Inflammation is a complex tissue reaction to injury that manifests in two main forms: acute (the classical variant) and chronic (an aberrant response). The onset rate, duration, and outcome of the process directly depend on the properties of the etiologic factor and the baseline reactivity of the organism.
Acute courseUnder normal organism reactivity, the acute process resolves completely within 1–2 weeks.
HyperergyA type of course characterized by dominant severe tissue alteration and destruction within the lesion.
ChronificationMorphologically manifested by monocytic-lymphocytic infiltration and granuloma formation.
LIRS syndromeA modern designation for the combination of the five classic local signs of inflammation.
Classification by Onset Rate and Course
The interaction of a phlogistic (injurious) agent with tissues leads to one of two forms of the inflammatory response. The classification is based on the rate of reaction development and the overall duration of the process.
Acute inflammation. This is the classical, evolutionarily conserved variant of the reaction. It develops intensely. With a normoergic course (adequate reactivity), the process takes 1–2 weeks. Mild to moderate phenomena of injury (alteration and destruction), fluid extravasation into tissues (exudation), and cellular proliferation are observed in the lesion.
Chronic inflammation. Considered a variant of an inadequate protective response.
The clinical presentation is critically influenced by the reactivity of the organism:
In a hypoergic course, all classical signs of inflammation are extremely weak, and the process is sluggish.
In a hyperergic course, the reaction is excessive: severe alteration and massive destruction of the body's own tissues come to the forefront.
Features of Chronic Inflammation
The chronification of the process can follow two distinct scenarios:
Primary chronic. Arises immediately after exposure to the phlogistic agent, completely bypassing the acute phase. Initially characterized by a persistent, prolonged, and sluggish nature.
Secondary chronic. Forms as an outcome of initially acute inflammation that failed to resolve in time and became protracted.
Morphological markers of a chronic course:
Appearance of foci of tissue necrosis.
Pronounced monocytic and lymphocytic infiltration in the injury zone.
Formation of specific structures—granulomas and protective capsules.
Main Causes of Chronification
Five key groups of etiologic factors sustaining prolonged inflammation are distinguished:
Persistence of infection (bacteria, protozoa, chlamydia, mycoplasmas, rickettsiae, spirochetes, fungi) with parallel development of delayed-type hypersensitivity.
Prolonged exposure of foreign factors to tissues (foreign bodies, organic and inorganic dust).
Endocrine shifts, specifically chronic stress with persistently high blood levels of catecholamines and glucocorticoids.
Immune autoaggression (observed in systemic lupus erythematosus, rheumatoid arthritis).
Phagocytic deficiency (congenital, hereditary, or acquired).
Local Signs of Inflammation (LIRS)
Manifestations of the inflammatory process are subdivided into local and general (systemic). Local signs were described in antiquity and are known as the classical pentad of Celsus-Galen. In modern medical literature, this symptom complex is designated by the term LIRS (Local Inflammatory Response Syndrome).
The pentad includes:
Rubor — redness;
Tumor — swelling;
Dolor — pain;
Calor — heat (local temperature elevation);
Functio laesa — loss of function of the organ or tissue.
Pathogenesis of Redness (Rubor)
Visually, this sign appears as hyperemia of the skin or mucous membranes directly over the inflammatory focus. This is due to profound vascular changes:
Active hyperemia develops.
Precapillaries dilate and their number increases.
The number of functioning capillaries sharply increases, and they become engorged with arterial blood.
Arterialization of venous blood is observed. Due to accelerated blood flow and reduced oxygen utilization by the damaged tissue, the oxyhemoglobin ($HbO_2$) content in the venous bed anomalously increases.
Mnemonic
The classical pentad of local signs is easily remembered as a rhythmic Latin tongue-twister: «Rubor, tumor, calor, dolor et functio laesa» (Redness, swelling, heat, pain, and loss of function).
Frequently asked questions
What is the pathogenesis of swelling (Tumor) development in inflammation?
The pathogenesis of swelling (Tumor) in inflammation consists of the escape of plasma and blood cellular elements into tissues with the formation of exudate.
The process of inflammatory edema formation includes the following mechanisms:
Exudation — the exit of the liquid part of the blood and cells from microvessels into tissues or body cavities.
Action of mediators — the release of histamine and bradykinin in response to injury.
Vascular reactions — vasodilation and a sharp increase in vascular wall permeability.
As a result of these changes, enhanced filtration of fluid with a high protein content occurs outside the vascular bed, leading to an increase in tissue volume.
Which inflammatory mediators cause the development of pain (Dolor)?
The development of pain (Dolor) in inflammation is associated with the action of pain mediators.
Pain mediators include:
Prostaglandins in complex with histamine, serotonin, bradykinin, and substance P.
Prostaglandins increase the sensitivity of pain receptors to algogens.
Decreased synthesis of PGE₂ prevents the sensitization of pain receptors to chemical irritants such as bradykinin and histamine released in the inflammatory focus.
Maximum release of pain mediators occurs during the exacerbation of a chronic inflammatory process.
What is the difference between primary and secondary chronic inflammation?
Primary chronic inflammation initially runs a sluggish and persistent course, bypassing the acute stage. Secondary chronic inflammation develops as a continuation of an acute process that did not resolve with recovery and became protracted.
Why does venous blood in the inflammatory lesion become 'arterialized'?
This occurs due to the acceleration of local blood flow and decreased oxygen consumption by damaged tissues. As a result, venous blood retains a high content of oxyhemoglobin ($HbO_2$), giving it a bright red color and causing the symptom of redness (Rubor).
How do hypoergy and hyperergy alter the picture of inflammation?
In a hypoergic course, the reactivity of the organism is reduced, so the signs of inflammation are weakly expressed. In a hyperergic course, the reaction is inappropriately strong: alteration (injury) and tissue destruction processes predominate in the lesion.
Go deeper
Mechanisms of active hyperemia and exudation development
Pathogenesis of granuloma formation in chronic inflammation
Role of delayed-type hypersensitivity in microbial persistence
Types and causes of phagocytic deficiency
Effects of glucocorticoids and catecholamines on the inflammatory response