Bacterial portals to pulp: caries (most common source), exposed dentinal tubules (tubule permeability ↓ by dentinal fluid, live odontoblastic processes, tertiary and peritubular dentin)

1.        Vital pulp is very resistant to microbial invasion but necrotic pulps are rapidly colonized

2.        Rarely does periodontal disease → pulp necrosis

3.        Anachoresis: microbes carried in blood to area of inflammation where they establish infection

Caries → pulp disease: infecting bacteria are immobile, carried to pulp by binary fission, dentinal fluid movement

1.        Smooth surface and pit and fissure caries: S. mutans (important in early caries) and S. sobrinus

2.        Root caries: Actinomyces spp.

3.        Mostly anaerobes in deep caries. 

4.        Once pulp exposed by caries, many opportunists enter (e.g., yeast, viruses) → polymicrobial infection

Pulp reaction to bacteria: non-specific inflammation and specific immunologic reactions

1.        Initially inflammation is a chronic cellular response (lymphocytes, plasma cells, macrophages) → formation of peritubular dentin (↓ permeability of tubules) and often tertiary dentin (irregular, less tubular, barrier)

2.        Carious pulp exposure → acute inflammation (PMN infiltration → abscess formation).  Pulp may remain inflamed for a long time or become necrotic (depends on virulence, host response, circulation, drainage, etc.)

Endodontic infections: most commonly Prevotella nigrescens; also many Prevotella & Porphyromonas sp.

1.        Actinomyces and Propionibacterium species can persist in periradicular tissues in presence of chronic inflammation; they respond to RCT but need surgery or abx to resolve infection

2.        Streptococcus faecalis is commonly found in root canals requiring retreatment due to persistent inflammation

Root canal ecosystem: lack of circulation in pulp → compromised host defense

1.        Favors growth of anaerobes that metabolize peptides and amino acids rather than carbohydrates

2.        Bacteriocins: antibiotic-like proteins made by one species of bacteria that inhibit growth of another species

Virulence factors: fimbriae, capsules, enzymes (neutralize Ig and complement), polyamines (↑ # in infected canals)

1.        LPS: G(-), → periradicular pathosis; when released from cell wall = endotoxin (can diffuse across dentin)

2.        Extracellular vesicles: may → hemagglutination, hemolysis, bacterial adhesion, proteolysis

3.        Short-chain fatty acids: affect PMN chemotaxis, degranulation, etc.; butyric acid → IL-1 production (→ bone resorption and periradicular pathosis)

Pathosis and treatment:

1.        Acute apical periodontitis (AAP): pulpal inflammation extends to periradicular tissues; initial response

2.        Chronic apical periodontitis (CAP): can be asymptomatic (controversial whether bacteria can colonize)

3.        Acute apical abscess (AAA), phoenix abscesses (acute exacerbation of CAP), and suppurative apical periodontitis: all characterized by many PMNs, necrotic tissue, and bacteria

Treatment of endodontic infections: must remove reservoir of infection by thorough debridement

1.        Debridement: removal of substrates that support microorganisms; use sodium hypochlorite (NaOCl) to irrigate canals (dissolves some organic debris in areas that can’t be reached by instruments); creates smear layer

2.        Intracanal medication: recommend calcium hydroxide (greatest antimicrobial effect between appointments) inserted into pulp chamber then driven into canals (lentulo spiral, plugger, or counterclockwise rotation of files) and covered with sterile cotton pellet and temporary restoration (at least 3mm thick)

3.        Drainage: for severe infections to ↓ pressure (improve circulation), release bacteria and products; consider abx

4.        Culturing: rarely needed but if so, sterilize tissue with chlorhexidine and obtain submucosal sample via aspiration with a 16- to 20-gauge needle

Root canal sealers are materials used in endodontics to fill the space between the root canal filling material (usually gutta-percha) and the walls of the root canal system. Their primary purpose is to provide a fluid-tight seal, preventing the ingress of bacteria and fluids, and to enhance the overall success of root canal treatment. Here’s a detailed overview of root canal sealers, including their types, properties, and clinical considerations.

Types of Root Canal Sealers

1. Zinc Oxide Eugenol (ZOE) Sealers

   • Composition: Zinc oxide powder mixed with eugenol (oil of cloves).
   • Properties:
     • Good sealing ability.
     • Antimicrobial properties.
     • Sedative effect on the pulp.
   • Uses: Commonly used in conjunction with gutta-percha for permanent root canal fillings. However, it can be difficult to remove if retreatment is necessary.

2. Resin-Based Sealers

   • Composition: Composed of resins, fillers, and solvents.
   • Properties:
     • Excellent adhesion to dentin and gutta-percha.
     • Good sealing ability and low solubility.
     • Aesthetic properties (some are tooth-colored).
   • Uses: Suitable for various types of root canal systems, especially in cases requiring high bond strength and sealing ability.

3. Calcium Hydroxide Sealers

   • Composition: Calcium hydroxide mixed with a vehicle (such as glycol or water).
   • Properties:
     • Biocompatible and promotes healing.
     • Antimicrobial properties.
     • Can stimulate the formation of reparative dentin.
   • Uses: Often used in cases where a temporary seal is needed or in apexification procedures.

4. Glass Ionomer Sealers

   • Composition: Glass ionomer cement (GIC) materials.
   • Properties:
     • Good adhesion to dentin.
     • Fluoride release, which can help in preventing secondary caries.
     • Biocompatible.
   • Uses: Used in conjunction with gutta-percha, particularly in cases where fluoride release is beneficial.

5. Bioceramic Sealers

   • Composition: Made from calcium silicate and other bioceramic materials.
   • Properties:
     • Excellent sealing ability and biocompatibility.
     • Hydrophilic, allowing for moisture absorption and expansion to fill voids.
     • Promotes healing and tissue regeneration.
   • Uses: Increasingly popular for permanent root canal fillings due to their favorable properties.

Properties of Ideal Root Canal Sealers

An ideal root canal sealer should possess the following properties:

• Biocompatibility: Should not cause adverse reactions in periapical tissues.
• Sealing Ability: Must provide a tight seal to prevent bacterial leakage.
• Adhesion: Should bond well to both dentin and gutta-percha.
• Flowability: Should be able to flow into irregularities and fill voids.
• Radiopacity: Should be visible on radiographs for easy identification.
• Ease of Removal: Should allow for easy retreatment if necessary.
• Antimicrobial Properties: Should inhibit bacterial growth.

Clinical Considerations

• Selection of Sealer: The choice of sealer depends on the clinical situation, the type of tooth being treated, and the specific properties required for the case.
• Application Technique: Proper application techniques are crucial for achieving an effective seal. This includes ensuring that the root canal is adequately cleaned and shaped before sealer application.
• Retreatment: Some sealers, like ZOE, can be challenging to remove during retreatment, while others, like bioceramic sealers, may offer better retrievability.
• Setting Time: The setting time of the sealer should be considered, especially in cases where immediate restoration is planned.

Conclusion

Root canal sealers play a vital role in the success of endodontic treatment by providing a seal that prevents bacterial contamination and promotes healing. Understanding the different types of sealers, their properties, and their clinical applications is essential for dental professionals to ensure effective and successful root canal therapy.

Cracked tooth syndrome denotes an incomplete fracture of a tooth with a vital pulp. The fracture involves enamel and dentin, often involving the dental pulp.

Prevalence
Molars of older individuals most frequently present with cracked tooth syndrome. Most cases occur in teeth with class I restorations (39%) or in those that are unrestored (25%), but with an opposing plunger cusp occluding centrically against a marginal ridge. Mandibular molars are most commonly affected , followed by maxillary molars and maxillary premolars.

Symptoms
The patient usually complains of mild to excruciating pain at the initiation or release of biting pressure. Such teeth may be sensitive for years because of an incomplete fracture of enamel and dentin that produces only mild pain. Eventually, this pain becomes severe when the fracture involves the pulp chamber also. The pulp in these teeth may become necrotic.

Clinical features

Close examination of the crown of the tooth may disclose an enamel crack, which may be better visualized by using the following methods:

Fiber optic light: this is used to transilluminate a fracture line. Most cracks run mesiodistally and are rarely detected radiographically when they are incomplete.

Dye: Alternatively, staining the fractute with a dye, such as methylene blue, is a valuable aid to detect a fracture.

Tooth slooth: this is a small pyramid shaped plastic bite block, with a small concavity at the apex of the pyramid to accommodate the tooth cusp. This small indentation is placed over the cusp, and the patient is asked to bite down. Thus, the occlusal force is directed to one cusp at a time, exerting the desired pressure on the questionable cusp.