necrosis

Necrosis is a form of cell death that results from acute cellular injury in living tissue. It is characterized by loss of plasma membrane integrity, uncontrolled enzymatic digestion of cellular components, and subsequent inflammation. Necrosis is distinct from programmed cell death such as apoptosis, which is orderly and non-inflammatory.

Types of necrosis are described by tissue appearance and underlying mechanism. Coagulative necrosis is the most common pattern after ischemia in solid organs; the architecture is initially preserved but cells are dead. Liquefactive necrosis involves enzymatic digestion that turns tissue into a liquid mass, typical of brain infarcts and abscesses. Caseous necrosis has a cheese-like appearance and is characteristic of tuberculosis. Fat necrosis involves the breakdown of adipose tissue, as seen in pancreatitis and breast tissue. Fibrinoid necrosis refers to immune complex– and antibody-mediated damage to vessel walls, with deposition of fibrin-like material.

Mechanistically, necrosis results from severe energy failure, loss of ion homeostasis, membrane rupture, and leakage of lysosomal enzymes that digest cellular components. Nuclear changes such as pyknosis, karyorrhexis, and karyolysis occur, and an inflammatory response is typically elicited.

Clinical significance involves tissue dysfunction and potential complications. Necrotic tissue may serve as a focus for infection or progress to gangrene in extremities. In the brain, liquefactive necrosis can cause permanent deficits depending on location and extent.

Diagnosis relies on histology and imaging to assess tissue integrity and the extent of damage. Treatment focuses on addressing the underlying cause, removing or debriding necrotic tissue when appropriate, and supporting organ function; antibiotics are used for infectious etiologies, and restoring blood flow is pursued when ischemia is reversible.