Inflammation

Physiological prototypes and the norm

Long before becoming a standard pathological process, components of the inflammatory response evolutionarily worked to maintain homeostasis. Inflammation is based on entirely physiological mechanisms:

• The expenditure of structures to ensure function became the prototype of alteration.
• Natural tissue homeostasis formed the basis of phagocytosis.
• Blood clotting and transudation reactions transformed into inflammatory exudation.
• Natural cell formation and maturation serve as the basis for proliferation.

According to Academician I.V. Davydovsky, there are analog processes that look like inflammation but represent the physiological norm. Vivid examples of dualistic processes are the menstrual cycle (where endometrial damage, fluid exit, and repair consistently succeed one another) and childbirth.

Three pillars of morphogenesis

To call a reaction true inflammation, a strict combination of three morphological phases is required. In each form of the disease (e.g., purulent or productive inflammation), one component may dominate, but all three are always present.

1. Alteration (from Lat. alter — other, changed). The initiating link. A phlogistic factor damages tissues, altering their metabolism, function, and physicochemical properties. The phase is divided into primary and secondary zones, encompassing biochemical and morphological stages. Vascular reactions and immune activation cannot be triggered without alteration.
2. Exudation. Movement of protein-rich fluid and formed blood elements from the microvasculature (capillaries and small veins) into surrounding tissues. Inflammatory hyperemia and leukocyte emigration develop.
3. Proliferation (from Lat. proliferatio: proles — offspring, ferre — to produce). The final phase. Its logic is to clear the lesion of damaged tissues using obligate phagocytes and restore structural integrity through local cell division.

Differential diagnosis

In pathomorphology and pathophysiology, it is extremely critical to distinguish the inflammatory process from adjacent conditions. The key lies in the absence of one or two mandatory components of the triad:

• Only alteration (without vascular reaction and cell proliferation) = necrosis.
• Only exudation (without prior tissue death and subsequent proliferation) = tissue edema.
• Only proliferation (without damage and exudate) = tumor process.

Biochemical foundation and microcirculation

At the molecular level, alteration instantly triggers the release of inflammatory mediators. Histamine and serotonin are released from mast cells and platelets. Arachidonic acid metabolites (leukotrienes, prostaglandins), the kinin system (bradykinin), and potent cytokines (TNF-α, IL-1, IL-6) become involved.

This humoral cocktail causes vasodilation and increased vascular permeability. At the systemic level, a strict sequence of vascular reactions develops:

1. Brief arteriolar spasm.
2. Arterial hyperemia.
3. Venous hyperemia.
4. Stasis.

It is against the background of these hemodynamic shifts that leukocyte emigration occurs: margination, adhesion to the endothelium, and diapedesis into the lesion.

Class and exam questions

What else to study on this topic

• Five cardinal clinical signs of inflammation (local manifestations).
• Classification of inflammation by predominant component (destructive, exudative, productive).
• Mechanisms of leukocyte emigration (margination, adhesion, diapedesis).
• Differences between the biochemical and morphological phases of alteration.
• Arachidonic acid metabolic pathways: cyclooxygenase and lipoxygenase.
• Extended 5-component diagram of the links of the inflammatory process.

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.