History of Endodontics aae/abe



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Inflammatory Mediators


Main objectives of pro-inflammatory mediators:

  1. Vasodilation and Increase Vascular Permeability

  2. Recruit/Activate Inflammatory cells (PMN, Mast cells, Macrophages, Lymphocytes, Bradykinin) & Complement system (C3a, C5a)

  3. Sensitize/Activate Nociceptors

Vasodilation


  1. Histamine – Mast cells (stimulated by C3a, SP, CGRP), Platelets

  2. Prostaglandins (Prostacyclin) – All leukocytes, Mast cells (COX pathwy)

  3. CGRP – Pulpal nociceptors

Increased Vascular Permeability

  1. Bradykinin – Plasma activated through kinin system cascade

  2. Leukotrienes – All leukocytes, Mast cells (LIPOX)

  3. C3a, C5a – Plasma complement system cascade

  4. Substance P – Pulpal nociceptors

Opsonization

  1. C3b, C5b – Plasma complement system cascade

Inflammatory Mediators (cont.)


Endothelial Adhesion Expression

  1. TNF (cytokine) – Macrophages


  2. IL-1 (cytokine) – Macrophages

  3. Chemokines – Macrophages, PMNs, Endothelial cells, Fibroblasts


Leukocyte Activation and Chemotaxis

  1. C3a, C5a – Plasma complement system cascade

  2. Leukotrienes – All leukocytes, Mast cells

  3. Chemokines – Macrophages, PMNs, Endothelial cells, Fibroblasts

  4. TNF – Macrophages


Tissue Damage

  1. Lysosomal enzymes – PMNs, Macrophages - phagocytosis

  2. Free oxygen radicals – Activated leukocytes

  3. Nitric oxide – Macrophages

What is the role of the neuropeptides?


Neurogenic Inflammation

  1. Vasodilation (via CGRP & mast cells  histamine)

  2. Increased Vascular Permeability (via SP & mast cells  Leukotrienes)

  3. Nerve sprouting/Pain (via SP/CGRP  Fibroblasts  NGF) - Byers

  4. Activate Macrophages/T lymphocytes  cytokines: IL-1, TNF-, IL-6

  5. Bone resorption and Immune regulation in AP development - Byers




  1. Sessle – Neuropeptides mediate release of inflammatory mediators from immune cells (i.e.: macrophages, mast cells, platelets) resulting in inflammatory cascade

  2. Byers – injury leads to “sprouting” of sensory nociceptors: Neuropeptides (SP/CGRP)  fibroblasts  NGF  Nerve sprouting =  Nociceptor receptive field + response

  3. Wakisaka 1990– neuropeptides may help regulate pulpal blood flow + pain transmission as well as promote inflammatory response

  4. Hargreaves – sympathetic transmission may modulate pain (capsaicin study)

Neuropeptides

5 Major Neuropeptides:

Wakisaka 1990, Hargreaves 1994, Caviedes-Bucheli IEJ 2006

SP (Substance P):

  1. Trigeminal 1 cell bodies (mainly C-fibers) – Trigeminal ganglion

  2. Interact with Mast cells: Release of histamine & leukotrienes

  3. Activates Macrophages/Lymphocytes: Release of inflammatory mediators (ie: Cytokines, PGs, Thromboxanes)

  4. Stimulate Pulpal cells (ie: Fibroblasts, Odontoblast like cells): NGF


CGRP (Calcitonin Gene Related Peptide):

  1. Trigeminal 1 cell bodies – Trigeminal ganglion

  2. Interact with Mast cells: Release of histamine & leukotrienes

  3. Stimulate Pulpal cells (ie: Fibroblasts, Odontoblast like cells): NGF

Neuropeptides
NKA (Neurokinin A):

  1. Trigeminal 1 cell bodies – Trigeminal ganglion

  2. Activates Macrophages/Lymphocytes: Release of inflammatory mediators (ie: cytokines, PGs, Thromboxanes)


NPY (Neuropeptide Y):

  1. Sympathetic efferent derived (co-localized with Norepinephrine) – Superior Cervical ganglion

  2. Sympathetic vasoregulation - Vasodilation ( Pulpal Blood Flow)


VIP (Vasoactive Intestinal Peptide):

  1. Parasympathetic efferent derived (co-localized with Acetylcholine)

  2. Vasodilation (Pulpal Blood Flow)

Vascular response = LOCALIZED Inflammation



Kim - Key components in pulpal inflammation:


  1. Microcirculation – increased PBF by C fiber stimulation (neurokinin A, substance P, CGRP released from C fiber nerve terminals)




  1. Sensory nerve activity – excitatory effect from increased pulpal blood flow via increased tissue pressure (effect on A delta fibers)


VHK:

  1. Van Hassel – 1st to discuss Localized Inflammationvascular collapse spreads incrementally from the site of injury, not by strangulation at the apex

  2. Heyeraas (Tonder)Pulpal lymphatics – drainage of interstitial fluid/proteins to  Interstitial tissue pressure

  3. Kim/TakahashiPulpal Collateral Circulation circumvents blood flow around the area of injury/inflammation (AV, VV shunts, Ushaped arteriole)
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