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Radang Kronik

Rahmiati
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-γ)
 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 γ production, by activated T-cell
which has antiviral role and will attracted
macrophage. While interferon α and β 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

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