Pulpal Diseases

- Inflammation is a protective attempt of living tissues to any type of injury which involves the
coordination & interaction of several responses.
- Pulpal inflammation is unique as it is influenced by:
1. Low compliance environment
2. Lack of collateral circulation
3. Limited caliber of the apical foramen

Classification of Pulpal Diseases

Inflammatory Diseases
1. Reversible pulpitis
2. Irreversible acute pulpitis
3. Chronic pulpitis
4. Pulp necrosis
Degenerative Diseases
1. Pulp atrophy
2. Pulpal calcification
3. Internal resorption

I- Inflammatory Diseases
1) Reversible pulpitis (Pulp Hypremia):
Definition: Reactive inflammatory process that resolves or diminishes with removal of the
irritant.
Etiology:
1. Increased dentin permeability.
2. Microbes.
3. Physical agents.
4. Thermal agents.
5. Chemical agents.
6. Leak around restoration
Histopathology: (figure 1)
1. Prolonged vasodilatation.
2. Erythrocyte extravasations.
3. Minimal amount of WBC infiltration.
Clinical symptoms:
-Pain: Sharp transient pain with thermal changes (cold > hot), sweat, sour: that subsides
immediately after removal of the cause.
-The hyperemic pulp is inflamed to the extent that these stimuli cause fluid movement inside the
dentinal tubules to stimulate odontoblasts and its associated fast conducting A-delta nerve fibers
to produce pain.
Diagnosis
- History: History of recent cavity preparation or recent restoration.
- Character of pain: Sharp pain, which subsides immediately after removal of the stimulus.
- Visual examination: Caries, cracked tooth, or traumatic occlusion.
- Vitality test: Response to electric pulp tester is lowered; cold elicits pain rather than hot
application.
-Palpation/percussion: Normal response.
-Radiograph: caries or restoration with normal periapical picture.

Figure 1: Histopathologic picture of pulp hyperemia showing dilated blood vessel.

2) Irreversible Acute Pulpitis:

Definition: response of clinically detectable inflammatory pulpal connective tissue.
Etiology:
1. As hyperemia stimulus not removed.
2. Acute exacerbation of chronic inflammation.
Histopathology: (figure 2)
*Different zones of the acute inflammatory response:
1. Zone of hyperemia: prolonged vasodilatation and fluid exudation will lead to increased intra-
pulpal pressure.
2. Zone of necrosis:Congestion and stasis.Dead cells as result of decreased oxygen.
3. Pulp abscess formation:
Clinical symptoms:
1. Pain is sharp, varies from mild moderate to severe.
2. Pain with thermal changes that persists after removal of the cause. Initially: Cold
elicits pain. Then Cold & Hot precipitate pain. Advanced stages; hot elicits severe pain
which can be relieved for few seconds with cold application.
3. Pain is spontaneous, continuous or intermittent.
4. Pain is not localized (diffuse).
5. Lying down increase pain intensity.
6. Pain could be referred.
Diagnosis:
-Pain character.
-Clinically carious exposure or fracture involving the pulp.
-Percussion/Palpation: negative.
-X-ray: normal.
-Vitality test: hot application increases pain due to increased vasodilatation and increased intra-
pulpal pressure. Cold relives pain because its contractile effect decreases the intra-pulpal
pressure below the threshold limit of the nerve fibers.
Note: After a while in the acute pulpits: cold cannot initiate pain because A-δ fibers are not vital
since they cannot tolerate oxygen depletion.

Figure 2: Histopathologic picture of symptomatic irreversible pulpitis (acute pulpitis)

3) Irreversible Chronic Pulpitis:

Definition: chronic inflammatory response of pulp connective tissue.
Types of chronic pulpits:
A. Open form (ulcerative pulpitis).
B. Closed form.
C. Hyperplasic pulpitis
A- Open form (ulcerative pulpitis):
Definition: chronic inflammatory response of pulpal connective tissue related to carious
exposure or following acute pulpitis.
Histopathology: (figure 3)
Zone of necrosis.
Zone of contamination.
Zone of irritation.
Diagnosis:
-Pain: usually absent or minimal.
-Clinically: Long standing carious cavity.
-Vitality test: require higher stimulation on electric pulp tester.
-Palpation/percussion : normal response
-Radiograph: normal picture / some widening in PDM space in advanced stages.

B- Closed form of chronic pulpitis:

Definition: chronic inflammatory response of pulpal connective tissue related to previous trauma
without pulp exposure.
Etiology: Low grade, long lasting irritation and increased host resistance. In addition to trauma,
rapid orthodontic movement or periodontal lesions may be the cause.
Histopathology: High infiltration of chronic inflammatory cells. (figure 3)
Diagnosis:
-Pain: usually absent or minimal.
-Clinically: sound tooth structure.
-Vitality test: require higher stimulation on electric pulp tester.
-Palpation/percussion: normal response unless there's periodontal involvement.
-Radiograph: normal picture/some widening in PDM space in advanced stages.

Figure 3: Histopathologic picture of chronic pulpitis

C- Hyperplastic pulpitis:
Definition: Chronic inflammatory response of pulpal connective tissue, characterized by
overgrowth of granulomatous C.T into the carious cavity.
Diagnosis:
Clinically:
-Pain: usually absent or minimal but the patient may complain of bleeding from the affected
tooth.
-Clinically: Over growth of granulomatous tissue, easily bleed, into the carious cavity usually in
the first permanent molar of young-aged patient.
-Vitality test: pulp responds to vitality testing.
-Palpation/percussion: normal response unless there's periodontal involvement.
-Radiograph: normal picture/some widening in PDM space in advanced stages.
Histopathology: (figure 4)
Chronic inflammatory response characterized by the presence of granulation tissue.
The granulation tissue composed of:
a. Fibroblast, collagen fibers and Blood vessels.
b. Infiltrated by chronic inflammatory cells as lymphocytes, plasma cells and macrophages.
The resulted polyp is lined by stratified squamous epithelium from the oral mucosa
Figure 4: Histopathologic picture of chronic hyperplastic pulpitis

4) Pulp necrosis:
Definition: Death of pulp tissue.
Diagnosis
-Pain Usually absent, unless seen in flare-up
-Clinically Sound, carious or discolored tooth.
-Vitality Negative or false positive response
-Palpation/percussion: Negative unless flare-up of apical lesion occurred.

II- Pulp Degenerative Diseases

1. Atrophy
Definition: Decreased pulp size
Etiology:
1. Normal aging process as with continuous formation of cementum leads to decrease in
diameter of the apical foramen with decrease in blood supply to the pulp.
2. Pulp capping.
3. Caries and trauma.
4. Persistent irritation.
Histopathology :
The cellular elements decreases while the collagen fibers increases.

2- Pulpal calcification:
Definition:
It is a deposition of calcium salts in dead or degenerated tissue, so that pulpal calcification may
be physiologic or pathologic process.
Types of pulpal calcification:
1. Dystrophic calcification: Pulp stones or Denticles
2. Diffuse calcification
*Pulp stones:
Pulp stones may present in the pulp chamber or in the root canal.
Classification:
A-according to location (in relation to dentin wall):
Free
Attached
Embedded
B-according to composition:
True stone
False stone
Histopathology:
- True pulp stones are composed of dentin as a result of detached dentinoblast, or
fragments of epithelial root sheath of Hertwig which may stimulate the undifferentiated
mesenchymal cells to form odontoblast.
- False stone formed of calcium salts, which are deposited in a dead or degenerated tissue.
* Diffuse calcification (calcific metamorphosis):
Definition:
Partial or complete obliteration of the pulp chamber by excessive deposition of mineralized
tissue on the dentin walls.
Diagnosis:
Clinical
-Give yellow crown
-Pain threshold to thermal & electrical stimuli or the tooth may be unresponsive.
-Normal palpation & percussion
Radiographic: Various degrees of radiographic obliteration (figure 5)

Figure 5: Radiograph showing diffuse calcification of the upper central incisors

3- Internal resorption:
Definition: Destruction of pre-dentin and dentin.
Clinical:
-Most cases are asymptomatic.
-If the internal resorption occurs in the pulp chamber, the crown of the tooth appears
clinically as having Pink Spot.
Radiograph:
Irregular enlargement in root canal space.(figure 6)

Figure 6: Radiographs showing internal resorption

 Periapical Diseases
Classification of periapical diseases:
1. Acute apical periodontits(AAP)
2. Acute apical abscess (AAA)

3. Chronic apical periodontitis (cap)

4. Chronic apical abscess(CAA)
5. Phoenix abscess
6. Periapical osteosclerosis (Condensing osteitis)

7. Periapical granuloma
8. Periapical or radicular cyst

1. Acute Apical Periodontitis:

Clinically; sensitivity on percussion, tooth felt in supra occlusion
Vitality: occur in vital or non-vital tooth
Radiographically: Widening of periodontal membrane space (figure 7)
Histopathology:
-Hyperemia, vascular congestion and edema.
-Extravasation of PMN by chemotactic factors
Treatment:
-Vital tooth; removal of the cause; removal of premature contact
-Non-vital; root canal treatment

Figure 7: Radiograph showing widening of the periodontal membrane space

2. Acute Apical Abscess:

Clinically:
-Severe, localized, throbbing pain continously.
-Raised temperature and malaise
Percussion/Palpation: positive
Radiographically: Widening of periodontal membrane space
Vitality test: non vital
Histopathology:
-Zone of necrosis; vascular congestion - neutrophil infiltration pus
-Zone of inflammation; fluid exudate - macrophages
-Zone of proliferation; granulation tissue - chronic inflammatory cells

3. Chronic Apical Periodontitis:

Clinically;
-Teeth do not respond to pulp sensitivity tests
-Tenderness to biting is mild
-Tenderness may be noted to palpation over the root apex
Radiographically: varies from minimal widening of periodontal ligament space to large area of
periapical radiolucency
Histopathology: Granulomatous tissue with infiltrate cells, fibroblasts.

4. Chronic Apical Abscess:

Etiology:
-low grade long lasting infection.
-Following acute apical pathosis

5. Phoenix Abscess:
Definition: Acute exacerbation of pre-existing chronic granulomatous lesion
Etiology: Invasion of chronic PA granuloma by micro-organisms from septic canal.
Clinically;
-Sensitive to percussion and palpation
-Vitality is negative
Radiographically: Large radiolucent area (figure 8)

Figure 8: Radiograph showing large apical radiolucency

 6. Condensing Osteitis (Periapical Osteosclerosis):
Definition: response of periapical bone to low grade long lasting pulp irritants
Etiology: Occurs in young age with chronic pulp inflammation
Histology:
-Osteoblastic hyperactivity
-Dimenished marrow space
Clinically:
-No clinical symptoms,
-Carious exposure
Percussion: negative
Radiographically: Increase radiopacity of PA bone (figure 9)

Figure 9: Radiographic picture of condensing osteitis

7. Periapical Granuloma:
Definition: Advanced chronic apical periodontitis
Etiology: low grade inflammation and increase host resistance
Histopathology:
-Granulation tissue
-Chronic inflammatory cell infiltration
-Fibrous capsule
Clinically: no pain
Percussion: negative
Vitality: negative
Radiographically: radiolucent lesion (figure 10)
Figure 10: Radiograph showing apical radiolucency

8. Periapical Cyst:
Definition:-Sequlae of chronic lesion.
Incidence: 6-55%
Classified into:
a) True cyst.
b) Pocket cyst.
Histopathology:
Treatment:?