Diseases of the Pulp

Pulp Introduction

The dental pulp consists of vascular connective tissue contained within the rigid dentin walls. It is the principal source of pain in the oral cavity and also a major site of attention in endodontics and restorative procedures. This, knowledge of pulp is essential not only for providing dental treatment but also to know the rationale behind the treatment provided.

Read And Learn More: Endodontics Notes

Important features of pulp:

• It is a coherent soft tissue, surrounded by dentin which limits the area for expansion and restricts its ability to tolerate
  edema.
• Odontoblasts present in the pulp have the ability to form dentin in response to caries and irritants.
• Pulp has an almost total lack of collateral circulation. This limits its ability to cope with bacteria, necrotic tissue, and inflammation.
• It gives a radiographic appearance as a radiolucent line.

Periapical Tissue Diseases

Etiology Of Pulpal Diseases

Classification of etiology according to WEINE beginning with the most common irritant

1. Bacterial:

The most common cause of pulpal injury is bacteria or their by-products which may enter the pulp through a break in dentin from

• Caries
• Accidental exposure
• Fracture
• Percolation around a restoration
• Extension of infection from gingival sulcus
• Periodontal pocket and abscess

Periapical Tissue Diseases

• Anachoresis (a process by which microorganisms get carried by the bloodstream from another source and localize on inflamed tissue)

2. Traumatic:

• Acute trauma like fracture, luxation, or avulsion of tooth
• Chronic trauma including parafunctional habits like bruxism

Radicular Cyst

3. Iatrogenic:

Pulp inflammation resulting from the clinician’s own procedures is referred to as entactogenic pulpitis. Iatrogenic causes of pulp pathologies can be

• Thermal changes are caused during tooth preparation, restoration, bleaching of enamel, electrosurgical procedures, etc.
• Orthodontic movement
• Periodontal curettage
• Periapical curettage
• Use of chemicals like temporary and permanent
• restorations, liners, bases, and use of cavity desiccants such as alcohol

Radicular Cyst

4. Idiopathic:

• Aging
• Resorption; internal or external

Radiation injury to pulp:

• Pulp cells exposed to ionizing radiation may become necrotic, and show vascular damage and the interference in mitosis of cells.
• Irradiation affects salivary glands resulting in decreased salivary flow, thereby increasing predisposition to dental caries and pulpal involvement.
• Effects of radiation damage to teeth depend on the dose, source, type of radiation, exposure factor, and stage of tooth development at the time of irradiation.

Progression Of Pulpal Pathologies

Pulp reacts to above mentioned irritants the same as other connective tissues. A normal pulp gives a mild-to-moderate response to pulp tests and this response subsides on the removal of stimulus. The degree of inflammation is proportional to the intensity and severity of the tissue damage.

For example, slight irritation like incipient caries or shallow tooth preparation causes little or no pulpal inflammation, whereas extensive operative procedures may lead to severe pulpal inflammation.

Depending on the condition of the pulp, severity, and duration of the irritant, and host response, the pulp may respond from mild inflammation to pulp necrosis. These changes may not be accompanied by pain and thus may proceed unnoticed.

Pulpal reaction to microbial irritation

Microorganisms present in carious
enamel and dentin
↓
Penetration of microorganisms in deeper
layers of carious dentin
↓
Pulp is affected before the actual invasion of bacteria via their toxic by-products
↓
By-products cause local chronic cell infiltration
↓
When actual pulp exposure occurs, pulp tissue gets locally infiltrated by PMNs to form an area of liquefaction necrosis at the site of exposure
↓
Eventually, necrosis spreads all across the pulp and periapical tissue resulting in severe inflammatory lesions

Pulp Inflammation and Its Sequelae:

The traditional theory which explained pulpal inflammation and its sequelae was referred to as strangulation theory. Strangulation theory is no longer accepted and a current theory explains the sequelae of pulpal inflammation.

Strangulation Theory:

It says that on irritation, there is local inflammation in the pulp, which results in vasodilation, increased capillary pressure, and permeability. These results in increased filtration from capillaries into tissues, thus increasing tissue pressure. By this, thin vessel walls get compressed resulting in decreased blood flow and increased venous pressure.

This results in a vicious cycle, because the increase in venous pressure further increases capillary pressure. Consequently, choking/strangulation of pulpal blood vessels occur because of increased tissue pressure. This results in ischemia and further necrosis.

Current Theory:

Many studies have shown that an increase of pressure in one area does not affect the other areas of the pulp. Therefore local inflammation in pulp results in increased tissue pressure in inflamed area and not the entire pulp cavity.

It is seen that injury to coronal pulp results in local disturbance, but if the injury is severe, it results in complete stasis of blood vessels in and near the injured area. Net absorption of fluid into capillaries in adjacent uninflamed areas results in increased lymphatic drainage thus keeping the pulpal volume almost constant.

A limited increase in pressure within the affected pulpal area is explained by the following mechanism:

• Increased pressure in inflamed areas favors the net absorption of interstitial fluids from adjacent capillaries in uninflamed tissues.
• Increased interstitial tissue pressure lowers the transcapillary hydrostatic pressure difference, and thus opposes further filtration.
• Increased interstitial fluid pressure increases lymphatic drainage.
• Break in the endothelium of pulpal capillaries facilitate the exchange mechanism.

Infectious sequelae of pulpitis include apical periodontitis, periapical abscess/cellulitis, and osteomyelitis of the jaw. Spread from maxillary teeth may cause purulent sinusitis, meningitis, brain abscess, orbital cellulitis, and cavernous sinus thrombosis. Spread from mandibular teeth may cause Ludwig’s angina, parapharyngeal abscess, mediastinitis, pericarditis, and empyema

Diagnosis Of Pulpal Pathology

1. Subjective symptoms: Most common symptom is pain

2. Objective symptoms:

• Visual and tactile inspection—3Cs
  • Color
  • Contour
  • Consistency
• Thermal tests:
  • Heat tests: Use of
    • Warm air
    • Hot water
    • Hot burnisher
    • Hot gutta-percha stick
  • Cold tests:
    • Ethyl chloride spray
    • Ice pencils
    • CO 2 snow (temperature −78°C)
• Electrical pulp testing
• Radiographs
• Anesthetic tests
• Test cavity

Recent advances in diagnostic aids for pulp pathologies include

3. Laser Doppler flowmetry

4. Liquid crystal testing

5. Hughes probe camera

6. Infrared thermography

7. Thermocouples

8. Pulse oximetry

9. Dual wavelength spectrophotometry

10. Plethysmography

11. Xenon-133 radioisotopes

Classifiation Of Pulpal Pathologies

Grossman’s Clinical Classification:

1. Pulpitis: Inflammatory disease of the dental pulp

• Reversible pulpitis
• Irreversible pulpitis
  • Symptomatic irreversible(previously known as acute irreversible pulpitis)
  • Asymptomatic irreversible(previously known as chronic irreversible pulpitis)
  • Hyperplastic pulpitis
  • Internal resorption

2. Pulp degeneration

• Calcifi (radiographic diagnosis)
• Atrophic (histopathological diagnosis)
• Fibrous

3. Necrosis

Baume’s Classifiation

Based on clinical symptoms:

• The asymptomatic, vital pulp which has been injured or involved by deep caries for which pulp capping may be done.
• Pulp with a history of pain which is amenable to pharmacotherapy.
• Pulp was indicated for extirpation and immediate root filling.
• Necrosed pulp involving infection of radicular dentin
  accessible to antiseptic root canal therapy.

Seltzer and Bender’s Classification:

Based on clinical tests of pulp and histological diagnosis:

Treatable without Pulp Extirpation and Endodontic Treatment

• Intact uninflamed pulp
• Transition stage
• Atrophic pulp
• Acute pulpitis
• Chronic partial pulpitis without necrosis

Untreatable without Pulp Extirpation and Endodontic Treatment

1. Chronic partial pulpitis with necrosis
2. Chronic total pulpitis
3. Total pulp necrosis

Ingle’s Classification:

1. Inflammatory Changes

• Hyper-reactive pulpalgia
  • Hypersensitivity
  • Hyperemia
•  Acute pulpalgia
  • Incipient (may be reversible)
  • Moderate (may be referred)
  • Advanced (relieved by cold)
• Chronic pulpalgia
• Hyperplastic pulpitis
• Pulp necrosis

2. Retrogressive Changes

• Atrophic purposes
• Calcifi purposes