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Clinical and Morphological Forms of Necrosis

Necrosis

For medical students2 min readUpdated 2026-10-10

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

Color of GangreneThe black color is due to the formation of iron sulfide from the reaction of hemoglobin iron with hydrogen sulfide.
Liquefactive NecrosisDevelops in fluid-rich tissues. A classic example is an area of gray softening in the brain.
SequestrumA dead piece of tissue (usually bone) that is not reabsorbed and causes purulent inflammation.
InfarctionVascular necrosis due to ischemia. The shape of the lesion directly depends on the branching pattern of arteries in the organ.

Coagulative and Liquefactive Necrosis

Coagulative (dry) necrosis occurs under specific conditions: high protein content, low fluid content, high pH, and reduced hydrolytic activity.

Key examples of dry necrosis include:

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

Gangrene: Features and Types

Gangrene (from Greek gangraina — a fire) refers to the necrosis of tissue that is exposed to the external environment. Affected areas acquire a characteristic black color. This color results from the formation of iron sulfide when hemoglobin iron reacts with hydrogen sulfide from the air. Gangrene can affect the extremities, lungs, intestines, or uterus.

There are three main types of gangrene:

  1. Dry gangrene. Tissues dry out (mummify). A clear demarcation line (zone of demarcation inflammation) is always visible at the border with living, preserved tissue. This process typically affects the extremities and body due to atherosclerosis, Raynaud's disease, frostbite, burns, and severe infections (e.g., typhus).
  2. Wet gangrene. Develops under the action of putrefactive bacteria. The tissue becomes edematous, swells, and emits a foul odor. Unlike the dry form, a clear demarcation zone is absent. It is found in the lungs, intestines, and uterus. In severely debilitated children (e.g., after measles), noma (cancrum oris) may develop — a form of wet gangrene affecting the skin of the cheeks or perineum.
  3. Pressure ulcer (bedsore). A form of gangrene of trophoneurotic origin. It forms in bedridden patients over areas subjected to prolonged pressure. Risk factors include debilitated patients with infectious, oncological, neurological, and cardiovascular diseases.

Infarction and Sequestrum

Infarction (from Latin infarcire — to stuff) is a type of vascular (circulatory) necrosis caused by tissue ischemia. Causes include arterial occlusion by a thrombus or embolus, prolonged arterial spasm, and functional overload of the organ under conditions of hypoxia.

The shape of an infarction depends on collateral circulation and angioarchitecture:

Aosequestrum is a piece of dead tissue that lies free within living structures. It has three key properties: it does not undergo autolysis, it is not replaced by connective tissue, and it causes purulent inflammation. Most commonly, sequestration affects bone tissue, and rarely, soft tissues. Sequestra may spontaneously eliminate from the body through developing sinus tracts.

Mnemonic

To easily remember the shape of an infarction, visualize the organ's blood supply. End-arteries resemble a tree trunk—when occluded, the necrotic zone forms a strict "wedge" (kidney, spleen). Dispersed arteries resemble a bush, resulting in an "irregular" infarction shape (myocardium, brain).

Frequently asked questions

In which organs and tissues does liquefactive necrosis develop?

Liquefactive (wet) necrosis predominantly develops in tissues rich in fluid and high in hydrolytic enzyme activity. A classic example and frequent location of this type of necrosis is the brain, where an area of gray softening forms (e.g., in ischemic stroke).

What microscopic nuclear changes occur during necrosis?

Necrosis involves sequential microscopic nuclear changes due to the activation of hydrolases (ribonucleases and deoxyribonucleases). The three main nuclear stages are:

  • Karyopyknosis — nuclear shrinkage.
  • Karyorrhexis — fragmentation of the nucleus.
  • Karyolysis — dissolution of the nucleus.
What are the favorable and unfavorable outcomes of necrosis?

Outcomes of necrosis are divided into favorable and unfavorable.

Favorable outcomes are associated with containment and repair processes:

  • Organization — replacement of necrotic debris by connective tissue (scarring).
  • Encapsulation — walling off the necrotic area with a connective tissue capsule.
  • Petrification — deposition of calcium salts (dystrophic calcification).
  • Ossification — formation of bone tissue.
  • Cyst formation or glial scar — specific outcomes in the central nervous system.

Unfavorable outcomes often lead to death or severe organ dysfunction:

  • Purulent liquefaction — enzymatic lysis of necrotic masses with a risk of infection spreading and sepsis.
What stages occur in the morphogenesis of infarction?

The morphogenesis of infarction (using myocardial infarction as an example) includes three sequential stages:

  • Ischemic stage — pre-necrotic stage characterized by worsening metabolic disturbances and energy deficit.
  • Necrotic stage — development of the actual area of cell death.
  • Organization stage — scarring, where the necrotic zone is replaced by maturing granulation tissue.

In cerebral infarction, microscopic changes are also divided into three stages: necrosis development, softening (resorption with lipid-laden macrophages / "gitter cells"), and the formation of a glial-mesodermal scar or cyst.

Why is necrosis in tuberculosis called caseous (cheesy)?

The name comes from the external resemblance of necrotic debris to cottage cheese in color and consistency. It consists of precipitated proteins and abundant lipids, formed in the center of a granuloma from mononuclear-derived cells.

What is the main difference between dry and wet gangrene?

In dry gangrene, the tissue mummifies, and a clear zone of demarcation inflammation is visible at the border with healthy tissue. Wet gangrene presents with edema, a foul odor due to putrefactive bacteria, and lacks a clear demarcation line.

What is noma and who gets it?

Noma (cancrum oris) is a type of wet gangrene. It localizes to the skin of the cheeks or perineum and occurs in severely malnourished or debilitated children, for example, following measles.

Why is a sequestrum dangerous in tissues?

A sequestrum does not undergo autolysis and is not replaced by a scar. Lying freely among living tissues, this dead fragment provokes purulent inflammation and sinus tract formation.

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