biology and histology of the pulp and PA tissues Flashcards
DST, seen with?
draining sinus tract, seen with necrotic pulp/ChronicPA abseces
main pulp components
conn tissues with fibroblasts, odontoblasts and osteoblasts
can pulp defend?
Yes
when does pulpal defense fail, leads to?
bacterial invasion, leads to inflam and necrosis
what is the direction of usual bacterial invasion
coronal to apical
Pulpal organ defined
cells? strucutres?
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)
Primary Function of pulp?
e
Formative:
odontoblasts – dentin (with dental epithelium)
ameloblasts – enamel
secondary pulpal functions
Supportive, Protection, Sensation, Defense, Repair
Fibroblast arises from_______________
Fibroblast arises from undifferentiated ectomesenchymal cell
most prevalent cell in pulp/ basic cell of all conn tissue
fibroblast
function of fibroblasts
secrete type 1 and 3 collagen and ground substance
fibroblasts important in which functions
wound helaing and pulpal regeneration
Odontoblast
responsible for? also plays a role in?
produces?
processes extend into?
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
dentinal tubules with odontoblasts
dentin
predentin
odontoblast layer
tubule destruction progression
sclerosis may occur to block bac
tracts die
tertiary dentin formed by fibroblasts to block off tubules
pulp chamber size with age
will decrease due to secondary dentin making endo treatment more difficult
response of pulp to injury
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.
Branstromm’s“Hydrodynamic Theory”
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
dental pulp anatomy components
lamina dura
cortical bone of the alveolar bone, appears more radiopaque
odontoblasts primary dentin/ tooth formation
pattern of deposition of secondary dentin
uniform, reduces the general size of the pulp but retains general form as the tooth matures
bacteria entering through the tubules, bacteria are much smaller in diameter allowing for this
what cells form tertiary dentin
fibroblasts
microabscess on the left and tertiary dentin formation
second response of the the pulp to aging and injury
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!
PCO only related to what factor
pt age
common etilogies of pulpal irritation
many of these are.
microbiological = primary cause
mechanical
chemical/ trauma (can allow bac to enter)
many of these can be iatrogenic
pulp resilience
The pulp amazingly resilient if covered by at least .5mm of healthy dentin. Reasonable trauma can be survived if bacteria are minimized or eliminated.
1 threat to pulp health
caries
presence of bacteria and pulpal injury, rat experiment
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
acute pulpitis histology
bacteria present with pus/ PMN
cracks in teeth
can allow bac to advance to the pulp and cause infection
may not be seen radiographically
Portals of ACCESS” of microbiological irritants
-most common cause?
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)
Mechanical Irritants, example
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
aspiration of odontoblasts mechanisms
can be due to exccessive heating
how should we dry dentin
cotton pellet not air
types of trauma
EXTERNAL: Falls & Sports Accidents
INTERNAL: Para-Normal Habits (Bruxism)
perio pockets may allow for?
bac invasion thru the apical foramen
with bac present, what necrosis may occur in the pulp?
coagulative necrosis
