8. EFFECT OF DENTAL MATERIALS ON
PULP
GIC – Well tolerated by pulp
• Calcium hydroxide – includes dentin bridge
formation.
• Zine oxide – eugenol- has an anti-bacterial
effect.
• Formocresol – Cause chronic inflammation of
the pulp.
• Dentin bonding agent – can irritate the pulp
causing inflammation
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18. Pulpal Pain
•
Deep, dull, aching pain of a threshold nature
•
Often difficult to localize
•
Occurs irrelevant to biomechanical(masticatory)
functions
19. Common Characteristics of Pulpal Pain
1. Quality of pain is dull, aching, throbbing and
occasionally sharp
2. An identifiable condition that reasonably explains the
symptoms
3. Response to local noxious stimulation is
proportionate and predictable
4. Pulpal pain tends to get better or worse, but rarely
stays the same over time
5. Local anesthesia of the suspected tooth eliminates
the pain
20. Site of Pain vs. Source of
Pain
Site of Pain
• The location where the patient feels the pain
• Easily located by asking the patient to point out the
region of the body that is painful
Source of Pain
• That area of the body from which the pain actually
originates
21. Primary Pain
Site (where it hurts) = Source (where it
originates)
Eg./ cut finger
Heterotopic Pain
Site ≠ Source
Eg./ cardiac pain
22.
23. Heterotopic Pain
Pain felt in an area other than its true site of
origin (associated with deep, somatic pain).
–Projected pain: perceived in the anatomic
distribution of the same nerve that
mediates the primary pain (painful
adjacent teeth).
–Referred pain: felt in an area innervated
by a different nerve from the one that
mediates the primary pain (teeth in
opposing arch, face, head, neck).
Does not cross the midline.
Convergence of afferent neurons.
24. TERMINOLOGY
Dental pulp – Tissue within each
tooth that contains the nerves, blood
vessels, and cells that make the tooth
a living organ
Pulpitis – A range of conditions from
inflammation all the way to pulpal
necrosis
25. TERMINOLOGY CON’T
Vitality – response of the pulpal tissue
to a stimulus(healthy to
nonresponsive)
Reversible/irreversible pulpitis –
Reactions of a vital pulp to stimuli
Necrotic – death of the pulp
Periapical Tissue
• chronic periodontitis
• acute periodontitis
29. Acute Pain
Associated with tissue damage or injury.
Recent onset.
Limited duration.
Stimulation of peripheral and central
nociceptors by algogenic substances
(bradykinin, prostoglandin, leukotrienes,
histamines, substance P, excitatory AAs).
30. Chronic Pain
Prolonged persistence of pain beyond
the healing of tissue.
Frequently experienced in the absence
of peripheral stimulation or lesions.
Result from changes in the dorsal horn
and brain.
31. TOOTHACHE PAIN
Toothache of odontogentic origin can be
visceral (pupal) or musculoskeletal
(periapical or periodontal).
– When the pulp is exposed to a noxious
stimulus, there is a reactive inflammatory
response.
– The resulting edema is unable to expand
because of the surrounding inflexible cementum
→ ↑ tissue pressure and ↓ blood flow that
causes damaging effects to the pulp.
32. Considerations:
Healthy pulp (cellular) v Aged pulp (fibrous)
As an increasing amount of pulp tissue is involved,
the inflammatory process progresses apically, until
it extends out into the periapical tissue → apex
becomes sensitive to palpation and percussion.
Periapical inflammation from non-pulpal causes
can exhibit similar symptoms:
– Hyperocclusion
– Bruxism
43. Pulpalinflamationanddegenerationnotexpectedtoimprove.
A physiologically older pulp has less ability to recover due to decrease in
vascularity andreparative cells.
As inflammation spreads apically, cellular organization begins to break
down.
Localized pressure slows venous return, resulting in buildup of toxins and
lowerpH thatcauseswidespreadcellulardestruction.
