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 Stimulus is persistent

 Recruitment of monocytes is maintained

 Existing macrophages are attached in place

 Proliferation of macrophages is stimulated

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ACUTE INFLAMMATION CHRONIC INFLAMMATION
 Rapid onset & short  Gradual onset & long
duration duration

 Marked vascular changes  Mild vascular changes,

vascular thickening
 Abundant fluid exudate  Usually scanty fluid
exudate

 Main inflammatory cells:  Main inflammatory cells:

neutrophils & macrophages,
macrophages lymphocytes, plasma cells
and giant cells.
 Absent or mild fibrosis  Marked fibrosis

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 Chronic non-specific inflammations:
◦ Conventional features of chronic inflammation
◦ Follow acute inflammation e.g. chronic osteomyelitis,
chronic ulcer etc.

 Chronic specific inflammations:

◦ Conventional features of chronic inflammation
◦ Characteristic microscopic picture
◦ They usually start chronic.
◦ Occurs in the form of Granulomas.
◦ Granulomas form when the immune system
isolates an antigen but is unable to completely
destroy it.
Chronic specific inflammation
 Focal accumulation of
macrophages that are transformed
into epithelioid cells.
 Surrounded by lymphocytes,
plasma cells
 Epithelioid cells fuse to form giant
cells in the periphery or center of
granulomas
 Older granulomas develop an
inclosing edge of fibroblasts &
connective tissue.

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1. Infective granuloma:
◦ a) Bacterial as tuberculosis, leprosy
◦ b) Parasitic as bilharziasis
◦ c) Fungal as cryptococcosis

2. Foreign body granuloma:

◦ a) Silicosis & asbestosis
◦ b) Granuloma around pieces of wood or
glass, catgut
3. Granuloma of unknown cause e.g.
Sarcoidosis

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 Repair is the replacement of damaged tissue by
a new healthy one.
TYPES OF REPAIR:
I. REGENERATION:
 Replacement of damaged cells by new cells of
the same type.
 This is done by proliferation of the surrounding
living cells.
II. HEALING BY FIBROSIS:
 Replacement of damaged tissue by granulation
tissue (fibroblasts & capillaries) which matures
to fibrous (scar) tissue.

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I. Local factors:
 Extent of tissue damage
 Type of damaged cells: Labile, stable or
permanent cells
 Blood supply: Poor blood supply and
ischaemia delays repair.
 Infection & presence of foreign bodies

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II. General factors:
 Age

 Malnutrition: Protein deficiency, Vitamins C &

D deficiencies, zinc deficiency.
 Glucocorticoid and cytotoxic drugs delay
repair.
 Diabetes mellitus is associated with defective
repair.

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 The type of repair is mainly determined by
the type of damaged cells.
 They are divided into three groups:
1- Labile cells
2-Stable cells
3-Permenant cells

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Labile cells:
 Proliferate continuously throughout life to replace
ageing cells.
 They have a good power of regeneration .e.g.
surface epithelium, lymphoid & hematopoeitic
tissues.
Stable cells:
 Proliferate only when there is a need,
 They have a moderate power of regeneration e.g.
parenchymal cells of liver, kidney & pancreas.
mesenchymal cells as smooth muscles, fibroblasts &
osteoblasts.
 Repair in these cells occur by regeneration & or by
fibrosis.

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Permanent cells:
Cannot proliferate at all (These cells do not
regenerate).
◦ Damaged cardiac and skeletal muscle cells
are healed by fibrosis, which is the
deposition of fibrous tissue by fibroblasts.
 Damaged nerve cells are healed by gliosis,
which is the deposition of glial fibers by the
astrocytes.

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MD 406, 2022
MECHANISM OF FIBROSIS:
Angiogenesis:
Formation of new capillaries budding from
old vessels

 Fibrogenesis:
Consisting of emigration & proliferation of
fibroblasts
Production of extracellular matrix proteins
& collagen, thus forming a scar

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 Scar remodeling by:
1. Resorption of capillaries by macrophages.

2. Scar decreases in size by the contractile

action of myofibroblasts (modified
fibroblasts) & the action of collagenases
produced by the macrophages.

 Mature scar consists of collagen, few or no

capillaries, matrix and inactive fibroblasts.

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