Acute & Chronic Inflammation Learning Objectives The student should be able to



Download 39.45 Kb.
Date conversion01.06.2018
Size39.45 Kb.
Acute & Chronic Inflammation
Learning Objectives
The student should be able to :


  1. Define Inflammation.

  2. Describe the types of Inflammation.

  3. What are the cells and tissues involved in inflammation?

  4. Describe the signs and symptoms of Inflammation?

  5. Describe the causes of acute inflammation.

  6. Describe the causes of chronic inflammation.

  7. What are the morphological features of Chronic Inflammation?

  8. What is granulomatous Inflammation?


Acute & Chronic Inflammation
Lecture Outline
General Facture of Inflammation:


  • In cell injury – various exogenous and endogenous stimuli can cause cell injury which involves the cells, nuclei and organelles of the cells.

  • In vascularized tissue – same exogenous and endogenous stimuli produce inflammation.


Inflammation



Role of Tissue and Cells in inflammation :
Many tissue and cells are involved in inflammation. The tissue & fluid are:


  • The fluid and proteins of plasma.

  • Blood vessels.

  • Cellular and extra cellular constituents of connective tissue (mast cells & fibroblast).



The circulating cells are:


  • Neutrophils.

  • Monocytes.

  • Eosinophils.

  • Lymphocytes.

  • Basophils.

  • Platelets.


Sign & symptoms of Inflammation:
These are:


  • Fever, (increase temperature).

  • Pain.

  • Tissue damage.

  • Swelling of tissue.

  • Redness of tissue.

  • Loss of movements or restricted movement, if near joints.


Types of Inflammation:

Inflammation is divided into:


I - Acute inflammation occurs over seconds, minutes, hours and days.
II - Chronic inflammation occurs over longer times, days & months.
Acute inflammation:


  • Acute inflammation begins within seconds to minutes following the injury of tissues.


Chronic inflammation:


  • Chronic inflammation is of longer duration and is associated histologically with the presence of:

  • Lymphocytes and macrophages.

  • The proliferation of blood vessels.

  • Fibrosis and tissue necrosis.


Response of Inflammation
The main processes are:
I - Increased blood flow.

II - Increased permeability.

III - Migration of neutrophils.

IV - Chemotaxis.

V - Leucocytes recruitment & activation.


I - Increased blood flow:

Due to dilation of blood vessels (arterioles) supplying the region.



II - Increased permeability:

Increased permeability of the capillaries, allowing fluid and blood proteins to move into the interstitial spaces.




III - Migration of neutrophils (and perhaps a few macrophages) out of the venules and into interstitial spaces.

IV – Chemotaxis


  • Once outside the blood vessel, a neutrophil is guided towards an infection by various diffusing chemotactic factors. Examples include the chemokines and the complement peptide C5a, which is released when the complement system is activated either via specific immunity or innate immunity.

V - Leucocytes recruitment & activation.


  • This is the first step is the binding of the neutrophils to the endothelium of the blood vessels.

  • The binding is due to molecules, called cell adhesion molecules (CAMs), found on the surfaces of neutrophils and on endothelial cells in injured tissue.

  • The binding of leukocytes occur in two steps:

  • In the first step, adhesion molecules called selectins tightly gather the neutrophil to the endothelium, so that it begins rolling along the surface

In a second step, a much tighter binding occurs through the interaction of ICAMs on the endothelial cells with integrins on the neutrophil.
Eosinophils:

However, in some circumstances eosinophils rather than neutrophils predominate in acute inflammation. This tends to occur with parasites (worms), against which neutrophils have little success.


Response of Acute Inflammation:


  • Increased Blood Flow, increased permeability and Edema in Inflammation:

  • The increased blood flow & increased permeability are readily visible within a few minutes following a scratch that does not break the skin.

  • At first, there is pale red line of scratch.

  • Later on there is accumulation of inflammatory cells lead swelling, (inflammation).

  • Finally, there is accumulation of interstitial fluid cause edema.



Chronic inflammation


  • It is the inflammation of prolong duration (weeks or months).

It occurred as:

  • Following acute inflammation.

  • Occurs, incidentally as active inflammation.

  • With tissue destruction.

  • With repair process.



Causes of Chronic inflammation:
I - Persistent infection.

II - Prolonged exposure to potentially toxic agents.

III - Autoimmunity.
I - Persistent infection:


  • Bacteria.

  • Viruses.

  • Fungi.

  • Parasites


II - Prolonged exposure to potentially toxic agents:


  • Endogenous, (atherosclerosis).

  • Exogenous,(by particulate silica-Silicosis).

III - Autoimmunity:

Occurs in:



  • Rheumatoid arthritis.

  • Lupus erythematosus.




  • Lymphocyte, macrophage, plasma cell (mononuclear cell) infiltration

  • Tissue destruction by inflammatory cells

  • Attempts at repair with fibrosis and angiogenesis (new vessel formation)

  • When acute phase cannot be resolved

    • Persistent injury or infection (ulcer, TB)

    • Prolonged toxic agent exposure (silica)

    • Autoimmune disease states (RA, SLE)


Morphological Features of Chronic Inflammation
These are characterized by:

I - Infiltration by mononuclear cells.

II - Tissue destruction.

III - Removal of damaged tissue, (healing).



Morphological Features of Chronic Inflammation
I - Infiltration by mononuclear cells:
The mononuclear cells are become predominant after 48 hours.
These include;


  • Macrophages.

  • Lymphocytes.

  • Plasma cells.

  • Eosinophils.

  • Mast cells.




  • Macrophages:




    • Scattered all over (microglia, Kupffer cells, sinus histiocytes, alveolar macrophages, etc.

    • Circulate as monocytes and reach site of injury within 24 – 48 hrs and transform.

    • Become activated by T cell-derived cytokines, endotoxins, and other products of inflammation.




  • T and B lymphocytes:




    • Antigen-activated (via macrophages and dendritic cells)

    • Release macrophage-activating cytokines (in turn, macrophages release lymphocyte-activating cytokines until inflammatory stimulus is removed)




  • Plasma cells:




    • Terminally differentiated B cells (of lymphocytes).

    • Produce antibodies.


Eosinophils :


    • Found especially at sites of parasitic infection, or at allergic (IgE-mediated) sites.

    • Eosinophils have highly cationic proteins, which are toxic to parasites.


II - Tissue destruction:
Occur due to:

  • Inflammatory cells.

  • Persistent infecting material.


III - Removal of damaged tissue, (healing):


  • Occur by proliferation of small blood vessels, (angiogenesis).

  • Proliferation of fibroblast, (fibrosis-repair).



Granulomatous Inflammation:


  • Clusters of T cell-activated macrophages, which engulf and surround indigestible foreign bodies (mycobacteria, H. capsulatum, silica, suture material)

  • Resemble squamous cells, therefore called “epithelioid” granulomas with peripheral lymphocytes, fibrosis & multinucleated giant cells.


Lymph Nodes and Lymphatics:


  • Lymphatics drain tissues







      • Lymphadenitis, lymphangitis

      • Usually contained there, otherwise bacteremia ensues

      • Tissue-resident macrophages must then prevent overwhelming infection.


Systemic effects


  • Fever

    • One of the easily recognized cytokine-mediated (esp. IL-1, IL-6, TNF) acute-phase reactions including

      • Anorexia

      • Skeletal muscle protein degradation

      • Hypotension




  • Leukocytosis




    • Elevated white blood cell count

    • Bacterial infection (neutrophilia)

    • Parasitic infection (eosinophilia)

    • Viral infection (lymphocytosis)


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

    Main page