Radang Kronik

Rino Pattiata
Dept. Patologi Anatomik
FKUI
DEFINITION

Long-term inflammation where the

inflammation process is active, while
tissue damage and repair was done
simultaneously
Chronic inflammation

Mononuclear cell infiltration such as :

macrophage, lymphocyte and plasma
cell
Tissue damage
Repair: angiogenesis and fibrosis
Causes of chronic
inflammation
Viral infection
Persistent microbes infection
Long term toxic agent
Autoimmune disease
Cells in chronic inflammation

Macrophage
Lymphocyte
Plasma cell
Eosinophyl
Mast cell
Makrofag (1)

Monocyte half-time is 1 day, under influence of

adhesion molecule and chemotactic factor will
go to inflammation area
Change into macrophage in tissue
Activated into epitheloid cells
Activated signal:
Sitokin (IFN-)
Endotoksin
Mediators produce during acute inflammation
Extracellular matrix such as fibronectin
Makrophage (2)

Activated macrophage could produce

certain producr that will lead tissue into
necrotic and fibrosis
Acid and basic proteases
Complement Komponen komplemen dan
faktor pembekuan
Oksigen reaktif dan NO
Metabolit asam arakhidonat (eikosanoid)
Sitokin : IL-1, TNF dan berbagai growth
factor
Cellular co-operation

Macrophage in the inflammation area cause by

MIF, while MAF will stimulate phagocytosis
Production of several inflammation mediators
Lymphocytes attracted
Target cell destruction
Interferon production, by activated T-cell
which has antiviral role and will attracted
macrophage. While interferon and will
activated NK-cell and macrophage
Granulomatosa inflammation

Chronic inflammation showed aggregate

of activated histiocyte (epitheloid)
Could be caused by persisten T-cell
response
Activated T-cell will produce cytokine
which will caused persistent macrophage
activation
Serous inflammation

Efussion
A few protein
Injury against pleural mesotel pleura,
peritoneum and pericardium
Burnt or viral infection at skin epidermis
Fibrinosa inflammation

More severe injury, so bigger molecules

can pass by including fibrin
fibrin exudate will be degraded by
fibrynolisis resolution
Failed: organisation
Resolusi
Organisation

Scar formation
Started with granulation tissue consisted of
endothelial cell proliferation and myofibroblast
Myofibroblas : collagen secretion and othe
matrix component; also have muscle filament
and ability to bind to surrounding cell
Granulation tissue will be change into mature
fibrous tissue
Suppurative/purulent
inflammation
Contain pus/purulent exudate consisted
of necrotic tissue, neutrophyl and
edematous solution
Caused by pyogenic bacteria
Could be formed as abscess
Ulcer

Loss of the entire surface

mucosal/epithelium
Base of ulcer is granulation tissues