History of Endodontics aae/abe

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Antibiotic Susceptibility

Baumgartner/Xia – (98 strains isolated from 12 endo abscesses – aspirational)

  1. Pen VK 1st choice - 85% effective – NARROW Spectrum

  2. Amoxicillin - 91% effective (broader spect./rapid absorp/longer ½ life)

  3. Amox + Clavulanic acid (Augmentin) - 100% effective

  4. Clindamycin - 96% effective

  5. Metronidazole - 45%*

  6. Metro + Pen V - 93%, Metro + Amox - 99% ( 8%)

*Metronidazole - Effective only on obligate anaerobic bacteria

Pen VK – Effective on Facultative & Obligate Anaerobes

Clindamycin – More effective on Gram + Facultative & Obligate Anaerobes

Note: Amoxicillin or Augmentin used in Immunocompromised patients due to broader spectrum, rapid absorption, longer ½ life, and higher serum levels

Antibiotic effect on Oral Contraceptives

Hersch – only effected by Rifampin, but still advise patient to use alternate BC due to legal issues.

Are bacteria present in traumatized teeth with intact crowns?


  1. Bergenholtz - found bacteria 64% of the time - mixed anaerobic infection, penetrated thru tubules or cracks

  1. Tronstad/Langeland – Bacteria gaining access to necrotic pulp via enamel/dentin cracks (trauma) establish infection within 2-3 weeks

  1. Love 1996In vitro, traumatized incisors - Bacterial penetration of trauma induced enamel/denin cracks  pathway for development of infections in devitalized pulps of intact crowns subjected to trauma

Does Anachoresis occur?

Anachoresis = bacterial infection of traumatized pulp via bacterial invasion of blood vessels from adjacent PDL/sulcus


  1. Robinson/Bolling – 2 requirements: pulpal inflammation & bacteria

  1. Gier/Mitchell 1968– Bacteria are attracted to inflamed pulps. Traumatized teeth – bacteria invade lymphatics/vascularture via periodontium infect pulp

  1. Tziafas 1989 – Dog study; Pulp exposures/CaOH2/Induced bacteremia (-streptococci) – 24/27 teeth infected,  Inflamm. Zone, Bacterial infection; Non-inflammed pulp-no infection; did NOT I.D. bacteria!


  1. Delivanis/Doyle – Could NOT demonstrate bacteria in unfilled root canals after repeated intravenous injections of bacteria

Focal Infection – Does it occur today?

Wahl - defines focal infection as “a localized or generalized infection caused by dissemination of microorganisms or toxic products from a focus of infection”.
Focal infection” term coined by WD Miller 1891 - found gangrenous pulps could act as centers of infection causing alveolar abscesses

William Hunter 1900 - Attributed a multitude of diseases to “oral sepsis”  EXT

Billings 1912 - Introduced “focal infection” theory to USA
No definitive evidence bacteremia causes systemic disease!

Pallasch; Ehrmann – Focal Infection theory does not exist, NSRCT least likely dental treatment to produce significant bacteremia (Pallasch)

Siqueira – No evidence that organisms from NSRCT cause disease in remote sites

TorabinejadChronic AP lesions can not cause systemic diseases via immune complexes
Premedicate those susceptible to infective endocarditis

Methods of Bacterial Identification

  1. Culturing: Aerobic, Anaerobic, excludes VBNC species

  2. Molecular Methods:

    1. Broad Range PCR

    2. Pyrosequencing

    3. DNA-DNA hybridization (eg: Checkerboard arrays, microarrays)

    4. Species specific PCR

    5. Nested PCR

    6. Mulitplex PCR

    7. Real time Quantitative PCR (qPCR)


Peripheral Sensitization
Peripheral Sensitization = Increased excitability of pulpal nociceptors due to inflammation and pro-inflammatory mediators
Direct Activators of Peripheral Nociceptors:




Sensitizers of Peripheral Nociceptors:



NGF – nerve growth factor

SP - neuropeptide


Peripheral Sensitization (Triad)

  1. Hyperalgesia = Increased/Prolonged response to noxious suprathreshold stimuli, aka after-firing

  2. Allodynia = Decreased threshold for AP  response to non-noxious stimuli

  3. Spontaneous pain

Sessle 2005 – Peripheral sensitization of afferent nocicptive endings is associated with a decreased threshold for generation of AP (Allodynia), increased responsiveness to noxious stimuli (Hyperalgesia), and spontaneous activity
Hargreaves 1991 – Peripheral sensitization (Hyperalgesia) is mediated by inflammatory mediators. Results in Triad of Spontaneous APs, Decreased threshold for AP (Allodynia), and Prolonged response to noxious stimuli (Hyperalgesia)
NarhiArterial pressure following heartbeat (non-noxious stimuli) stimulates sensitized nociceptors to fire = “throbbing” pain

Central Sensitization

Sessle 2005/2011, Hargreaves 1991

  1. Central sensitization - Afferent C fiber barrage secondary to peripheral sensitization/activation may lead to an Increased Receptive field and Recruitment of long range fibers in Medullary dorsal horn; Plasticity of central neurons – Sprouting and Unmasking of 2nd order neurons

  1. Trigeminal brain stem complex - somatotopically arranged: main sensory nucleus, spinal trigeminal nuclear tract (subnuclei: oralis, interpolaris, caudalis aka Medullary dorsal horn)

  1. Interneurons (local circuit neurons) - inhibitory (GABA) or excitatory

  1. Decending pathways - Down regulation by opioid pathways (Enkephalins, GABA) in Periaqueductal Gray (PAG)/Nuclear Raphe Magnus (NRM) of brainstem

Pain Pathways

Detection, Processing, and Perception of Pain – Trigeminal nociceptive afferents


1st order neuron - Peripheral pulpal tissue -> Trigeminal ganglion (1º cell body) -> Medullary dorsal horn (Subnucleus Caudalis) of spinal trigeminal nuclear tract (brainstem)

Processing: (Trigeminothalamic tract)

2nd order neuron - Medullary dorsal horn of spinal trigeminal nuclear tract (2º cell body) -> Thalamus (contralateral due to crossing midline while ascending)

Perception: (Thalamocortical tract)

3rd order neuron – Thalamus (3º cell body) -> Cerebral cortx/higher centers

Pain Pathways

  1. Holland/Michaelson – Silent pulpitis leads to pulpal necrosis (40-60%)

  1. Jaber/Dionne - opioid receptors present peripherally within the pulp

  1. Wadachi/Hargreaves 2006 – Direct activation of peripheral nociceptors – TRPV1 C fiber pulpal nociceptors express TLR4 and CD14 receptors (PRRs = Pattern Recognition Receptors) which react to LPS

  1. Narhi – peripheral inflammatory cells contain endogenous opioids and somatostatin that can inhibit nociceptor AP generation

  1. Mudie/Holland – peripheral lymphocytes contain endorphins

Opioids mimic Endogenous Opioids – act centrally at level of spinal trigeminal nuclear tract and peripherally

Referred Pain
Sessle 2005Convergence theory: Superficial and Deep 1st order neurons synapse with the same WDR and NS 2nd order neuron cell bodies within the medullary dorsal horn of the spinal trigeminal nuclear tract. Afferent barrage leads to increased receptive field/activation of long range neurons/central sensitization (central neuroplasticity – sprouting and umasking of 2nd order neurons) and inability of higher levels to determine pain specific location
Falace 1996 – Referred pain:

  1. Pain severity is the most reliable predictor for referred pain

  2.  intensity of nociceptive barrage,  Referred pain

  3. 89.9% of patients w/ severe pain have referred pain

  4. Most common site = Adjacent tooth (80%)

C fiber stimuation:

See Bender 2000 and Van Hassel 1969

Deafferentation & Chronic Pain
Nixdorf 2010– Meta-analysis of Frequency of Persistent tooth pain post Endodontic procedures, ie: Pulpectomy, NSRCT, Retx, Endodontic microsurgery, (6 months or >): 5.3% (>7% in well-controlled studies). (Pain = spontaneous pain or percussion, palpation, or bite induced pain)
Holland – Deafferentation and chronic pain – Possible neuroma formation of periapical nerve fibers due to inflammation of periapical tissues at time of re-organization/healing following RCT
Sessle/Hu – Cat study, post RCT pain - Deafferenation (pulpotomy)   Receptive Field +  Spontaneous Firing = Central neuroplastic changes & Chronic Pain. (Neuroplastic changes = unmasking and nerve sprouting)
Nixdorf 2010 – Meta-analysis of Frequencey of Persistent (> 6months) dento-alvoelar pain of non-odontogenic origin post Endodontic treatment: 3.4%
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