History of Endodontics aae/abe

Download 0.95 Mb.
Date conversion20.11.2016
Size0.95 Mb.
1   ...   4   5   6   7   8   9   10   11   ...   29

Who studied pulpal vasculature & localized inflammation?

  1. VanHassel 1st to discuss localized inflammation in pulp – vascular collape spreads incrementally from site of injury (pressure differences)

  1. Heyeraas (Tonder)localized increased tissue pressure may persist in the inflamed area w/out a circumferential spread to the rest of the pulp. Negative feedback system prevents pulpal strangulation (lymphatic drainage)

  1. Kim & Takahashi – discovered presence of arteriovenous anastomosis and venous-venous anastomosis and u shaped arterioles (unique feature of pulpal vascular network) = collateral circulation – circumvents blood flow around the area of inflammation (localized)

--Also found sympathetic adrenergic vasoconstritor fibers (NPY) =  Vasodilation ( Pulpal Blood Flow)
No Pulpal Strangulation Theory!

Are Mast Cells in the Pulp ?


Farnoush - Found in inflamed and non-inflamed pulpal tissue


Suda – Mast Cells are NOT present in normal pulps

Who found lymphatics in the pulp ?

  1. Bernick – demonstrated lymphatics in the pulp

  1. Heyeraas (Tonder) - Pulp may have a beneficial blood flow increase during inflammation in spite of simultaneously increased tissue pressure. This supports the concept of lymphatic drainage. Localized increased tissue pressure without circumferential spread! Lymphatic drainage of interstitial fluid/proteins prevents spread of tissue pressure

Are antibodies present in the healthy pulp?


  1. Langeland Antigens in the root canal system can initiate an immune response with antibodies

  1. Hahn – IgG, major class of immunoglobulins in normal and irreversible groups


  1. Pulver Normal pulps do NOT have immunoglobulins-containing cells. In inflamed pulps, IgG most common, IgA, IgE, IgM containing cells are also seen.

  1. Jontell/BergenholtzB lymphocytes, mast cells, and Abs are NOT present in normal pulp

Describe the Compliment cascade

Activated by pro-inflammatory cytokines, neuropeptides, bacterial antigens

  1. Mediate vascular responses: C3a, C5a  Mast Cells  Histamine (vasodilation), Leukotrienes ( Vascular Permeability)

  2. Leukocyte chemotaxis: C3a, C5a  PMNs, T/B cells, Bradykinin

  3. Opsonizination of targets for phagocytic cells (C3b, C5b)

  4. Directly damage of target cells (C5-9, MAC)

Most important step is cleavage of C3

Classical pathway: activated by Ab coated targets or Ag-Ab complexes (IgM, IgG – Type III foreign body rxn)

Alternate pathway: activated by LPS, aggregated IgM or IgG, Ag-IgG complexes, plasmin
Immune Modulators & Silent Pulpitis

  1. Holland/MichaelsonSilent pulpitis: 40-60%

  1. Jaber/Dionne -  opioid receptors present peripherally within the pulp on primary nociceptors

  1. NarhiEndogenous opioids and somatostatin released by inflammatory cells are capable of inhibiting firing of sensory nerve fibers

  1. Mudie/Holland 2006Endorphins are located within lymphocytes in inflammed pulps

Endogenous Opioids (neuromodulators): Beta-Endorphins, Met- and Leu-Enkephalins, Dynorphins

Targets: Mu, Delta, Kappa receptors

Periapical Pathophysiology

Apical Periodontitis – Etiology - BACTERIA

AP is caused by entry into PA tissues either by bacterial toxins, enzymes, or byproducts (TEBs) or direct invasion by microbes from the canal system

Exogenous Factors

I. Microorganisms:

  1. Kakehashi 1965 – Pulp exposure - germ free vs conventional rats - germ free rats: vital/hard tissue repair; conventional rats: pulp necrosis/AP

  2. Sundqvist 1976 – Human study, evaluated necrotic traumatized teeth – w/o AP: no bacteria; w/ AP: Bacteria present (90% Anaerobes)

  3. Moller/Fabricius 1981– Monkey study, Devitalized pulps/sealed 6-7 months: Sterile necrotic pulps – No AP changes; Infected necrotic pulps – AP inflammation/destruction

II. Bacterial Toxins/Bacterial Enzymes/Metabolic Byproducts (TEBs)

  1. Toxins: LPS, LTA, Peptidoglycan

  2. Enzymes: Hyaluronidases, Chondroitin sulfatases, Collagenases

  3. Byproducts: Sulfur

Apical Periodontitis – Etiology

Nair 1995

III. Physical Insults (Foreign bodies)

  1. Overinstrumentation of the canal system

  2. Extrusion of obturating materials, dentin debris

  3. Traumatic injury of the periapical tissues

IV. Chemical Insults (Foreign bodies)

  1. Extrusion of Irrigants

  2. Extrusion of Intracanal Medications

  3. Extrusion of Root canal filling materials/sealers

Endogenous Factors

  1. Cholesterol crystals

Ricucci/Siqueira – Intraradicular biofilms are responsible for AP (CAGE)

Periapical Pathology – Inflammatory Reactions

  1. Apical Inflammation: Periapical tissue reaction to irritants emerging from the root canal system, Resulting inflammation characterized by vasodilation, increased vascular permeability, and exudate

  1. Apical Infection: Direct invasion of the periapical tissues by microorgansims that establish an extraradicular infection, evoke purulent inflammation, and subsequently produces tissue damage


  1. Innate Immune Response (1st 48 hours)

  2. Adaptive Immune Response (>48 hours)

  3. Neurogenic Inflammation (24 hours +)

Periapical Bone Destruction

  1. Stashenko/Wang - Host immune response mediates tissue destruction and bone resorption in response to bacterial infection. TNF-, IL-1, IL-2, IL-6

  1. Byers 1990Sprouting of CGRP containing nociceptors in the periapical tissues occurred while vital pulp tissue remained coronally, suggesting neuropeptides may contribute to periapical lesion development

  1. Stashenko – Animal model (rats), kinetics of bone resorption:

    1. Bone destruction appeared radiographically ~10 days (post p.e.)

    2. Active phase 0-15 days: rapid bone destruction, TH > TS

    3. Stationary phase > 20 days: slower bone destruction, TS > TH

    4. T cells responsible for immunoregulation of bone destruction

RANKL: via IL-1, IL-6, TNF, PGs, Bradykinin, LPS = osteoclast,  bone dest.
Periapical Pathogenesis

Granuloma vs. Granulation Tissue:

Trowbridge 1990

  1. Granuloma

    1. Round, circumscribed inflammatory lesion consisting of an accumulation of macrophages, lymphocytes, and a variable number of plasma cells, neutrophils, giant cells and mast cells all enclosed within a collagenous stroma.

    2. Periapical Granuloma = Localized mass of chronic inflammatory tissue consisting of macrophages, T lymphocytes, plasma cells, mast cells, giant cells and epithelium formed in reaction to infection of the dental pulp which serves as a constant source of antigenic material.

  1. Granulation Tissue

    1. Proliferative phase of wound repair consisting of fibrin CT matrix containing endothelial cells and fibroblasts mixed with inflammatory cells of lymphocytes and macrophages
1   ...   4   5   6   7   8   9   10   11   ...   29

The database is protected by copyright ©dentisty.org 2016
send message

    Main page