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Endodontic microbiology (Pathways of Infection: (Developmental anomalies,…

- - - - Normal mice had:
        
        Pulpal necrosis
        
        Periapical granulomas and abscesses
      - Germ free mice:
        
        No necrosis
        
        No periapical inflammation
        
        Dentinal bridge @ site of exposure
  - - - after 7 mos no periapical inflammation
    - - Periapical inflammation
- - - - Extra-cusp or bump on the posterior teeth
        
        are equivalent to each other, both can be worn away from occlusion and the pulpal extensions can be exposed leading to pulpal necrosis or periapical disease
    - - Enlarged cingulum on anterior teeth
    - - infolding of enamel into dentin, most commonly seen in maxillary lateral incisors
        
        Tooth affected by this condition has a higher risk of developing caries and periradicular pathology. The thin layer of the infolding enamel could be chipped off easily, providing entrance for microorganisms into the tooth canal. This can cause abscess formation
  - - - no recent evidence for this
        
        The main pathway of pulpal infection in traumatic injuries is from the gingival sulcus through dentinal exposure as result of enamel cracks or the microvasculature of the traumatized PDL
- - - - During tx
        
        Leaking rubber dam
        
        Contaminated instruments (endo)
        
        Remnants of caries, dental plaque, calculus on the crown
        
        Undetected crack
      - B/w apps
        
        Fracture of tooth or restoration
        
        Tooth left open for drainage
        
        Leakage via temporary restoration
        
        Defective coronal restoration/old filling
      - After RC filling
        
        Fracture of tooth
        
        Recurrent decay
        
        Fracture/loss of temp/ permanent restoration
        
        Undetected crack
        
        Leakage through temp/permanent restoration
        
        Tooth left unrestored/delayed permanent restoration
  - - - Involved microorganisms are remnants of a 1º or 2º infection (failed RCT)
        
        Factors 4 persistent RL
        
        Intraradicular infection
        
        Procedural Mishaps
        
        Missed canals
        
        Inadequate instrumentation
        
        Poor access cavity design
        
        Leaking temporary or permanent restoration
        
        Inadequate aseptic control
        
        Foreign body rxn
        
        Cysts
        
        Extraradicular infection by bacteria of the species (Actinomyces israelii and Propionibacterium propionicum)
        
        Fibrous scar tissue healing**
        
        Healing of bone is slower than healing of CT
        
        CT heals faster than bone –> scar tissue formed in empty space in bone
        
        Take MHx, sometimes RL is fibrotic tissue
        
        Microbiology of canals
        
        Gram + facultative bacteria particularly E. Faecalis are predominant
        
        Can survive + reproduce in highly alkaline environments
        
        Calcium hydroxide is ineffective b/c E.faecalis can endure pH around 11.5, E Faecalis contains cell wall associated H+ pump that keeps cytoplasm acidic
        
        Natural buffering capacity of dentin also helps to protect this bacterium
        
        Resistant to antibiotics
        
        Can survive prolonged periods of starvation
        
        Grows in anaerobic + aerobic conditions
        
        Frequently isolated in cases of persistent apical periodontitis
        
        Adhesion and penetration into dentinal tubules to escape from intracanal instrumentation and irritants
        
        Fungi like C. albicans present here > than in 1º infections
        
        they can overgrow after inefficient intracanal antimicrobial procedures
        
        Survive as monoinfection
        
        Grow and invade dentin
        
        Candida may resist CaOH which may be a factor for selection of Candida in persistent RC infections
        
        NaOCl and EDTA are effective at killing Candida
        
        1 or a few species
      - Clinically indistinguishable can cause:
        
        Persistent exudation
        
        Persistent symptoms
        
        Inter appointment exacerbations
        
        Failure of endo (characterized by persistence of apical periodontitis lesion)
  - - - Obligate anaerobic bacteria
      - Gram - (porphyromonas spp., Prevotella, Fusobacterium, Treponema)
      - 10-30 species
      - Some Gram + (actinomyces, lactobacillus, streptococcus)
      - Polymicrobial nature
      - Teeth with long standing infections and large lesions harbour more bacterial species and have a higher density of bacteria in their RCs than teeth with small lesions
  - - - Periapical Cysts/pocket cysts (communication with the canal)
      - Extruded material/contaminated dentin debris
        
        increase likelihood of transferring bacteria to PA tissues
      - Acute apical Abscess
      - Periapical Actinomycosis
        
        independent extraradicular infection
        
        Can also be found in RC of re-tx teeth, possibly from a communication b/w periapical tissues and RC
        
        Actinomyces israelii is the most prevalent isolated from human abscesses
        
        Properties
        
        Resistance to antimicrobials used in endo tx
        
        Ability to grow in mono-infections
        
        Growth pattern of cohesive filaments or chains that escape PMN phagocytosis
        
        Ability to evade host response
- - - - resist environmental ∆s
    - - enhanced pathogenicity
    - - possess the ability to self organize
    - - response to environmental ∆s as a unit
        
        cell-cell communication/genetic exchange