GRANULOMATOUS INFLAMMATION
1- Definition
Granulomatous inflammation is a particular aspect of chronic inflammatory reaction
where cellular phenomena predominate. This is a histiocytic inflammation formed
of circumscribed lesions corresponding to a grouping of macrophages: the granuloma.
A GRANULOMA is defined as an agglomeration of histiocytic cells, often very
limited, often surrounded by lymphocytes and which may contain varying proportions of
epithelioid cells and multinucleated giant cells.
Inflammatory granuloma always reflects the persistence of the pathogenic agent, even if it
is not always visible. This persistence is linked to:
– or incomplete phagocytosis: resistance of germs, non-resorbable foreign bodies, enzymatic deficiency.
– or a +/- complete inefficiency of the immune system.
– either an overflow of the 2 defense phenomena by the permanent arrival of agents
inflammatory, or a natural resistance specific to certain germs.
In the granuloma, histiocytes transform into epithelioid cells and by fusion into
multinucleated giant cells.
– epithelioid cells : large cells of various shapes, rounded, elongated or
fusiform. Their nuclei are ovoid, elongated or notched. Their cytoplasm is abundant.
Their name comes from the resemblance to epithelial cells.
Epithelioid cells are highly activated histiocytes secreting cytokines and enzymes. On the other hand, their phagocytic activity is reduced.
The mechanisms of histiocyte activation into epithelioid cells are poorly understood.
– giant cells: 2 types:
– Langhans cells by fusion of epithelioid cells.
– Muller cells by nuclear division without cytoplasmic division
2- Main etiologies of granulomatous inflammation
Granulomatous inflammation can be nonspecific, or specific, that is,
allowing an etiological diagnosis:
By a characteristic aspect: epithelioid and gigantocellular granuloma
By the presence of an identifiable infectious agent
Etiologies:
– Infectious lesions
Bacterial lesions: Typical mycobacterium (Koch’s bacillus) or atypical.
Fungal lesions-mycoses: candidiasis, aspergillosis
Viral lesions: herpes virus
Parasitosis: echinococcosis
– Non-infectious lesions : Crohn’s disease, Sarcoidosis, beryllium disease, stroma of certain
tumors, granulomatous vasculitis
3- Pathogenesis
There are 2 types of granulomas, with different pathogenesis
A- Foreign body granuloma
It is very common. It is triggered by relatively inert foreign bodies.
Granuloma occurs mainly when the material is too large to be phagocytosed by a single macrophage, and does not induce an inflammatory or immune reaction of its own.
Examples:
– Exogenous foreign bodies: mineral or plant fragments introduced into a wound, threads
suture, silica, asbestos, talc.
– Endogenous foreign bodies: lipids released during cell necrosis.
Microscopic appearance
This granuloma is generally richer in giant cells than in epithelioid cells.
Sometimes there are small granulomas with a foreign body embedded in a cell.
giant. More often, the foreign body is surrounded by several giant cells which mold
on it. The foreign body can usually be identified in the center of the granuloma, especially
when it is birefringent in polarized light.
Evolution: the inflammatory reaction to foreign bodies does not tend to regress and heal
if the foreign body that triggers it is not resorbable and cannot be eliminated.
GRANULOMATOUS INFLAMMATION
B- Immune granuloma: epithelioid and giant cell granuloma
It is caused by insoluble particles capable of inducing an immune response to
cell-mediated (delayed hypersensitivity type IV).
5- Examples of granulomatous lesions
Tuberculosis
This is an example of granulomatous inflammation. This is the typical example of a granuloma.
epithelioid and gigantocellular (immune). The presence of Mycobacterium tuberculosis in the tissues triggers an inflammatory reaction that follows the successive phases of inflammation: exudative, cellular, repair with fibrosis.
It has 2 specific characteristics :
– epithelioid and giant cell granulomatous lesions
– appearance of a specific necrosis: caseous necrosis
Different phases
Acute phase : this is an exudative phase rich in bacilli, with non-infectious lesions.
specific, consisting of edema, polymorphonuclear neutrophils and histiocytes.
At this stage caseous necrosis appears . The name “caseum” comes from the appearance
macroscopic, resembling curdled milk. This is a focus of tissue destruction.
Histologically, it is a homogeneous eosinophilic substance devoid of cells,
of uniform appearance.
The caseum can change: liquefy which allows the evacuation and drainage of the focus
tuberculous with formation of a cavity (cavern) and contamination of neighboring tissues. It
may also dry out or calcify.
Cellular phase : granulomatous lesions (immunological granuloma indicating the onset of
cell-mediated immunity game).
Macroscopy: Well-defined and persistent nodules in the tissues: miliary granulations (1-2
mm), miliary tubercles (2-3 mm), encysted tubercles (1-3 cm).
Histology : Granulomas forming rounded nodules composed of epithelioid cells
arranged in a palisade, mixed with a variable number of giant cells . On the periphery we
note a crown of lymphocytes . Further outward, and in more advanced lesions, there is
fibroblasts and collagen. These nodules are sometimes centered with caseous necrosis .
.
Repair phase: scar fibrosis
Debridement of the caseum is difficult and maintains persistent chronic inflammation; sclerosis will most often be encircling sclerosis around the caseous foci.
Please note that caseum never resolves spontaneously. There are 3 possible developments:
– persistence
– elimination after fistulization in a cavity
– calcification
Location
Pulmonary localization is the most frequent spontaneous form, other localizations
parenchymatous are multiple and responsible for urinary, meningeal,
genitals…..
Sarcoidosis or Besnier Boeck Schaumann (BBS) disease
It is a condition of unknown cause characterized histologically by a reaction
inflammatory granulomatous: epithelioid and giant cell granulomas without caseous necrosis, often well-defined, more or less confluent. Giant cells may contain inclusions called asteroid bodies and Schaumann bodies. It can affect all organs (mediastino-pulmonary in 90% of cases, lymph nodes, spleen, liver, skin).
The evolution is towards fibrosis. The microscopic lesions are evocative but not
pathognomonic, not allowing the diagnosis to be confirmed on their own. The anatomo-pathological diagnosis can be made on bronchopulmonary, lymph node, cutaneous, accessory salivary gland and hepatic biopsies.
Other examples
– giant cell temporal arteritis or Horton’s disease
– Takayashu arteritis
– Crohn’s disease
GRANULOMATOUS INFLAMMATION
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