growing lesion associated with the root apex of a non - vital tooth
 External root resorption possible

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27
Q

PA cyst radiograph

A

radioluceny at apex

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28
Q

can we know a cyst from radiography?

A

no we need histo/biopsy

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29
Q

are multiple PA cyst possible

A

yes, multiple non vital teeth

30
Q

PA cyst histo/ strucutre

A

wall made of inflam cells
lining usually hyperplastic epithelium
empty lumen

31
Q

PERIAPICAL ABSCESS
cells?
tooth vital?
may arise as?
symptomatic? why or why not?

A

 Accumulation of acute inflammatory cells at the apex of a non - vital tooth
 May arise as the initial periapical pathosis or as an acute exacerbation of chronic periapical lesion ( P h oenix a b s ces s)
 Generally symptomatic , but may be asymptomatic if there is a lack of accumulation of purulent material due to a chronic path of drainage

32
Q

PA abscess histo

A

lots of PMN= similar to acute inflamm

33
Q

PA abscess tx and healing

A

RCT indicated, removal of pulp may allow bone to heal

34
Q

POTENTIAL DRAINAGE PATHWAYS OF ACUTE PERIAPICAL INFECTIONS
determined by?

A

DETERMINED BY LOCATIONS OF APEX
1 . Surface of the gingiva (parulis)
2 .Palate (palatal abscess)
3 . Max sinus
4 . soft tissue spaces (cellulitis)
5 . Floor of mouth (ludwig’s)

35
Q
A

palatal abscess

36
Q

PARULIS (GUM BOIL)
due to?
mechanism of formation?
consists of?

A

acute PA inflammation
purulent material perforates thru bone, periosteum, soft tissue, epithelium and drains through intraoral sinus
Parilus=intraoral opening of the sinus tract
consists of a mass of inflammed granulation tissue with an epithlialized sinus tract

37
Q
A

gum boil/ parulis

38
Q

abscess

A

localized collection of pus that has accumulated in a tissue cavity, producing flucutance

39
Q

cutaneous sinus tract

A

dental abscesses can drain extraorally to the skin by forming these tracts thru bone

40
Q

oroantral fistula
usually from?

A

not from pathology, usually trauma
open communication btwn the sinus and the oral cavity

41
Q

oroantral fistulas commonly have?

A

granulation tissue form within them

42
Q

SINUS TRACT VS. FISTULOUS TRACT

A

sinus tract: from interior to exterior, parulis is the end of the tract
fistulous tract: connects two anatomic cavities (many types)

43
Q

types of fistulas

A

oroantral (mouth to sinus)
oronasal
tracheoesphogeal

44
Q

cellulitis

A

diffuse spread of an acute inflammatory process thru fasical planes/soft tissue producing the cardinal signs of inflamm
abscess unable to establish a drainage path into the mouth or onto skin

45
Q

what occurs with cellulitis often?

A

trismus= hard to open mouth

46
Q

Ludwigs angina

A

agressive, rapidly spreading cellulitis involving multiple anatomic spaces: submental, sublingual and submandibular
produces massive swelling of neck that can extend to the clavicles and block airway=death
medical emergency

47
Q

canvernous sinus thrombosis
emergency?
how can this happen?
associated with infections in what teeth?

A

medical emergency
valveless vv of face allow retrograde spread of infectious materials from middle third of face
blood clot may form in the cavernous sinus which is life threatening
associated with spread of infection from maxillary teeth

48
Q

cavernous sinus contents

A
49
Q

osteomyelitis can be caused by?
predispositions?

A

bacterial infection of bone: odontogenic infections, trauma to bone, NUG, NOMA (developing countries)

Predispositions: chronic systemic disease, immune def, decreased vascularity of bone

50
Q

acute osteomyelitis
spreads thru what part of bone?
tissue rxn? due to?

A

spread thru medullary spaces
minimal tissue reaction due to rapid onset/ minimal time to react

51
Q

chronic osteomyelitis
tissue rxn?
what forms? what occurs?
why would antibiotics be hard to use?

A

prominent tissue reaction-granulation tissue forms and fibrosis occurs
granulation tissue may wall of site making Antibiotics hard to use

52
Q

osteomyeltits possible drainage?

A

can occur via a sinus tract

53
Q

traumas that can cause osteomyelitis?

A

extraction, fracture

54
Q

chronic osteomyelitis radiograph

A

mixed lucent and opaque lesion, ill defined

55
Q

acute osteomyelitis histo

A

lots of PMN in bone

56
Q
A

acute osteomyelitis

57
Q

sequestrum

A

fragment of necrotic bone separated from adjacent vital bone that usually undergoes spontaneous exfoliation

58
Q

sequestrum histo with gram stain

A

would see bone and bacterial debris, lack of cells in lacunae

59
Q

involucrum

A

non-vital bone encased by vital bone

60
Q

PROLIFERATIVE PERIOSTITIS/ GARRE OSTEOMYELITIS
form of?
rxn?
most frequently seen in? where?

A

form of chronic ostemyelitis, osteomylelitis with proliferative periostitis/garre osteomyelitis

periosteal rxn occur which layers of reactive vital bone are formed producing cortical expansion (onion skin)

seen most frequently in children/young adults in man molar/PM areas involving the lower border/ buccal cortex

61
Q

proliferative periostitis radiograph

A

must be occlusal view to see onion skin

62
Q

proliferative periostitis progression

A

may need to recontour bone

63
Q

CHRONIC FOCAL SCLEROSING OSTEOMYELITIS/ CONDENSING OSTEITIS
seen in? where?

A

localized area of bone sclerosis associated with the apices of teeth with pulpal disease

seen in children/young adults involving the man molars and PM
reaction of bone to inflammation

64
Q

ACTINOMYCOSIS
spp names
morpholgy
gram/O2
commensual?

A

means ray fungus but is bacterial infection caused by actinomyces spp
A. israelii and A. vicosus
filamentous bacteria: branching
gram +/ anaerobic
part of normal oral flora

65
Q

CLASSIFICATION OF ACTINOMYCOSIS

A

Cervico-facial – 5 5 %
 Abdomino-pelvic – 2 5 %
 Pulmonary – 1 5 %

66
Q

entry of actinomycoses?
can extend thru?
can disregard?

A

area of prior trauma: soft tissue injury, perio pocket, non-vital tooth, extraction site, infected tonsil
direct extension thru soft tissue
disregards fascial planes and lymphatics

67
Q

presentation of cervico-facial actinomycosis

A

woody induration and fibrosis= hard
draining sinus tracts
suppuration with sulfur granules

68
Q

cervicofacial actinomycosis radiograph

A

Ill defined lucency at the site of entry/ infection

69
Q
A

CF actinomycosis, sinus tracts

70
Q
A

sulfur granule

71
Q

what is present in the radiolucency of actinomycosis

A

bacteria

Pathology (20 decks)

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