Necrosis

Necrosis (from the Ancient Greek νεκρός — “dead”) is a pathological process of irreversible cell and tissue death in a living organism, caused by various damaging factors. Necrosis must be distinguished from apoptosis, which is programmed, physiological cell death that occurs without an inflammatory reaction.

Cellular swelling, protein denaturation, and destruction of cellular organelles are the key characteristics of necrosis. Intracellular contents released into the surrounding tissue provoke inflammation — an important diagnostic feature.

Aetiology and Pathophysiology

Necrosis tends to develop in response to an extremely aggressive irritant when the tissue is no longer able to adapt. Necrosis may be classified by etiology.

Main causes:

• Vascular (ischemic): This is the most common cause. It results from cessation or sharp reduction of blood supply to the tissue, leading to hypoxia and cell death. Myocardial infarction is a typical illustration of this mechanism.
• Traumatic: This type of necrosis develops following direct physical destruction of the tissue (blunt injury, rupture) or exposure to physical factors (burns, frostbite, radiation).
• Toxic: Necrosis may be triggered by chemical substances or toxins. This includes bacterial toxins (e.g., in gas gangrene) or chemical agents (acids, alkalis, poisons).
• Allergic (immune-mediated): Necrosis develops as a result of immune reactions in sensitized tissues, such as in the Arthus phenomenon.

Clinical and Morphological Forms

Depending on tissue structure and the cause of cell death, necrosis can take different forms, which vary in appearance and consistency.

Basic forms include:

• Coagulative (dry) necrosis: Typical of protein-rich organs (heart, kidneys, spleen). Necrotic tissue becomes firm, dry, and grayish-yellow. Structural outlines of the tissue are preserved for some time. It may also develop following exposure to aggressive acids. Acid causes protein denaturation and the formation of a dense, crust-like film on the tissue surface. This film acts as a protective barrier, preventing further acid penetration.
• Liquefactive (wet) necrosis: Enzymatic digestion of dead tissue, producing a liquid or semi-fluid mass. This type of necrosis is typical of protein-poor, fluid-rich tissues (e.g., the brain in ischemic stroke). It may also develop when tissue is exposed to concentrated alkaline solutions. The process is dangerous, as tissue continues to be damaged until the alkali is neutralized or diluted, and alkali can penetrate deeply into tissue.
• Gangrene: A form of necrosis affecting tissues in contact with the external environment. Gangrene may present as dry, wet, or gas lesions.
• Caseous (cheese-like) necrosis: A form of coagulative necrosis in which dead tissue resembles dry, crumbly cheese. It is pathognomonic for tuberculosis.
• Sequestrum: A fragment of necrotic bone that does not undergo autolysis and remains separated within sound bone.

Clinical Significance and Outcomes

The outcome of necrosis depends on its type, extent, and localization. Dead tissue may undergo organization and be replaced by connective tissue (scarring); encapsulation (when a fibrous capsule is formed); or petrification (calcium salt deposition). Wet necrosis and gangrene are particularly dangerous due to absorption of toxic breakdown products, which can lead to severe intoxication and sepsis. Treatment often requires surgery — necrectomy, i.e., excision of nonviable tissue.