General Pathology for Lecture6 Dr. Mukhallad A.

Ramadhan
College of Dentistry

INFLAMMATION AND REPAIR

II. Chronic inflammation: Chronic inflammation can be considered to be

inflammation of prolonged duration (weeks to months to years) in which active
inflammation, tissue injury, and healing proceed simultaneously.

Chronic inflammation is characterized by the following:

• Infiltration with mononuclear ("chronic inflammatory") cells,

including macrophages, lymphocytes, and plasma cells.
• Tissue destruction, largely directed by the inflammatory cells.
• Repair, involving new vessel proliferation (angiogenesis) and fibrosis.

Chronic inflammation arises in the following settings:

a) Viral infections: Intracellular infections of any kind typically require

lymphocytes (and macrophages) to identify and eradicate infected
cells.

b) Persistent microbial infections: most characteristically by a selected

set of microorganisms including mycobacteria (tubercle bacilli).

c) Prolonged exposure to potentially toxic agents: Examples include

nondegradable exogenous material such as inhaled particulate silica.

d) Autoimmune diseases: in which an individual develops an immune

response to self-antigens and tissues (e.g., rheumatoid arthritis or
multiple sclerosis).

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General Pathology for Lecture6 Dr. Mukhallad A. Ramadhan
College of Dentistry

 Chronic Inflammatory Cells:

1. Lymphocytes.
2. Plasma Cells.
3. Eosinophils.
4. Mast Cells.
5. Macrophages: Constituting the critical mainstay and heart of chronic
inflammation, macrophages are tissue cells that derive from circulating blood
monocytes after their emigration from the bloodstream. Macrophages, normally
diffusely scattered in most connective tissues, may also be found in increased
numbers in organs such as the
• Liver (called Kupffer cells).
• Spleen and lymph nodes (called sinus histiocytes).
• Central nervous system (called microglial cells).
• Lungs (called alveolar macrophages).

 Granulomatous Inflammation:
Granulomatous inflammation is a distinctive pattern of chronic inflammation
characterized by aggregates of activated macrophages that assume a squamous cell-
like (epithelioid) appearance.

 Granulomas can form in the setting of persistent T-cell responses to certain

microbes (such as Mycobacterium tuberculosis, Treponema pallidum causing
the syphilitic gumma, or fungi), where T-cell-derived cytokines are
responsible for persistent macrophage activation.
 Granulomas may also develop in response to relatively inert foreign bodies
(e.g., suture, splinter, breast implant), forming so-called foreign body
granulomas.
 Notably, granuloma formation does not always lead to eradication of the
causal agent, which is frequently resistant to killing or degradation.
Nevertheless, the formation of a granuloma effectively "walls off" the
offending agent and is therefore a useful defense mechanism.

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General Pathology for Lecture6 Dr. Mukhallad A. Ramadhan
College of Dentistry

MORPHOLOGY

The aggregates of epithelioid macrophages are surrounded by a collar of

lymphocytes secreting the cytokines responsible for ongoing macrophage activation.
Older granulomas also develop a surrounding rim of fibroblasts and connective
tissue, due to cytokines elaborated by the activated macrophages; this rim of scarring
is useful in containing the injurious agent that caused formation of the granuloma in
the first place, although it may also be a cause of tissue injury and dysfunction.

Multinucleated giant cells: are also found in granulomas. They consist of a large
mass of cytoplasm and multiple nuclei and derive from the fusion of 20 or more
macrophages.

Acentral zone of necrosis. Grossly, this has a granular, cheesy appearance and is
therefore called caseous necrosis.

L
EC

GC

Typical granuloma consist of central necrosis (N), epithelioid cells (EC),

Gaint cels (GC), lymphocytes (L).

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General Pathology for Lecture6 Dr. Mukhallad A. Ramadhan
College of Dentistry
MORPHOLOGIC PATTERNS OF ACUTE AND CHRONIC
INFLAMMATION:

1. SEROUS INFLAMMATION: This is characterized by the outpouring of a

watery, relatively protein-poor fluid (effusion). The skin blister resulting from a burn
or viral infection is a good example of a serous effusion accumulated either within
or immediately beneath the epidermis of the skin.

Blister Serous effusion

2. FIBRINOUS INFLAMMATION: This occurs as a consequence of more severe

injuries, with a resultant greater vascular permeability allowing larger molecules
(specifically, fibrinogen) to pass the endothelial barrier.

Consequence of fibrinous exudates:

A. Resolution: may be degraded by fibrinolysis.

B. Organization: if there is a failure to completely remove the fibrin it will lead

to ingrowth of fibroblasts and blood vessels, leading ultimately to scarring.

Fibrinous Exudate

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General Pathology for Lecture6 Dr. Mukhallad A. Ramadhan
College of Dentistry

3. SUPPURATIVE (PURULENT) INFLAMMATION: This is manifested by the

presence of large amounts of purulent exudate (pus) consisting of neutrophils,
necrotic cells, and edema fluid.
 Abscesses are focal collections of pus ( surrounded by fibrous capsule) that may
be caused by deep seeding of pyogenic organisms into a tissue or by secondary
infections of necrotic foci.

Suppurative inflammation

4. ULCERATION: This refers to a site of inflammation where an epithelial surface

(skin, gastric epithelium, colonic mucosa, bladder epithelium) has become necrotic
and eroded, often with associated subepithelial acute and chronic inflammation.

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