Granulomatous

Inflammation
 Granulomatous Inflammation
• It is a distinctive type of chronic inflammation that is
characterized by collection of
Epitheloid cells
Other inflammatory cells
Multinucleate giant cells may also be present

• When granulomatous inflammation is focal,

circumscribed and surrounded by fibrous tissue, it is
known as granuloma.

• Epitheloid cell is derived from macrophage. They are

called epitheloid because of their resemblance to
epithelial cells.
• Granulomas tend to form because the
body is unable to eliminate the
offending agent by the usual process of
phagocytosis and digestion.

• Agents that tend to invoke

granulomatous response actually prefer
to reside in phagocytes. Instead of
being eliminated, they thrive inside
these cells.
Morphological patterns of Gran. Inflammation
Different morphologic patterns of GI are seen. It is
important to recognize these patterns, as they can
provide a clue for diagnosis.

Different patterns seen are:

Diffuse granulomatous inflammation: e.g.

lepromatous leprosy.

Tuberculoid granulomatous inflammation

Non caseating: e.g. sarcoidosis

Caseating: e.g. mycobacteriosis

Suppurative: e.g. cat scratch disease

 Causes of Granulomatous Inflammation
1. Specific infections:
Bacterial: TB, leprosy, brucellosis, lymphogranuloma venereum
and syphillis.
Many fungal diseases: e.g. histoplasmosis
Some parasites: e.g. schistosoma

2. Due to foreign bodies:

Endogenous: keratin, cholesterol, urates
Exogenous: suture material, talc powder, silicone implants.

3. Due to specific chemicals:

e.g. berrylium.

4. Due to certain drugs :

Hepatic granuloma due to phenylbutazone or allupurinol.

5. Idiopathic: Crohn’s disease, sarcoidosis

 Pathogenesis of Granuloma Formation
 Granuloma is a cell mediated hypersensitivity response to the
offending agent.

 On contact with the inciting agent, naïve CD4+ lymphocytes (helper

lymphocytes) are activated.

 This activation is facilitated by IL-12 secretion from macrophages.

 Activated lymphocytes mature into TH1 cells.

 TH1 cell secretes IFN-γ. In turn, IFN-γ stimulates macrophages to

secrete GFs like PDGF, TNF, IL-1, IL-2 etcetera.

 These PRFs incite accumulation of inflammatory cells at the site of

injury.

 IFN-γ is also responsible for converting macrophages into epitheloid

cells and giant cells.
Inflammatory
cell
Pathogenesis
accumulate of granuloma
Contact with
antigen
formation
PDGF, IL 1
TNF, IL 2

IL12
CD4+ T H 1 cell
Macrophage lymphocyte

IFN γ
Tubercular
Lymphadenitis
Scrofula
Tuberculosis
Tuberculosis
Multiple Granulomas Spleen
Miliary TB - Spleen
Granulomatous Inflammation
Epitheloid Cells in a Granuloma
Granuloma showing Giant Cells
Caseation Necrosis
Langhan’s Giant cell and Caseation
Suture Granuloma
Foreign Body Granuloma