Chronic Inflammation Bpt
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Lecture 4 Chronic Inflammation
Dr. Mehzabin Ahmed 24 September 2008
Chronic Inflammation, tissue destruction and fibrosis Introduction
When a damaging stimulus persists, complete healing cannot occur, and chronic inflammation results In chronic inflammation the tissue damage continues along with attempts to repair
Types: 5) Chronic non specific inflammation 6) Chronic granulomatous inflammation
Causes of chronic inflammation
Persistence of infections by organisms of low toxicity
Cause an delayed type of immune reaction
Results in a granulomatous inflammation
Prolonged exposure to potentially toxic substances
Bacteria like M. tuberculosis, T. pallidum; viruses; fungi; parasites etc Exogenous- silica particles - silicosis Endogenous- toxic plasma lipid componentsatherosclerosis
Autoimmunity
reaction against the body’s own tissues
Results in chronic tissue damage and inflammation
Rheumatoid arthritis, systemic lupus erythematosus
Features of chronic inflammation
Infiltration with mononuclear cells- lymphocytes, plasma cells and macrophages
Tissue destruction- seen as areas of necrosis in the affected tissues- caused by the persisting microorganisms and the inflammatory cells
Attempt at healing- seen as areas of fibrosis (connective tissue replacement of the damaged tissues) accompanied and helped by angiogenesis (the proliferation of new vessels)
Mononuclear infiltrate associated with immune response
Immune mechanisms dominate the cellular response in chronic inflammation The macrophage is the main effector cell in chronic inflammation Lymphocytes and plasma cells are also present in chronic inflammatory reactions
macrophage
lymphocyte Plasma cells
Chronic peptic ulcer is an example of chronic inflammation where tissue damage due to acid-peptic digestion and tissue repair are going on at the same time
Peptic ulcer
fibrosis Chronic Inflammation, tissue destruction and fibrosis
Peptic ulcer
Granulomatous inflammation:
It is a distinct type of chronic inflammation.
There is a focal collection of activated macrophages called epithelioid cells.
Granuloma: it is the focus of chronic inflammation consisting of
Epithelioid cells
Lymphocytes
Plasma cells and
Giant cells- formed by fusion of epithelioid cells
Types of granulomas
Based on mechanism:
Immune granuloma - there is a cell mediated immune response against an insoluble particle like microbes
Foreign body granuloma- they result form a relatively inert substances- the foreign body may be seen in the center of the granuloma
Eg: tuberculosis, Sarcoidosis, Fungal infections
Eg: talc, sutures
Based on morphology:
Caseating granulomas: there are areas of caseous necrosis (seen as cheesy white areas) in the affected tissues. Seen in cases of tuberculosis. Noncaseating granulomas- there is no central caseation. It is seen in sarcoidosis, fungal infection.
Granuloma formation is seen in some chronic diseases In chronic inflammations macrophages form groups called granulomas Granulomatous inflammation is seen when an organism is of low pathogenicity but excites an immune response e.g. Mycobacterium tuberculosis Mycobacterium leprae Fungus Virus Parasite
Granuloma
Langhans Giant Cell
Granuloma
Lymphocytic Rim
sis
Ca
cro e N s seou
Epithelioid Macrophage
Granulomatous inflammation
lymphocytes
Granuloma made up of macrophages
Tuberculosis is an example of granulomatous inflammation
A granuloma in TB is called a tubercle A tubercle is composed of activated macrophages with surrounding lymphocytes and fibroblasts In TB the granulomas undergo caseation necrosis and heal by fibrosis when the immunity is good
Caseating granulomas are seen commonly in TB
epithelioid cells
lymphocyte
giant cells Area of caseation necrosis
Granulomatous inflammation can be a tissue response to some foreign materials
Granulomas form when a non-living material is deposited in the tissue and cannot be degraded easily
e.g. urate crystals in gout, inhaled organic dust
Foreign body giant cells are formed by the fusion of macrophages around the material
Sarcoidosis is a granulomatous disease of unknown cause in which the granulomas do not show caseation and heal by fibrosis
Giant cells form by fusion of macrophages
Langhan giant cell
Foreign body giant cell
Non caseating granulomas
Granuloma healing by fibrosis
Noncaseating granuloma in Sarcoidosis
The outcome of tubercle formation depends on the adequacy of the host immune response
In primary TB the initial lung lesion (Ghon focus) remains small but the infection spreads to the hilar lymph nodes (primary complex)
Primary TB
The primary complex will heal in most cases with development of immunity to TB
Rarely the primary complex will progress in patients with poor natural immunity
Bronchial spread of organisms produces tuberculous pneumonia
Blood stream spread of organisms produces miliary TB
Miliary TB
Pulmonary dissemination
Miliary tuberculosis, Spleen
Slide 16.31
Secondary TB
In adults secondary TB heals by fibrosis around the caseating granulomas
In adults with poor immune response secondary TB progresses locally and spread to other sites
Blood stream spread of the organism can lead to spread to other organs
Tuberculous lesions may become reactivated long after healing
Secondary tuberculosis
In secondary TB initial tuberculous infection is at the apex of the upper lobe of a lung with little lymph node involvement
Spinal TB - Potts Disease
Outcome of infection in TB
Dr. Mehzabin Ahmed 24 September 2008
Chronic Inflammation, tissue destruction and fibrosis Introduction
When a damaging stimulus persists, complete healing cannot occur, and chronic inflammation results In chronic inflammation the tissue damage continues along with attempts to repair
Types: 5) Chronic non specific inflammation 6) Chronic granulomatous inflammation
Causes of chronic inflammation
Persistence of infections by organisms of low toxicity
Cause an delayed type of immune reaction
Results in a granulomatous inflammation
Prolonged exposure to potentially toxic substances
Bacteria like M. tuberculosis, T. pallidum; viruses; fungi; parasites etc Exogenous- silica particles - silicosis Endogenous- toxic plasma lipid componentsatherosclerosis
Autoimmunity
reaction against the body’s own tissues
Results in chronic tissue damage and inflammation
Rheumatoid arthritis, systemic lupus erythematosus
Features of chronic inflammation
Infiltration with mononuclear cells- lymphocytes, plasma cells and macrophages
Tissue destruction- seen as areas of necrosis in the affected tissues- caused by the persisting microorganisms and the inflammatory cells
Attempt at healing- seen as areas of fibrosis (connective tissue replacement of the damaged tissues) accompanied and helped by angiogenesis (the proliferation of new vessels)
Mononuclear infiltrate associated with immune response
Immune mechanisms dominate the cellular response in chronic inflammation The macrophage is the main effector cell in chronic inflammation Lymphocytes and plasma cells are also present in chronic inflammatory reactions
macrophage
lymphocyte Plasma cells
Chronic peptic ulcer is an example of chronic inflammation where tissue damage due to acid-peptic digestion and tissue repair are going on at the same time
Peptic ulcer
fibrosis Chronic Inflammation, tissue destruction and fibrosis
Peptic ulcer
Granulomatous inflammation:
It is a distinct type of chronic inflammation.
There is a focal collection of activated macrophages called epithelioid cells.
Granuloma: it is the focus of chronic inflammation consisting of
Epithelioid cells
Lymphocytes
Plasma cells and
Giant cells- formed by fusion of epithelioid cells
Types of granulomas
Based on mechanism:
Immune granuloma - there is a cell mediated immune response against an insoluble particle like microbes
Foreign body granuloma- they result form a relatively inert substances- the foreign body may be seen in the center of the granuloma
Eg: tuberculosis, Sarcoidosis, Fungal infections
Eg: talc, sutures
Based on morphology:
Caseating granulomas: there are areas of caseous necrosis (seen as cheesy white areas) in the affected tissues. Seen in cases of tuberculosis. Noncaseating granulomas- there is no central caseation. It is seen in sarcoidosis, fungal infection.
Granuloma formation is seen in some chronic diseases In chronic inflammations macrophages form groups called granulomas Granulomatous inflammation is seen when an organism is of low pathogenicity but excites an immune response e.g. Mycobacterium tuberculosis Mycobacterium leprae Fungus Virus Parasite
Granuloma
Langhans Giant Cell
Granuloma
Lymphocytic Rim
sis
Ca
cro e N s seou
Epithelioid Macrophage
Granulomatous inflammation
lymphocytes
Granuloma made up of macrophages
Tuberculosis is an example of granulomatous inflammation
A granuloma in TB is called a tubercle A tubercle is composed of activated macrophages with surrounding lymphocytes and fibroblasts In TB the granulomas undergo caseation necrosis and heal by fibrosis when the immunity is good
Caseating granulomas are seen commonly in TB
epithelioid cells
lymphocyte
giant cells Area of caseation necrosis
Granulomatous inflammation can be a tissue response to some foreign materials
Granulomas form when a non-living material is deposited in the tissue and cannot be degraded easily
e.g. urate crystals in gout, inhaled organic dust
Foreign body giant cells are formed by the fusion of macrophages around the material
Sarcoidosis is a granulomatous disease of unknown cause in which the granulomas do not show caseation and heal by fibrosis
Giant cells form by fusion of macrophages
Langhan giant cell
Foreign body giant cell
Non caseating granulomas
Granuloma healing by fibrosis
Noncaseating granuloma in Sarcoidosis
The outcome of tubercle formation depends on the adequacy of the host immune response
In primary TB the initial lung lesion (Ghon focus) remains small but the infection spreads to the hilar lymph nodes (primary complex)
Primary TB
The primary complex will heal in most cases with development of immunity to TB
Rarely the primary complex will progress in patients with poor natural immunity
Bronchial spread of organisms produces tuberculous pneumonia
Blood stream spread of organisms produces miliary TB
Miliary TB
Pulmonary dissemination
Miliary tuberculosis, Spleen
Slide 16.31
Secondary TB
In adults secondary TB heals by fibrosis around the caseating granulomas
In adults with poor immune response secondary TB progresses locally and spread to other sites
Blood stream spread of the organism can lead to spread to other organs
Tuberculous lesions may become reactivated long after healing
Secondary tuberculosis
In secondary TB initial tuberculous infection is at the apex of the upper lobe of a lung with little lymph node involvement
Spinal TB - Potts Disease
Outcome of infection in TB
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