biology and histology of the pulp and PA tissues Flashcards

1
Q

DST, seen with?

A

draining sinus tract, seen with necrotic pulp/ChronicPA abseces

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2
Q

main pulp components

A

conn tissues with fibroblasts, odontoblasts and osteoblasts

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3
Q

can pulp defend?

A

Yes

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4
Q

when does pulpal defense fail, leads to?

A

bacterial invasion, leads to inflam and necrosis

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5
Q

what is the direction of usual bacterial invasion

A

coronal to apical

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6
Q

Pulpal organ defined
cells? strucutres?

A

Central mass of a tooth consisting of soft tissue that is densely innervated by afferent (sensory) fibers, sympathetic fibers, vascular structures, lymphatics and specialized cells such as odontoblasts (characteristic cells of pulp) and fibroblasts (most
common/prevalent cell type in pulp)

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7
Q

Primary Function of pulp?
e

A

Formative:
odontoblasts – dentin (with dental epithelium)
ameloblasts – enamel

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8
Q

secondary pulpal functions

A

Supportive, Protection, Sensation, Defense, Repair

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9
Q

Fibroblast arises from_______________

A

Fibroblast arises from undifferentiated ectomesenchymal cell

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10
Q

most prevalent cell in pulp/ basic cell of all conn tissue

A

fibroblast

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11
Q

function of fibroblasts

A

secrete type 1 and 3 collagen and ground substance

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12
Q

fibroblasts important in which functions

A

wound helaing and pulpal regeneration

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13
Q

Odontoblast
responsible for? also plays a role in?
produces?
processes extend into?

A

Cell unique to the pulp
–Responsible for dentinogenesis
–Important in amelogenesis
–Produces collagen fiber and proteoglycan matrix which becomes mineralized
–Processes extend into tubules, cell present in the pulp

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14
Q
A

dentinal tubules with odontoblasts

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15
Q
A

dentin
predentin
odontoblast layer

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16
Q

tubule destruction progression

A

sclerosis may occur to block bac
tracts die
tertiary dentin formed by fibroblasts to block off tubules

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17
Q

pulp chamber size with age

A

will decrease due to secondary dentin making endo treatment more difficult

18
Q

response of pulp to injury

A

TERTIARY (REPARATIVE) DENTIN is deposited over time in the immediate area of the injury
by fibroblasts in an attempt to repair, protect or insulate the pulp from further injury.
General FORM of PULP is altered.

19
Q

Branstromm’s“Hydrodynamic Theory”

A

Anything that causes movement of the fluid w/in the dentinal tubules causes pain in the pulp (hot/cold)
fluid movement moves nn fibers to cause pain
removal=no pain is good, removal with pain may indicate RCT

20
Q

dental pulp anatomy components

A
21
Q

lamina dura

A

cortical bone of the alveolar bone, appears more radiopaque

22
Q

odontoblasts primary dentin/ tooth formation

A
23
Q

pattern of deposition of secondary dentin

A

uniform, reduces the general size of the pulp but retains general form as the tooth matures

24
Q
A

bacteria entering through the tubules, bacteria are much smaller in diameter allowing for this

25
Q

what cells form tertiary dentin

A

fibroblasts

26
Q
A

microabscess on the left and tertiary dentin formation

27
Q

second response of the the pulp to aging and injury

A

Calcific Metamorphosis
Pulp sclerosis or Dystrophic calcification=PCO: pulp canal obliteration
•Probably a combination of 2ndary and Tertiary dentin formation in response to extensive and chronic injuries before the pulp became necrotic. (no deposition unless pulp is vital)
•This canal is not negotiable by normal means – Refer – MICROSCOPE, CBCT!

28
Q

PCO only related to what factor

A

pt age

29
Q

common etilogies of pulpal irritation
many of these are.

A

microbiological = primary cause
mechanical
chemical/ trauma (can allow bac to enter)
many of these can be iatrogenic

30
Q

pulp resilience

A

The pulp amazingly resilient if covered by at least .5mm of healthy dentin. Reasonable trauma can be survived if bacteria are minimized or eliminated.

31
Q

1 threat to pulp health

A

caries

32
Q

presence of bacteria and pulpal injury, rat experiment

A

The #1 cause of pulpal injury
Kakehashi exposed pulps of germ free and conventional rats to their own flora. The gnotobiotic rats did not develop pulpal or periradicular lesions.*
Without MO & their products, LEOs (Lesions of Endodontic Origin) do NOT occur

33
Q

acute pulpitis histology

A

bacteria present with pus/ PMN

34
Q

cracks in teeth

A

can allow bac to advance to the pulp and cause infection
may not be seen radiographically

35
Q

Portals of ACCESS” of microbiological irritants
-most common cause?

A

cracks/ tooth fracture
Caries/leaking Restoration (Most common Causes)*
Exposed lateral or accessory Canals
CEJ defects
open tubules (bac=.2-.5um, tubule=50um)
initial pocket allowing invasion at apical foramen (uncommon)

36
Q

Mechanical Irritants, example

A

Most operative procedures are accompanied by significant opportunity for
iatrogenic and irreversible damage to the pulp.
•CUTTING WITH INSUFFICIENT COOLANT CAUSES> Aspiration of odontoblasts into
tubules
•If beyond limits of repair = Pulp Necrosis. 10ºC

37
Q

aspiration of odontoblasts mechanisms

A

can be due to exccessive heating

38
Q

how should we dry dentin

A

cotton pellet not air

39
Q

types of trauma

A

EXTERNAL: Falls & Sports Accidents
INTERNAL: Para-Normal Habits (Bruxism)

40
Q

perio pockets may allow for?

A

bac invasion thru the apical foramen

41
Q

with bac present, what necrosis may occur in the pulp?

A

coagulative necrosis