The Normal Pulp

● Free of symptoms with no spontaneous symptoms.

● Responds normally to pulp testing.
● Radiographically, there may be pulpal calcifications but no resorption (but still normal
functioning pulp).
● No caries.
● No mechanical pulp exposure.
● No endodontic treatment is indicated for these teeth.

Tissue damage won’t necessarily elicit pain immediately, it requires a long time.

1) A noxious stimulus is an external or internal physical change that induces an afferent

input in the nervous system, with or without sensory experience or a behavioral
response.
★ Not all stimuli are noxious (cause physical changes) to the pulp. It must be
noxious for a change to occur.
★ A noxious stimulus is actually, or potentially, damaging to the tissues and liable
to cause pain, but does not invariably do so.
★ Some noxious stimuli, especially in the viscera, do not cause nociceptive
responses.

What is a nociceptive response? What are nociceptive receptors?

➔ They are receptors that send impulses to the brain to notify it that a threat is present.

➔ Teeth cannot respond except by pain. That’s why we only experience pain in our teeth.
Because nociceptive receptors in the pulp are not as effective as they are in periapical
tissues.

➔ That’s why, when inflammation occurs up until necrosis, no pain is felt. It is only when a
periapical involvement starts that the patient will start feeling pain; because nociceptive
receptors are much more sensitive in periapical tissues than in the pulp.

Disease Progression
The microcirculation and sensory nerve activity are the 2 key components in pulpal
inflammation.

2) The earliest signs of pulp reaction to insult are morphological changes and overall
reduction in the number & size of odontoblast cell bodies .

3) Sensory nerves respond to noxious stimuli with pain sensation only, regardless of
stimulus in dentin or pulp.
 4) Pulp injury activates the interdental sensory nerves to release neuropeptides that
cause alteration in microcirculatory hemodynamics → by vasodilation and increase in
vascular permeability.

5) Tissue injury leads to destruction of nerve fibers at the injured site then
hypersensitivity to the surviving nerve fibers and then release of inflammatory
mediators → bradykinin, PG, and CGRP.

6) This will lead to increase in tissue pressure, decreased blood flow, aggregation of
RBCs, elevation in blood viscosity, and tissue hypoxia.

7) Tissue necrosis will follow, CO2 increases, and pH decreases, then vasodilation in
adjacent areas and spread of inflammation (discoloration may be evident, but not
necessarily pain).

The stimulus (whether mechanical, thermal, bacterial, or chemical) must reach a noxious level
for changes to start taking place.

If the noxious stimulus is removed, the pulp goes back to normal. If it persists, it will lead to
irreversible pulpitis and pulp necrosis.

Causes of Pulp Inflammation

I- Bacterial Causes

Coronal Ingress A. Caries:

● Most common means of ingress to the dental pulp for infecting bacteria and/or their
toxins.
● The pulp becomes inflamed from irritation by the preceding bacterial toxins, long
before the bacteria reaches it.
● The active carious lesion is composed of: an outer infected layer and a deeper affected
layer, which has been demineralized by acids produced by the bacteria in the infected
layer.
● In early pulpitis, the pulp is affected but not infected by bacteria, which is why it should
be reversible.

B. Incomplete fracture (bacterial cause, not trauma)

C. Anomalous tract (Radicular-lingual tract/Palato-gingival tract):
● Rare developmental defect
● Appears in the cervical ⅓ of the upper lateral incisor.
● Starts coronally → gingival irritation → plaque retention → pulp affection.
 Radicular A. Caries (less frequent than coronal caries)
Ingress B. Periodontal pocket: increases atrophy and dystrophic calcifications in the dental pulp.
C. Hematogenic infection (septicemia/bacteremia/anachoresis)

II- Traumatic Causes

Acute Trauma A. Coronal fracture: pulp death following coronal fractures is mainly due to bacterial invasion
that follows.
B. Radicular fracture will lead to disruption of pulp vascular supply, thus the injured coronal
pulp loses its vitality (pulp may not be always involved).
C. Luxation (movement of the tooth inside its socket): extrusive and lateral luxation, as well as
intrusion, always results in pulp death.

Chronic Trauma Attrition, abrasion, or erosion: pulp death due to incisal wear or gingival erosion is not very
common, as the reparative power of the pulp to lay down dentin as it recedes ahead of this stimulus is
phenomenal. (Low-grade trauma for a long time).

III- Iatral Causes

1. Cavity A. Heat of preparation:

Preparation The basic factors in rotary instrumentation that cause temperature rise in the pulp in order of
importance are:
1. Force applied by the operator (intermittent force is favorable)
2. Size, shape, and condition of cutting tool (a larger tool causes more heat due to its larger
surface area - dull burs cause more heat generation).
3. Revolutions per minute
4. Duration of actual cutting time

The goal is to avoid or minimize any heat generation during cutting into the tooth structure and the
use of proper cooling is very important.

B. Depth of preparation: the deeper the penetration, the more extensive the pulp inflammation will
be, where the degree of pulp response is inversely proportional to the remaining thickness of dentin.

C. Pulp horn extension

D. Dehydration: constant drying and chip blowing with warm air during cavity preparation can result
in pulp inflammation and possible necrosis. This mainly happens with an already stressed pulp.

E. Pulp exposure
F. Pin insertion

2. Restorations A. Insertion: Severe hypersensitivity and pulpalgia (symptoms of underlying pulp inflammation
& subsequent necrosis) have been noted following the insertion of gold foil and less frequently
with silver amalgam restorations.

B. Force of cementation: due to the chemical irritation of the cement liquid and also the
 tremendous hydraulic force exerted during cementation drives the liquid away from the pulp.

C. Heat of polishing

3. Orthodontic Rapid orthodontic movement can cause external root resorption. Usually, the resorption is minor and
Movement results in blunting of the root apex. But in some cases, the root can be shortened to a point that the
tooth becomes loose.

Dental pulps also become hyperplastic, devitalized, or experience internal resorption following
orthodontic movement.

4. Periodontal Extended, aggressive scaling curettage can cause hypersensitivity of teeth, pulpitis, and even pulp
Curettage devitalization.

**Usually, orthodontic movements and curettage pose no threats when done normally.

IV- Chemical Causes

1. Filling How do bacteria get into a position to irritate the pulp after a filling has been placed?
materials ➔ Microleakage.
➔ Bacteria left behind in the smear layer may also contribute toxins if allowed to remain viable by
being fed substrate through microleakage.

Some toxicity exists from materials, but it’s very minimal. It’s primarily bacteria that cause continuing
pulp inflammation.

2. Disinfectants ---

V- Idiopathic Causes

1. Aging The decreased numbers and size of cells and increase in collagen fiber content occurs with aging. Also,
the constant recession of the normal pulp and its production of secondary and irrational dentin is a
certain process.

2. Internal It can be either idiopathic or due to chronic pulpal inflammation.

Resorption

3. External It cannot be decided that external root resorption is a pulp dystrophy, since its origin lies within the
Resorption tissues of the periodontal membrane space.

Good luck :)
Loujine Elrafey