Wa0029

Chronic inflammation
Chronic=process has extend over a

long period of time.
Def: process in which lymphocytes,
plasma cells, Mc predominate,
granulation tissue & scar tissue are
also formed.
Chronic inflammation can develop as:
1/ progression from acute inflammation.
-Usually suppurative type= abscess deeply
seated & drainage delayed or inadequate
- by time abscess wall become thicker &
rigid fail to come together after drainage
- pus within the cavity become organized
(granulation tissue replaced by fibrous
scar).
Eg. abscess in BM  osteomyelitis .
The presence of a foreign body acts as a
continuing inflammatory stimulus
2/ Recurrent episodes of acute inflam.
eg. chronic cholecystitis due to presence of
gallstone
3/ Primary chronic inflammation
It is chronic inflam. from the onset and
there is no initial acute phase.
Causes:
-Prolonged exposure to non-degradable, more toxic
sub. Exogenous = silica, asbestos (lung disease)
Endogenous = atherosclerosis (response to lipids
damaging the intimal layer of arteries)
- Certain micro-organisms – persistent infections

(TB, viruses, leprosy, fungal infection)
- Some disease (autoimmune) eg. Rheumatoid

arthritis & chronic inflammatory bowl disease.
Examples of chronic disease:
Extremely variable eg.

-Chronic ulcer ( peptic ulcer)
- chronic cholecystitis
- fistula
- chronic granulomatous inflammation
Microscopic features of chronic inflam.
• cellular infiltrate , lymphocytes,
eosinophils, plasma cells, fibroblast and
macrophages & their derivatives ( giant
cells and epitheliod cells)
• exudate is not prominent
• may be production of fibrous tissue
• may be evidence of continuing
destruction of tissue at the same time of
tissue regeneration & repair.
• tissue necrosis may be prominent feature
especially in granulomatous conditions eg.
T.B.
-Lymphocytes + plasma cells  Immune

response at the site of chronic inflam.
- Eosinophils secret protein (toxic)
- Fibroblast + capillary healing & repair
-Macrophages
• are a part of mononuclear
phagocytic system (RES)
• BM stem cells monocyte in blood,
tissue Mc ( fixed & free)
• at the site of inflam. Mc become
activated(increased protein synthesis
Phagocytic &bactericidal activity)
• produce cytokines, IF alfa & B, IL-1,6,8,
TNF
• engulf wider rang of foreign material
• efficient scavengers of inflam. debris
• certain micro-organisms survive in it for

long period eg. Mycobacterium.
The mononuclear phagocytic system
• BM stem cell promonocyte blood
monocyte tissues eg.
-connective tissue ( Histiocyte )
- Lung (Alveolar macrophage )
- Peritonium (peritoneal macrophage )
- Liver (Kuffer cell )
- Skin (Melanophag )
- Bone (Osteoclast)
- Brain (Microglial cell )
* Specalised histiocytes :
Histiocytic giant cell Langhans cell
Foreign body
Touton
Granuloma formation
- accumulation of modified macrophages, called
epitheliod cells, arranged in small clusters or nodular
collection surrounded by lymphocytes.
• Giant cell granuloma  macrophages fused together,
forming large cells with multiple nuclei (Langhan’s
giant cells).
• Caseating (tuberculoid) granuloma  caseous necrosis
eg. T.B.
- the center of granuloma undergoes necrosis (caseous)
- histologically it is an amorphous, acellular material
staining pink with H/E stain.
- macroscopically this necrosis is solid, hard, cheese-like
and yellowish in color (caseous necrosis).
Histiocytic giant cells :
Formed when particles or bacteria
indigestible by macrophage.
Mc fused  multinucleated giant cells.
Types of these according to their
microscopic appearance:
a- Langhans giant cells= have horseshoe
arrangement of nuclei, characteristically
seen in T.B, sarcodosis.
b- Touton giant cells = central ring of
nuclei and clear peripheral
cytoplasm, seen in adipose tissue
breakdown.
c- Foreign body giant cell = nuclei
randomly scattered through their
cytoplasm, seen in foreign body
material.
Examples of granulomatous disease
• Tuberculosis
Caseating, epitheliod cell granuloma
- Neutrophils are unable to kill mycobacterium
- Macrophages phagocytose the bacilli and act as APCs
to Th1 lymphocytes
- IL-1 secreted by the macrophages activates Th1 cells,
which in turn secrete TNF and INF-γ, that activate the
macrophages to kill the organisms (inactivated
macrophages are unable to kill the multiplying
mycobacterium)
- Macrophages transform into epitheliod cells.
- Tubercular granulomas fuse to form masses visible to
the naked eye.
- Are not diagnostic of TB but suggests the possibility of
T.B.
Tuberculoid leprosy
• Limited to the skin and peripheral nerve
• Shows infiltration by epitheliod & Langhan’s giant
cells & peripheral lymphocytic infiltration (usually in
the deep dermal nerves)
• The granulomatous reaction destroys the nerve &
causes anesthesia.
• Sarcoidosis
• Histoplasmosis
• Schistosomiasis
• Cat scratch disease
• Rheumatic fever
• Crohn’s disease
• Rheumatoid arthritis

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Chronic inflammation

Chronic=process has extend over a

- Certain micro-organisms – persistent infections

- Some disease (autoimmune) eg. Rheumatoid

Extremely variable eg.

-Lymphocytes + plasma cells  Immune

• engulf wider rang of foreign material

• efficient scavengers of inflam. debris

• certain micro-organisms survive in it for

- Brain (Microglial cell )

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