Dental Anatomy: Dead Tract and Sclerotic Dentin

Dead Tract and Sclerotic Dentin

• Dead tract: a layer of impermeable calcified tissue that seals off the proximal end of tubules near the pulp, protecting the pulp.
• Sclerotic dentin: a mineral deposition in dentinal tubules due to aging or slowly progressing caries, resulting in the gradual occlusion of dentinal tubules and decrease in dentine permeability.
• Characteristics of sclerotic dentin:
  • Shiny, darkly colored, and feels hard to explorer tip.
  • Less sensitive and more protective of the pulp against subsequent irritations.
  • Often found under old restorations, which show a great amount of discoloration.

Sclerotic Dentin Formation

• Sclerosis can occur due to aging (physiologic dentin sclerosis) or irritation (reactive dentin sclerosis).
• Peritubular dentin becomes wider and thicker as tubules are filled and obliterated with calcifying minerals.
• Continued intratubular mineralization of dentin may result in complete obturation of the tubules.

Clinical Appearance of Sclerotic Dentin

• Sclerotic dentin appears translucent under the light microscope due to a reduction in light scattering through the affected tissue.
• It is referred to as the translucent or transparent dentin or zone.

Tertiary Dentin (Reparative Dentin, Reactionary Dentin, or Irregular Secondary Dentin)

• Tertiary dentin is classified into reactionary dentin and reparative dentin.
• Reactionary dentin: formed by surviving post-mitotic odontoblast cells as a reaction to stimuli such as caries.
• Reparative dentin: formed by odontoblast-like cells differentiated from stem cells of the pulp in response to rapid caries progression.

Characteristics of Tertiary Dentin

• Reactionary dentin:
  • Outcome of odontoblastic response to irritation caused by dental abrasion, attrition, cavity preparation, erosion, or dental caries.
  • Modified atubular dentinal matrix with altered biochemical properties.
• Reparative dentin:
  • Confined to the localized irritated area of the pulp cavity wall.
  • Structure is more often irregular, atubular dentin depending on the severity of the stimulus.
  • A defense reaction localized to the area of injury.

Infected Dentin

• Very softened and contaminated with bacteria.
• Includes the superficial necrotic dentin tissue or zone.
• Clinically, necrotic dentin is a wet, mushy, easily removable mass.

Affected Dentin

• Softened (demineralized) dentin due to the acidic products of bacteria present in the superficial infected layer of the carious lesion.
• Not invaded by bacteria and has intact tubules containing odontoblastic processes.
• Capable of remineralization, provided the pulp remains vital.

Hyperemia

• A physiologic term meaning an increase in blood flow through tissue.
• Histologically, dilated and congested vessels were seen.
• The pulp could not be inflamed.

Acute Pulpitis

• Occurs as a sequent to various operative procedures including mechanical pulp exposure, also following deep scaling and curettage.
• Always an acute reaction develops beneath the affected dentinal tubules.
• Histologic changes associated with inflammation:
  • Odontoblast cells may be destroyed or ruptured by edema.
  • Increased eosinophilia of the connective tissue.

Characteristics of Acute Pulpitis

• Marked dilatation of lymphatics and blood vessels.
• Infiltration of leukocytes is soon evident around the dilated vessels.
• Clinical manifestation is mild pain during hot and/or cold application, which remains as long as the stimulus remains.
• Categorized as reversible pulpitis, as the pulp can reverse to a healthy condition due to the absence of partial necrosis and if the stimulus is removed.

Chronic Total Pulpitis with Partial Necrosis

• Develops with the extension of the inflammation to involve the entire pulp tissue (coronal and radicular) due to the persistence of the irritant and the development of liquefaction necrosis within the inflammatory area or coagulation necrosis.
• Clinical manifestation is severe pain, sometimes lasting for many hours or when the patient sleeps, which increases the pressure inside the pulp and causes throbbing pain.
• Categorized as irreversible pulpitis, as the pulp is not able to reverse to a healthy condition due to the presence of partial necrosis.

Total Necrosis of the Pulp

• The pulp in which the cells have died as a result of coagulation or liquefaction necrosis.
• Treatment of choice is root canal treatment or tooth extraction.

Acute Pulpitis Superimposed on Chronic Pulpitis

• Severe pain, especially at night, until the abscess is formed, then there's slight relief but not complete relief unless drainage is done through the tooth (access opening) or surgical incision with antibiotic cover.
• Treatment is continued by root canal treatment or extraction.

Defense Mechanisms of the Dentino-Pulp Complex

• The dentine and pulp should be considered as one vital organ, similar in development, structure, and function.
• The reaction of the pulp and dentin to injury is mainly related to the activity of odontoblast cells.

Types of Dentin

• Reparative Dentin (Tertiary Dentin)
  • Formed by odontoblast-like cells differentiated from stem pulp cells after the death of primary odontoblasts.
  • Structured as irregular, atubular dentin, depending on the severity of the stimulus.
  • A defense reaction localized to the area of injury.
• Infected Dentin
  • Softened and contaminated with bacteria.
  • Includes the superficial necrotic dentin tissue or zone.
  • Clinically, it appears as a wet, mushy, and easily removable mass.
• Affected Dentin
  • Softened (demineralized) dentin due to the acidic products of bacteria.
  • Has intact tubules containing odontoblastic processes with a porous surface and containing crystalline material.
  • Capable of remineralization, provided the pulp remains vital.

Reduced Dentin Permeability

• Caused by the diffusion of plasma proteins into the dentinal tubules.
• Factors contributing to intratubular occlusion include:
  • Coagulation of plasma proteins (fibrin) from pulpal blood vessels in the tubules.
  • Pathological precipitation of intratubular materials (e.g., mineral deposits, collagen fibrils, proteoglycan linings, and bacteria).
  • Formation of a smear layer of dentine debris on the cut surface during cavity preparation.

Dead Tracts

• Regions of empty tubules in primary dentin resulting from degeneration of the odontoblastic process.
• Often found under most carious cavities.

Inflammatory Conditions of the Pulp

• The status of the pulp must be determined with accuracy to select the proper treatment.
• Inflammation is a protective response, but it may destroy normal cells as well as foreign substances.
• The pulp has a compromised blood supply, making it unable to cope with severe damage.
• The status of the pulp in response to injury progressively worsens:
  1. Healthy pulp
  2. Hyperemia
  3. Acute pulpitis
  4. Chronic partial pulpitis (without necrosis)
  5. Chronic partial pulpitis (with necrosis)
  6. Chronic total pulpitis with partial necrosis
  7. Total necrosis of the pulp
  8. Acute pulpitis superimposed on chronic pulpitis