Chronic Inflammation
            M
Dr Mohammad Manzoor Mashwani
Chronic Inflammation
Chronic inflammation is inflammation
 of prolonged duration
(weeks or months)
in which

inflammation, tissue injury, and attempts at repair
  coexist, in varying combinations.
CAUSES OF CHRONIC INFLAMMATION

1.Persistent Infection
2. Immune-mediated
 inflammatory diseases
3. Toxic Agents
Causes of chronic inflammation

• Acute inflammation:
   – Progressive: osteomyelitis
   – Recurrent: cholycystitis, gastritis.
• Primary: (abinitio) abinitio means "from the beginning“
• Contents
   – TB, fungal inf.
   – HSR.
• Persistent factor : foreign bodies
Primary Chronic Inflammation
It is the cause of tissue damage in some of the most
   common and disabling human diseases, such as

rheumatoid arthritis, atherosclerosis, tuberculosis,
  and pulmonary fibrosis.



It has also been implicated in the progression of
  cancer and in diseases once thought to be purely
  degenerative, such as Alzheimer disease.
Mechanism of chronic inf
                          Macrophages
             TH
                           Activation


            Free                              TGF-B       EGF
            radicals
            Enzymes
                            Cytokines         FGE     +
            NO                                GCSF



               e                        Fibrosis      Angiogenesis
            s u ge
         Tis ma
           da          Healing            Granulation tissue


© Dr.yasir 2oo7
MORPHOLOGIC FEATURES
Chronic inflammation is characterized by:
1. Infiltration with mononuclear cells, which include
  macrophages, lymphocytes, and plasma cells
2. Tissue destruction, induced by the persistent
  offending agent or by the inflammatory cells
3. Attempts at healing by connective tissue
  replacement of damaged tissue, accomplished by
  proliferation of small blood vessels (angiogenesis)
  and, in particular, fibrosis.
A, Chronic inflammation in the lung, showing all three characteristic
histologic features: (1) collection of chronic inflammatory cells (*), (2)
destruction of parenchyma (normal alveoli are replaced by spaces
lined by cuboidal epithelium, arrowheads), and (3) replacement by
The roles of activated macrophages in chronic inflammation. Macrophages are activated by
nonimmunologic stimuli such as endotoxin or by cytokines from immune-activated T cells
(particularly IFN-γ). The products made by activated macrophages that cause tissue injury and
fibrosis are indicated. AA, arachidonic acid; PDGF, platelet-derived growth factor; FGF,
fibroblast growth factor; TGFβ, transforming growth factor β.
GRANULOMATOUS INFLAMMATION
Granulomatous inflammation is a distinctive pattern
  of chronic inflammation that is encountered in a
  limited number of infectious and some
  noninfectious conditions. Immune reactions are
  usually involved in the development of
  granulomas.
A granuloma is a cellular attempt to contain an
  offending agent that is difficult to eradicate.
In this attempt there is often strong activation of T
  lymphocytes leading to macrophage activation,
  which can cause injury to normal tissues.
A granuloma is a focus of chronic
 inflammation consisting of
a microscopic aggregation of
 macrophages
that are transformed into epithelium-
  like cells, surrounded by a collar of
  mononuclear leukocytes, principally
  lymphocytes and occasionally
  plasma cells.
Giant Cells
Older granulomas develop an enclosing rim of
  fibroblasts and connective tissue.
Frequently, epithelioid cells fuse to form giant cells
  in the periphery or sometimes in the center of
  granulomas.
These giant cells may attain diameters of 40 to 50
  μm. They have a large mass of cytoplasm
  containing 20 or more small nuclei arranged either
  peripherally (Langhans-type giant cell) or
  haphazardly (foreign body–type giant cell).
Types of Granulomas
I. Foreign body granulomas
II. Immune granulomas
Foreign body granulomas
Incited by relatively inert foreign bodies.
Typically, foreign body granulomas form around
  material that are large enough to preclude
  phagocytosis by a single macrophage and do not
  incite any specific inflammatory or immune
  response.
The foreign material can usually be identified in the
  center of the granuloma, particularly if viewed
  with polarized light, in which it appears refractile.
Immune granulomas
Caused by agents that are capable
 of inducing an immune response
 which produces granulomas
 usually when the inciting agent is
 poorly degradable or particulate.
Methods of identification of Specific etiologic agent
           in Granulomatous diseases
1. Special stains for organisms
 (e.g., acid-fast stains for tubercle bacilli),


 2. Culture                methods
(e.g., in tuberculosis and fungal diseases),

3. Molecular techniques
(e.g., the polymerase chain reaction in tuberculosis),


4. Serologic studies
(e.g., in syphilis).
Chronic inflammation

Chronic inflammation

  • 1.
    Chronic Inflammation M Dr Mohammad Manzoor Mashwani
  • 2.
    Chronic Inflammation Chronic inflammationis inflammation of prolonged duration (weeks or months) in which inflammation, tissue injury, and attempts at repair coexist, in varying combinations.
  • 3.
    CAUSES OF CHRONICINFLAMMATION 1.Persistent Infection 2. Immune-mediated inflammatory diseases 3. Toxic Agents
  • 4.
    Causes of chronicinflammation • Acute inflammation: – Progressive: osteomyelitis – Recurrent: cholycystitis, gastritis. • Primary: (abinitio) abinitio means "from the beginning“ • Contents – TB, fungal inf. – HSR. • Persistent factor : foreign bodies
  • 5.
    Primary Chronic Inflammation Itis the cause of tissue damage in some of the most common and disabling human diseases, such as rheumatoid arthritis, atherosclerosis, tuberculosis, and pulmonary fibrosis. It has also been implicated in the progression of cancer and in diseases once thought to be purely degenerative, such as Alzheimer disease.
  • 6.
    Mechanism of chronicinf Macrophages TH Activation Free TGF-B EGF radicals Enzymes Cytokines FGE + NO GCSF e Fibrosis Angiogenesis s u ge Tis ma da Healing Granulation tissue © Dr.yasir 2oo7
  • 7.
    MORPHOLOGIC FEATURES Chronic inflammationis characterized by: 1. Infiltration with mononuclear cells, which include macrophages, lymphocytes, and plasma cells 2. Tissue destruction, induced by the persistent offending agent or by the inflammatory cells 3. Attempts at healing by connective tissue replacement of damaged tissue, accomplished by proliferation of small blood vessels (angiogenesis) and, in particular, fibrosis.
  • 8.
    A, Chronic inflammationin the lung, showing all three characteristic histologic features: (1) collection of chronic inflammatory cells (*), (2) destruction of parenchyma (normal alveoli are replaced by spaces lined by cuboidal epithelium, arrowheads), and (3) replacement by
  • 13.
    The roles ofactivated macrophages in chronic inflammation. Macrophages are activated by nonimmunologic stimuli such as endotoxin or by cytokines from immune-activated T cells (particularly IFN-γ). The products made by activated macrophages that cause tissue injury and fibrosis are indicated. AA, arachidonic acid; PDGF, platelet-derived growth factor; FGF, fibroblast growth factor; TGFβ, transforming growth factor β.
  • 21.
    GRANULOMATOUS INFLAMMATION Granulomatous inflammationis a distinctive pattern of chronic inflammation that is encountered in a limited number of infectious and some noninfectious conditions. Immune reactions are usually involved in the development of granulomas. A granuloma is a cellular attempt to contain an offending agent that is difficult to eradicate. In this attempt there is often strong activation of T lymphocytes leading to macrophage activation, which can cause injury to normal tissues.
  • 23.
    A granuloma isa focus of chronic inflammation consisting of a microscopic aggregation of macrophages that are transformed into epithelium- like cells, surrounded by a collar of mononuclear leukocytes, principally lymphocytes and occasionally plasma cells.
  • 26.
    Giant Cells Older granulomasdevelop an enclosing rim of fibroblasts and connective tissue. Frequently, epithelioid cells fuse to form giant cells in the periphery or sometimes in the center of granulomas. These giant cells may attain diameters of 40 to 50 μm. They have a large mass of cytoplasm containing 20 or more small nuclei arranged either peripherally (Langhans-type giant cell) or haphazardly (foreign body–type giant cell).
  • 27.
    Types of Granulomas I.Foreign body granulomas II. Immune granulomas
  • 28.
    Foreign body granulomas Incitedby relatively inert foreign bodies. Typically, foreign body granulomas form around material that are large enough to preclude phagocytosis by a single macrophage and do not incite any specific inflammatory or immune response. The foreign material can usually be identified in the center of the granuloma, particularly if viewed with polarized light, in which it appears refractile.
  • 29.
    Immune granulomas Caused byagents that are capable of inducing an immune response which produces granulomas usually when the inciting agent is poorly degradable or particulate.
  • 31.
    Methods of identificationof Specific etiologic agent in Granulomatous diseases 1. Special stains for organisms (e.g., acid-fast stains for tubercle bacilli), 2. Culture methods (e.g., in tuberculosis and fungal diseases), 3. Molecular techniques (e.g., the polymerase chain reaction in tuberculosis), 4. Serologic studies (e.g., in syphilis).