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Inflammation

Inflammatio

For medical students2 min readUpdated 2026-10-10

Inflammation is a complex local vascular-mesenchymal reaction of the body to tissue injury. The process is protective and adaptive in nature, aimed at destroying the injurious agent and restoring tissue integrity.

Core ProcessLocal vascular-mesenchymal reaction
Three ComponentsAlteration, exudation, proliferation
Classical SignsFive cardinal signs by Celsus and Galen
CausesBiological, physical, and chemical phlogogens

History and Classical Signs

The doctrine of inflammation dates back to the works of Hippocrates. Classical pathology defines five cardinal signs of inflammation:

  1. Rubor (redness) — described by A. Celsus.
  2. Tumor (swelling) — identified by A. Celsus.
  3. Calor (heat) — noted by A. Celsus.
  4. Dolor (pain) — identified by A. Celsus.
  5. Functio laesa (loss of function) — added by C. Galen.

Etiology and Causes

Factors that cause the pathological process are called phlogogens. They are divided into three major groups:

Essential Components of the Process

Full-fledged inflammation consists of three inseparable local reactions:

  1. Alteration — primary damage to structures.
  2. Exudation — escape of the liquid portion of blood and blood elements into the lesion.
  3. Proliferation — cell multiplication for tissue repair.

Diagnostic benchmark: isolated damage is termed necrosis, exudation alone is termed edema, and pure proliferation is characteristic of tumors.

Biological Significance

From a general biological perspective, inflammation is evaluated as an optimal protective and adaptive reaction developed throughout evolution. According to I.V. Davydovsky's concept, for humanity as a whole, it is a crucial mechanism for adaptation and acquiring immunity. However, for an individual with reduced reactivity, the inflammatory response may take on severe disease features and lead to a fatal outcome due to imperfect compensatory mechanisms.

Mnemonic

The triad of inflammation: A-E-P (Alteration, Exudation, Proliferation). Without all three components, the diagnosis of "inflammation" cannot be established!

Frequently asked questions

Which specific substances are classified as endogenous chemical phlogogens?

Endogenous chemical phlogogens include substances formed directly within the body:

  • Toxins produced during uremia or azotemia.
  • Excess enzymes.
  • Reactive oxygen species.
What types of exudative inflammation are distinguished based on the nature of the exudate?

Depending on the composition of the formed exudate, four main types of exudative inflammation are distinguished:

  • Serous — main type.
  • Fibrinous — main type.
  • Purulent — main type.
  • Putrid (gangrenous) — main type.

Additionally, there are variants that are not independent types:

  • Catarrhal (catarrh) — develops on mucous membranes, with mucus mixed into the exudate.
  • Hemorrhagic — erythrocytes are mixed into the exudate.
  • Mixed — a combination of different exudates.
What are the types of productive (proliferative) inflammation?

Productive (proliferative) inflammation is classified into several main forms:

  • Interstitial — diffuse inflammation.
  • Granulomatous — formation of granulomas.
  • Inflammation around animal parasites and foreign bodies — aimed at walling off the irritant.

Inflammatory hyperplastic growths (polyps, condylomata acuminata) are not productive inflammation by nature, representing a hyper-regenerative epithelial reaction to chronic exudative inflammation.

Which inflammatory mediators are cellular and which are plasma-derived?

Inflammatory mediators are subdivided into cellular and plasma (humoral) based on their origin.

Mediator GroupRepresentatives
CellularHistamine, heparin, serotonin, granulocytic factors, monokines, lymphokines.
PlasmaComponents of the complement system, plasmin system, and blood coagulation system.

These substances act in concert, providing chemical links between reactions in the inflammatory focus and concentrating efforts on removing injurious factors.

Which cells are the first to emigrate from blood vessels into the lesion during acute inflammation?

Neutrophilic leukocytes are the first to emigrate from blood vessels into the acute inflammatory lesion. Their egress occurs within the first 6–24 hours of the inflammatory process. After 24–48 hours, the picture changes, and monocyte and lymphocyte emigration begins to predominate. After performing their digestive function, polymorphonuclear leukocytes die, and the synthesis of enzymes in macrophages increases within the lesion to clean up the inflammatory field.

How are the names of inflammatory processes correctly formed?

In most cases, the suffix "-itis" is added to the Latin or English name of the organ (e.g., myocardium — myocarditis, liver — hepatitis). Historical exceptions include angina, pneumonia, and empyema.

How does inflammation differ at the species level versus the individual level?

At the human species level, inflammation acts as a flawless protective reaction that forms adaptation and immunity. In a specific patient, it can become a disease and lead to death due to individual insufficiency of protective forces.

What are phlogogens?

These are pathogenic factors of exogenous or endogenous origin (biological, chemical, physical) capable of triggering an inflammatory reaction.

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