Lesson 6 Flashcards
ZONES OF THE PULP
-› mature dentin
-› odontoblastic zone
-> cell-free zone
cell-rich zone
-› central zone
reaction of tooth
stimuli
explains tooth sensitivity even when pulp tissue is not diseased
HYDRODYNAMIC THEORY
HYDRODYNAMIC THEORY BY?
BRANNSTROM
stimulation of A-delta fibers
HYDRODYNAMIC THEORY BY BRANNSTROM
an external stimuli causes movement of dentinal fluid found inside the tubules causing an outward flow
HYDRODYNAMIC THEORY BY BRANNSTROM
nerve fibers extend into the dentinal tubules (______) and respond to the stimuli or movement
A-delta fibers
_______are found mainly in the central zone of the pulp
C fibers
formation of sclerotic dentin and formation of reparative or tertiary dentin
MILD INJURY
no pulp inflammation
MILD INJURY
no formation of sclerotic or reparative dentin
SEVERE PROLONGED INJURY
stimulus continues to act on pulp tissue developing into inflammation and furthermore pulp disease
SEVERE PROLONGED INJURY
pulp cannot repair and odontoblasts are damaged
SEVERE PROLONGED INJURY
a complex sequence of vascular and cellular changes of tissues in response to injury that subsides only after the effects of the causative factors have been eliminated and the damaged tissue is repaired or returned to a healthy state
PAIN DUE TO INFLAMMATION
rubor
Redness
calor
Heat
Tumor
Swelling
dolor
Pain
function laesa
Loss of function
irritant /stimulus
transient vasoconstriction
vasodilation due to release of inflammatory mediators
increased vascular permeability
transudation/exudation
edema
increased pulpal tissue pressure
compression of blood circulation
increased blood viscosity
stasis of blood flow
localized pulp inflammation
VASCULAR RESPONSE
The ________ occurs first as it is what brings the inflammatory cells to the area of injury.
vascular response
margination
diapedesis
chemotaxis
phagocytosis
CELLULAR RESPONSE
inflammatory cells move into side of blood vessels
Margination
movement through endothelial lining of the blood vessel
Diapedesis
attraction to the irritant
Chemotaxis
removal of irritant or stimulus
Phagocytosis
INFLAMMATION ACCORDING TO ONSET
Acute
Chronic
exudative or immediate
response of tissue to
neutralize injurious agent
Acute
> increase of PMNL
-> rapid course
Acute
-> sudden and intense
short onset
Acute
-> proliferative phase
• > persistent or long-standing
Chronic
-May follow an acute phase or may develop from onset
- (-) pain
Chronic
FEATURES OF THE PULP THAT PLAY A ROLE IN PULP INFLAMMATION
- LOW COMPLIANT ENVIRONMENT
- RESILIENT CONNECTIVE TISSUE (GROUND SUBSTANCE)
- PRESENCE OF ARTERIO-VENOUS ANASTOMOSES (AVA’S)
> the pulp is a soft tissue surrounded by hard tissue (dentin)
when there is presence of inflammation, vasodilation causes increased flow into the area, edema, and increase in intracellular fluid leading to an increase in blood volume
-> because of that, the pulp cannot expand and there is an increase in pressure causing some sort of pain to the patient
LOW COMPLIANT ENVIRONMENT
the ground substance is a gel-like material that becomes watery when damaged
RESILIENT CONNECTIVE TISSUE (GROUND SUBSTANCE)
in its gel-like state, it is able to stop or control the immediate spread of inflammation but when the irritant is too strong, it damages the gel-like consistency leading to further spread of inflammation
RESILIENT CONNECTIVE TISSUE (GROUND SUBSTANCE)
direct connections between arterioles and venules; no capillary bed
PRESENCE OF ARTERIO-VENOUS ANASTOMOSES (AVA’S)
open up to bring blood to the area of inflammation in order to decrease pressure in the pulp
PRESENCE OF ARTERIO-VENOUS ANASTOMOSES (AVA’S)
FACTORS CAUSING INJURY TO THE PULP
BACTERIA
PHYSICAL, THERMAL, MECHANICAL,
-direct pulp invasion via carious -lesion bacterial toxins
BACTERIA
anachoresis
BACTERIA
-trauma
-iatrogenic
**etched dentin: washed and overdried
**desiccation: collapsed collagen layer
**vibration or heat
PHYSICAL, THERMAL, MECHANICAL, CHEMICAL, ELECTRICAL CAUSES
-> regressive changes
-> barodontalgia or aerodontalgia
PHYSICAL, THERMAL, MECHANICAL, CHEMICAL, ELECTRICAL CAUSES
galvanism
PHYSICAL, THERMAL, MECHANICAL, CHEMICAL, ELECTRICAL CAUSES
increase of pressure to pulp tissue because of high altitude levels
barodontalgia or aerodontalgia
contact of metal restorations
galvanism
radiograph:
clearly delineated canals
(-) periapical radiolucency, resorption, calcifications
NORMAL PULP (PULP DISEASE)
-› asymptomatic
-> mild or moderate response to thermal test or stimuli
-> (-) percussion, palpation, mobility
NORMAL PULP (PULP DISEASE)
mild transient localized inflammatory response of the pulp
REVERSIBLE PULPITIS
non-spontaneous pain or pain that occurs only when there is stimuli
REVERSIBLE PULPITIS
quick, sharp pain to cold, less to hot
REVERSIBLE PULPITIS
(-) percussion, palpation, tooth mobility
REVERSIBLE PULPITIS
> less current with the electrical >pulp (EP) test recent dental treatment
REVERSIBLE PULPITIS
RADIOGRAPHIC FEATURES
-› normal PDL and lamina dura
REVERSIBLE PULPITIS
-> slight disruption of odontoblastic layer and inflammatory cell infiltration adjacent to area of irritation
REVERSIBLE PULPITIS
-> pulp hyperemia
-> inflammatory cell infiltrates
REVERSIBLE PULPITIS
TREATMENT
-> removal of damaged dentin >placement of liner or base
REVERSIBLE PULPITIS
IRREVERSIBLE PULPITIS are:
ACUTE IRREVERSIBLE PULPITIS
CHRONIC ULCERATIVE PULPITIS
CHRONIC HYPERPLASTIC PULPITIS
irreversible condition characterized by intense inflammatory response
ACUTE IRREVERSIBLE PULPITIS
-> pain
Moderate to severe
Spontaneous
Intermittent
Continuous
ACUTE IRREVERSIBLE PULPITIS
sharp (A-delta fibers)
dull and throbbing (C filers)
localized or referred
ACUTE IRREVERSIBLE PULPITIS
-> thermal response:
immediate response to hot stimuli but may be relieved with cold stimuli
immediate response to cold stimuli
ACUTE IRREVERSIBLE PULPITIS
immediate response to hot and cold stimuli but cold causes more pain than hot
ACUTE IRREVERSIBLE PULPITIS
reacts to low levels of current with the electric pulp test
ACUTE IRREVERSIBLE PULPITIS
-> may be (+) percussion
-> (-) palpation and tooth mobility
ACUTE IRREVERSIBLE PULPITIS
RADIOGRAPHIC FEATURES
-> deep caries
> extensive restorations thickened or widening apical portion of PDL
ACUTE IRREVERSIBLE PULPITIS
HISTOLOGIC FEATURES of
ACUTE IRREVERSIBLE PULPITIS
Early Phase
Late Stage
What phase?
> odontoblasts near the cause are destroyed
Early phase
What phase?
increased inflammatory cell infiltration
Early Phase
What phase?
vascular dilation and edema
Early Phase
What phase?
-> destruction of pulp zones
Late Stage
What phase?
inflammation involves entire pulp
Late stage
What phase?
inflammatory cells fill pulp
Late Stage
TREATMENTof ACUTE IRREVERSIBLE PULPITIS
RCT or pulpectomy
FORMATION OF PULP ABSCESS
ischemia
necrosis
degeneration of leukocytes
release of lysosomal enzymes
abscess formation
persistent inflammatory reaction of the pulp characterized by the presence of granulation tissue over the exposed pulp surface
CHRONIC ULCERATIVE PULPITIS
CLINICAL FEATURES
-> presence of carious lesion on either as a closed carious lesion or a cavity
CHRONIC ULCERATIVE PULPITIS
-> in an open carious lesion, pain is present when lesion is packed with food
CHRONIC ULCERATIVE PULPITIS
› possible (+) percussion
-> varied thermal response
CHRONIC ULCERATIVE PULPITIS
RADIOGRAPHIC FEATURES
-› near pulp exposure or presence of pulp exposure
CHRONIC ULCERATIVE PULPITIS
HISTOLOGIC FEATURES
-> localized excavation of the pulp surface
-> (+) of ulcer on the pulp surface
CHRONIC ULCERATIVE PULPITIS
-> plasma cell infiltration
> drainage of the inflammatory exudate through necrotic dentin
-> inflammation remains localized because drainage prevents build-up of pressure
CHRONIC ULCERATIVE PULPITIS
TREATMENT
-> RCT or extraction depending on the severity of crown involvement or restorability of the tooth
CHRONIC ULCERATIVE PULPITIS
-> hyper means “increase”; plastic means “tissue”
CHRONIC HYPERPLASTIC PULPITIS
excessive and exuberant overgrowth of a chronically inflamed dental pulp outside the pulp chamber
CHRONIC HYPERPLASTIC PULPITIS
complete exposure of pulp tissue which responds by growing or increase in terms of number and size
CHRONIC HYPERPLASTIC PULPITIS
-> the overgrowth of tissue is called a pulp polyp
CHRONIC HYPERPLASTIC PULPITS
common on young immature teeth
CHRONIC HYPERPLASTIC PULPITS
TREATMENT
> depends on restorability of the tooth
-> RCT or extraction
CHRONIC HYPERPLASTIC PULPITS
epithelial cells from surrounding oral tissue can fall into this growing granulation tissue to form lining epithelium of polyp
PULP POLYP WITH STRATIFIED SQUAMOUS EPITHELIUM
- plasma cell infiltration
- granulation tissue with delicate CT, filers and blood vessels
PULP POLYP WITH STRATIFIED SQUAMOUS EPITHELIUM
True or false
early polyps without stratified squamous lining will bleed while mature polyps with the lining will not
True
end stage of pulp inflammation
PULP NECROSIS
with or without crown discoloration
»_space;as the pulp breaks down, products of the cells release and cause discoloration
PULP NECROSIS
-› can be partial or total necrosis
-> no presence of blood vessels in pulp
-> root canal will appear radiolucent
PULP NECROSIS
TREATMENT
-> RCT or extraction
-depends on restorability of the tooth
PULP NECROSIS
Bacteria from another part of the body
Anachoresis
No capillary bed
Arterio-venous anastomoses
