The inflammatory process is the set of local and systemic reaction processes of the body in response to any form of exogenous and endogenous tissue aggression.

It is recognized clinically by the 4 cardinal signs of Galen: heat, redness, swelling (tumor), pain.

It tends to mitigate and repair the effects of the attack but his sometimes its deleterious effects.

It proceeds in two phases: the vascular and exudative phases and cell phase. It ends with injury repair.

A- Phase vascular inflammation:

Vascular and blood reactions include three phenomena: active congestion, inflammatory edema, leukocyte diapedesis.

• Active congestion is due to vasodilation occurred after vasoconstriction phase which promotes hemostasis.

It arteether-riolaire and capillary.

It is determined by a nervous mechanism (vasomotor nerves), chemical mechanism involving histamine, serotonin, kinins and prostaglandins.

• The inflammatory edema is a phenomenon due to the passage of plasma close to the liquid in the interstitial medium.

Associated with the increase of the hydrostatic pressure and especially to increase the permeability of the vascular wall.

The edema result: ① dilute harmful agents; ② circumscribe the inflammatory focus by fibrinogen barrier; ③ focus on site means humoral defense (Ig, complement); ④ slow the bloodstream by the hemoconcentration (5) promotes leukocyte diapedesis.

The inflammatory edema in a cavity gives a protein-rich exudate.

The predominance of vascular reaction characterizes acute inflammations.

B- Phase cell inflammation:

– Most often PNN are gradually replaced the inflammatory site by mononuclear cells.

Macrophages -> debridement.

When inflammation becomes chronic, inflammatory infiltrate consists of a majority of mononuclear cells (lymphocytes, macrophages …).

Cellular reactions are accompanied by a significant neogenesis.

C- Healing:

* The normal healing:

The tissue formed after the vascular and exudative phase is the fleshy bud or regeneration blastema.

It includes: an abundant interstitial substance edematous; numerous dilated capillaries, congested with radial disposition; cells that forms the inflammatory granuloma (dense polymorphic population that associates sometimes polymorphonuclear eosinophils, lymphocytes, macrophages, fibroblasts, mast cells).

From the granulation tissue (or regeneration blastema) will be wound with usually a complete restoration of pre-existing fabrics.

Three conditions are necessary for proper healing:

– Debridement is mandatory if there is an outbreak of necrosis or tissue debris.

Macrophage-mediated necrotic debris is so scarce.

If necrotic products are abundant, you have an external debridement: Spontaneous -> liquefying necrotic material (pus) and removal by fistula in a natural conduit or fistula to the skin; Sometimes removing block -> bourbillon the boil.

Or surgical debridement.

– The coaptation is the contraction of inflammatory focus rapprochement and even confrontation with its banks.

– Good vascularization: the contribution is essential for cells and substances needed to repair.

If vascularisa-tion is bad the chronicity is a risk (varicose ulcer …)

Some pathological situations prevent or delay the normal healing. It is then a chronic inflammation.

* The pathological scarring:

-> (Fibrosis)

Exaggeration of the development of granulation tissue -> Inflammatory pseudotumor; Pyogenic granuloma or at the skin or mucosa.

Destroyed many organs do not have the ability to regenerate due to the existence of specialized cells (myocardial fibers, renal glomeruli, neurons …).

Destroys parenchyma is replaced by fibrosis.

The fibrosis is defined as an increase of the conjunctiva weft of a fabric.

– Young Fibrosis: firm, but not hard, just very dense cell-rich inflammatory elements

– Converted: hard, very little cell, particularly consisting of collagen fiber.

Maximum is composed of hyaline sclerosis (glassy and homogeneous safranophiles coloring).

Fibrosis can be: atrophic, hypertrophic (keloid).

Can be mutilating (cirrhosis); systematized (portal fibrosis).

The fi-brosis is usually of inflammatory origin, but it may be due to tissue aging, metabolic cause, or a reaction to a tumor process.

D- The clinical forms of inflammation:

* Acute inflammation:

– Congestive: active congestion -> sunburn

– Hemorrhagic: increased vascular permeability (altered vascular wall) aboutis extravasation GR (érythrodiapédèse) -> Malignant flu

– Oedematous: serous exudation poor fibrin -> urticaria, angioedema

– Fibrinous inflammation: plasma exudation more or less rich in fibrin, which may result in the formation of solid deposits. Example: false membranes of diphtheria angina.

– Fibrin-leukocyte Inflammation: associated with a fibrinous exudate leukocyte influx is more or less important, diapedesis. Example: alveolitis fibrin-leukocyte pneumonia.

– Purulent: the presence of a large number of altered PNN (pus cells) -> pyogenic infection

– Necrotizing or gangrenous: ischemic or bacterial necrosis (Clostridium perfringens).

Dry gangrene is suppuration, for against the wet gangrene is an suppuration.

* Subacute Inflammation:

It is a cellular inflammation (productive).

It is characterized by an inflammatory granulation tissue (inflamma-tory granuloma) rich in mononuclear cells (monocytes, lymphocytes, and plasma cells).

It can be characterized by an abundance of histiocytes -> Aschoff nodule of the CEOS.

Lipophilic granulomas are characterized by the presence of macrophages charged with grease (acute pancreatitis).

Syphilis in the perivascular granuloma is rich in plasma cells (plasma cell granuloma). Granulomatous infections (nodule tuberculoid).

Foreign body granuloma (giant cells).

Autoimmune diseases.

* Chronic inflammation:

It is characterized by the importance of fibrosis.

In some chronic inflammation cell can remain predominant reaction and fibrosis remains lightly.

These are readily epithelioid granulomas.


The abscess was formed in 2 phases,

-> Phase phlegmonous: marked by major vascular and exudative phenomena (congestion, edema, diapedesis).

Reached the home is large, extended by lymphangitis.

-> Collection phase: purulent necrosis; the lesions are circumscribed;pus occupies the center of an inflammatory pocket.

The wall includes two intertwined areas, the external part is the repair phenomenon corresponds to the inner part pheno- nomena vascular congestion.

-> Evolution: positive by debridement (spontaneous or surgical). By unfavorable progression of suppuration by fistula (with inadequate debridement) enkystement exaggerated …


• Érythrodiapédèse: pathological phenomenon -> vascular walls are damaged.

It leads to interstitial hemorrhage. -> Serious infections.

• The cell phase productive phase that involves three types of cells: lymphocytes; macrophages; fibroblasts

• In the cell phase adaptive modification: Metamorphosis (monocytes -> macrophages), mobilization and multiplica-tion. And neogenesis (new MEC)


• Phlegmon: variety of suppurative inflammation much rarer than the abscess, characterized by the diffusion of pus without trend collection

• Healing: stabilizes after several months.

Poor debridement prevents scarring (it must be caused in the event of significant necrosis: Surgical incision drainage).

The good trophicity accelerates healing.

• Effect of inflammation on the epithelium:

-> Metaplasia (it is acquired; heterotopia is congenital)

-> Hypertrophic Regeneration