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Pathological Anatomy · Necrosis. Apoptosis

Clinical and morphological forms of necrosis

Necrosis

The classification of clinical and morphological forms of necrosis is based on a combination of factors: etiology, clinical manifestations, morphological picture, and the structural and functional characteristics of the affected organ. The main types of tissue death include dry and wet necrosis, gangrene, infarction, and sequestration.

Color of gangreneThe black hue is due to the formation of iron sulfide when hemoglobin reacts with hydrogen sulfide.
Wet necrosisDevelops in fluid-rich tissues. A classic example is an area of gray softening of the brain.
SequestrumA dead piece of tissue (most often bone) that does not resorb and causes purulent inflammation.
InfarctionVascular necrosis due to ischemia. The shape of the lesion directly depends on the type of arterial branching in the organ.
5 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Coagulative and liquefactive necrosis

Coagulative (dry) necrosis forms under specific conditions: when the tissue has abundant protein, low fluid content, high pH, and reduced activity of hydrolytic processes.

Several characteristic examples of dry necrosis are distinguished:

  • Waxy (Zenker's) necrosis: a lesion of muscle tissue described by Zenker. It occurs in severe infections such as typhoid and epidemic typhus.
  • Caseous necrosis: specific for tuberculosis. Accumulations of monocytic cells in the very center of the granuloma undergo necrosis. The masses consist of precipitated protein and a large amount of lipids, and resemble cottage cheese in color, consistency, and appearance.
  • Fibrinoid necrosis: develops in the setting of allergic and autoimmune diseases.

Liquefactive (wet) necrosis, by contrast, occurs in structures rich in fluid and characterized by high activity of hydrolytic enzymes. A typical example of such a process is an area of gray softening in the brain.

Gangrene: specifics and types

Gangrene (from Greek gangrania — a fire) is the necrosis of tissues that are in contact with the external environment. Affected areas acquire a characteristic black color. This color arises from the formation of iron sulfide when hemoglobin iron reacts with hydrogen sulfide from the air. Gangrene can be localized in the extremities, lungs, intestines, or uterus.

Three main types of gangrene are distinguished:

  1. Dry gangrene. Tissues dry out (mummify). A zone of demarcation inflammation is always clearly defined at the border with living, preserved tissue. The process affects the extremities and body in vascular atherosclerosis, Raynaud's disease, frostbite, burns, and severe infections (e.g., epidemic typhus).
  2. Wet gangrene. Develops under the action of putrefactive microorganisms. The tissue becomes edematous, swells, and emits a foul odor. Unlike the dry form, the demarcation zone is not defined here. It occurs in the lungs, intestines, and uterus. In severely debilitated children (e.g., after measles), noma (cancrum orgis) can occur — a wet gangrene of the skin of the cheeks or perineum.
  3. Pressure ulcer (bedsore). This is a variant of gangrene of trophoneurotic origin. It forms in bedridden patients in areas of greatest pressure on the skin. The risk group includes debilitated patients with infectious, oncological, neurological, and cardiovascular diseases.
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Infarction and sequestrum

Infarction (from Latin infarcire — to stuff, to cram) is a vascular (circulatory) necrosis that arises due to tissue ischemia. Its causes include arterial occlusion by a thrombus or embolus, prolonged arterial spasm, and functional overstrain of an organ under conditions of hypoxia.

The shape of an infarction depends on the development of collaterals and angioarchitecture:

  • Wedge shape: typical for organs with a magistral (stem) type of vascular branching and poorly developed collaterals (kidney, spleen, lung).
  • Irregular shape: characteristic of organs with a mixed or dispersed type of arterial branching (brain, myocardium).

Sequestrum is an area of dead tissue that lies freely among living structures. It possesses three important properties: it does not undergo autolysis, is not replaced by connective tissue, and causes purulent inflammation. Most often, bone tissue undergoes sequestration, and soft tissue only rarely. Sequestra can be independently eliminated from the body through developing fistulous tracts.

Briefly: answers to topical questions

In which organs and tissues does liquefactive necrosis develop?

Liquefactive (wet) necrosis predominantly develops in tissues that are rich in fluid and characterized by high activity of hydrolytic enzymes. The most characteristic example and frequent localization of this type of necrosis is the brain, where a focus of gray softening forms (e.g., in ischemic cerebral infarction).

What microscopic changes in the cell nucleus occur during necrosis?

During necrosis, sequential microscopic changes in the cell nucleus occur, associated with the activation of hydrolases (ribonucleases and deoxyribonucleases). Three main stages of nuclear change are distinguished:

  • Karyopyknosis — shrinking of the nucleus.
  • Karyorrhexis — fragmentation of the nucleus into clumps.
  • Karyolysis — dissolution of the nucleus.

What favorable and unfavorable outcomes of necrosis exist?

Outcomes of necrosis are divided into favorable and unfavorable.

Favorable outcomes are associated with processes of demarcation and repair:

  • Organization — replacement of necrotic masses with connective tissue (scarring).
  • Encapsulation — delimitation of the necrotic area by a connective tissue capsule.
  • Petrification — deposition of calcium salts (dystrophic calcification).
  • Ossification — formation of bone tissue.
  • Cyst or mesoglial scar — specific outcomes in the brain.

Unfavorable outcomes often lead to death or severe organ dysfunction:

  • Purulent liquefaction — purulent lysis of necrotic masses with the risk of infection generalization and the development of sepsis.

What stages are distinguished in the morphogenesis of infarction?

In the morphogenesis of infarction (using myocardial infarction as an example), three consecutive stages are distinguished:

  • Ischemic stage — the pre-necrotic stage, characterized by the buildup of metabolic disorders and the formation of an energy deficit.
  • Necrotic stage — the development of the focus of necrosis itself.
  • Stage of organization — scarring, during which the necrosis zone is replaced by maturing granulation tissue.

In cerebral infarction, microscopic changes are also divided into three stages: development of necrosis, softening (resorption with the formation of "gitter cells" [fat granule cells]), and the formation of a glio-mesodermal scar or cyst.

How to memorize

To easily remember the shape of an infarction, picture the organ's blood vessels. Magistral arteries resemble a tree trunk — when they are occluded, the necrosis zone forms a strict "wedge" (kidney, spleen). Dispersed arteries resemble a bush, so the shape of the infarction turns out to be "irregular" (myocardium, brain).

Class and exam questions

Why is necrosis in tuberculosis called caseous?

The name is due to the external resemblance of necrotic masses to cottage cheese in color and consistency. They consist of precipitated protein and a large amount of lipids, forming in the center of a granuloma from cells of monocytic origin.

What is the main difference between dry and wet gangrene?

In dry gangrene, the tissue mummifies, and a zone of demarcation inflammation is clearly visible at the border with the healthy area. Wet gangrene proceeds with edema and a foul odor due to putrefactive bacteria, and the demarcation line is not defined in it.

What is noma and in whom does it occur?

Noma, or cancrum orgis, is a type of wet gangrene. It is localized on the skin of the cheeks or perineum and occurs in severely debilitated children, for example, after a previous measles infection.

Why is a sequestrum in tissues dangerous?

A sequestrum does not undergo autolysis and is not replaced by a scar. Lying freely among living tissues, this dead area provokes purulent inflammation and the formation of fistulous tracts.

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What else to study on this topic

  • Mechanisms of iron sulfide formation in gangrene
  • Morphology and significance of demarcation inflammation
  • Pathogenesis of trophoneurotic necrosis in pressure ulcers
  • Influence of angioarchitecture on the development of infarction
  • Cellular composition of the granuloma in caseous necrosis

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