3. The degree of inflammation is proportional to the intensity and
severity of tissue damage.
Depending on the severity and duration of the insult and the host
response
pain
Thepain depends on:
4. Age Changes in the Pulp
volume
vascularity & cellularity.
collagen fiber content.
healing potential.
pulp stones and diffuse calcification
4
7. Healing of Pulp
• Injured odontoblasts
removal of irritant
reactionary dentin
Ca(OH)2 agents stimulate
formation of a calcified barrier.
7
Pulp Necrosis
8. LESION PROGRESSION
localized inflammation
inflammatory mediators.
vascular permeability.
capillary pressure capillary permeability
an exudate forms.
rigid walls
passive compression
collapse of the venules
"compartmentalized“
9.
10. Pain is often caused by
different factors.
Release of mediators of inflammation
causes pain directly by lowering the
sensory nerve threshold.
These substances also cause pain indirectly
by increasing both vasodilation in arterioles
and vascular permeability in venules,
resulting in edema and elevation of tissue
pressure. This pressure acts directly on
sensory nerve receptors.
Increased tissue pressure, the inability of
pulp to expand, and the lack of collateral
circulation may result in pulpal necrosis and
the development of a subsequent
periradicular pathosis.
Pain of Brannstrom
back-and-forth
movements of fluids within the dentinal
tubules stretch and stimulate the nerve
fibers.
11. Physiology of Pulpal Pain
Odontogenic pain
Sensibility of the dental pulp
2typesofsensorynervefibres
1. myelinated Afibres (A-deltaand
A-betafibres)
2.Unmyelinated C fibres
12. Dentin tubule fluid movement
Dehydration Heat Cold
Dentinal
tubule
and fluid
Dentin
Odontoblast
movement
A-delta
fibers
15. Common Characteristics of Pulpal Pain
Quality of pain
An identifiable condition
Response to local noxious stimulation
Pulpal pain tends to get better or worse
Local anesthesia
