3-DentinCaries3.Sınıf24-25_3744fd24e17e387feecc40da511c87f4-1

Dentin Caries Overview

• Definition: Dentin Caries - decay process in dentin, requires understanding of its histology and response to carious lesions.

• Source: Prof. Dr. Bilinç Bulucu, Restorative Dentistry Department

Histology of Dentin

• Dentin Structure:

  • Hard tissue covered by enamel on the crown and cementum on the root.

  • Calcified product formed by odontoblasts lining the inner surface.

  • Dentin Tubules: Extensions (Tomes fibers) of odontoblasts traverse the thickness of dentin, enabling fluid movement and ion transport.

  • Intertubular Dentin: Rigid, bone-like matrix with hydroxyapatite crystals embedded in collagen fibers.

  • Peritubular Dentin: Smooth mineral layer lining the tubules, providing structural integrity.

Clinical and Histologic Characteristics of Dentinal Caries

• Progression of Dentin Caries:

  • Dentin is less mineralized than enamel and contains microscopic tubules, facilitating acid ingress and mineral egress.

  • Caries in dentin have a V-shaped cross-section, spreading rapidly once it penetrates enamel at the DEJ (Dentino Enamel Junction).

  • Pain and Sensitivity:

    • Often, pain is not reported until deep lesions approach the pulp, causing fluid movement through open tubules.

    • Short, sharp pains indicate reversible pulpitis; sustained pain indicates irreversible pulpitis.

Response Mechanisms of the Pulp-Dentin Complex

• Three Levels of Response:

  1. Low-Level Acid Demineralization:

     • Vital pulp can remineralize affected dentin when caries progress slowly.

     • Initial demineralization does not require direct microbial exposure to elicit a response.

  2. Moderate-Intensity Attack:

     • Bacterial invasion leads to degeneration of odontoblasts; resultant dead tracts are identified in affected tubules.

     • Changes include formation of reparative dentin by secondary odontoblasts.

  3. Severe, Rapidly Advancing Caries:

     • High acid production overwhelms defenses, leading to pulp necrosis and abscess formation.

     • Characterized by increased inflammatory response and tissue degeneration.

Zones of Dentinal Caries

• Five Zones in Carious Dentin (clarified in slowly advancing lesions):

  1. Normal Dentin: No bacteria; sharp pain upon stimulation indicates health.

  2. Subtransparent Dentin: Demineralized area; still capable of remineralization but painful on stimulation.

  3. Transparent Dentin: Softer, contains large crystals; capable of self-repair if pulp remains vital.

  4. Turbid Dentin: Bacterial invasion evident; irreversibly denatured collagen and no self-repair capability.

  5. Infected Dentin: Structurally decomposed, heavily infested with bacteria; immediate removal necessary for successful restoration.

Advanced Carious Lesions

• Cavitation occurs as demineralization weakens the enamel surface, enhancing cariogenic plaque retention.

• Necrotic Dentin: Clinically noted for its mushy consistency; requires removal to access deeper infected zones.

• Sclerotic Dentin: Seen as a reparative barrier; less permeability, challenges bonding for restorative materials.

Dentin Management Techniques

• Use of Calcium Hydroxide: Employed in indirect pulp capping for deep lesions to promote healing.

• Stepwise Excavation: A selective carious dentin removal strategy over two stages; aims at environment modification for arrested caries that become inaccessible for bacteria.

• Hydraulic Calcium Silicate Cements (HCSCs): Emerging materials in restorative dentistry noted for bioactivity and moisture-setting capabilities.

Key Terms

• Reparative Dentin: Formed by secondary odontoblasts in response to irritants.

• Pulp Vitality: High blood supply and activity are essential for effective dentin repair or dentinogenesis.

• Affect vs. Infected Dentin: Affected dentin (zones 2 and 3) is soft but retains vitality; infected dentin (zones 4 and 5) requires removal due to bacterial activity.