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1. the death of one or more cells in the body, usually within a localized area, as from an interruption of the blood supply to that part
2. death of plant tissue due to disease, frost, etc.



the death within the living organism of individual organs or their component tissues or cells.

A necrosis is classified according to the pathological condition that causes it. Thus, frostbite and burns can cause traumatic necrosis; neurotropic necrosis arises with syringomyelia and the nervous form of leprosy; infarcts and gangrene are associated with circulatory, or ischemic, necrosis; caseous necroses occurring in tuberculosis and syphilis are forms of septic necrosis; and fibrinoid necrosis associated with allergic diseases is a type of allergic necrosis.

Necrosis is accompanied by characteristic changes in the cell and in the intercellular substances. The nucleus shrinks and coagulates, a process known as pycnosis, and the cytoplasm breaks up into clumps. The cell eventually lyses, that is, it degenerates and dissolves. The lysis is due to the activation of the lysosomal hydrolytic enzymes, such as ribonuclease, deoxyribonuclease, and acid phosphatase. The activation of the lysosomes occurs as a result of an increase in the permeability of the cell membranes, changes in the osmotic equilibrium, and acidosis—an abnormal increase in the intracellular hydrogen-ion concentration. Fibrinoid changes appear in the connective tissue, and nerve fibers become fragmented and disintegrate into clumps.

The clinical and morphological manifestations and further consequences of necrosis depend on the localization and distribution of the necrosis and on the mechanisms and conditions of origin. The following types of advanced necrotic conditions can develop: dry necrosis, such as Zenker’s degeneration of infected muscles; colliquative, or liquefactive, necrosis, which occurs for example, when a focus of softening arises in the brain in response to cerebral hemorrhage; gangrene; and bed sores. Necrotic tissue tears away; then, either connective tissue grows through it or the necrotic tissue undergoes autolytic or purulent liquefaction. Finally, the necrotic tissue becomes encapsulated and petrified.

The two most serious consequences of necrosis are a loss of function owing to the death of the structural elements of the necrotic tissues or organs and poisoning caused by the actual presence of a necrotic focus and by the inflammation that arises in response to this presence.



Death of a cell or group of cells as a result of injury, disease, or other pathologic state.
References in periodicals archive ?
The histological findings of acute hepatitis and focal necrosis and zonal necrosis were reversed 10% to 20% in groups A2 and B2 at 30th days.
Type of Standard reaction Stage alteration 1 Alteration of Deformation of the cell contour I the Hepatocytes Cellular hypertrophy I Cellular atrophy I Melanomacrophagous centers I, II and III Vacuolization of the cytoplasm I Degeneration of the cytoplasm II Fatty degeneration II Cell rupture II Inflammation II and III Congestion II 2 Alteration of Congestion II the blood vessels Hepatitis II and III 3 Necrosis Focal necrosis III Table 2.
Significant eosinophil infiltration of liver tissue and spotty and focal necrosis of hepatocytes around central veins are pathological characteristics of DILI.
Additional changes in the liver included sinusoidal congestion, focal necrosis, and haemorrhage in the fat tissue (near and around intestine); however, these changes were less common.
Figure 3 demonstrates an area of endocapillary proliferation with an area of focal necrosis or karyorrhexis (white arrow).
Histopathological study on cobra bite wounds in humans revealed focal necrosis within the epidermis with thrombosis and fibrinoid deposits in the superficial and deep dermal vessels, as well as features of leukocytoclastic vasculitis.
Necropsy indicated that the gray brocket deer had pulmonary congestion and edema, mild renal congestion, and renal focal necrosis.
Microscopically, this tumor features pleomorphic oncocytes with increased mitosis, focal necrosis, perivascular and perineural invasion, and an infiltrative growth pattern.
Biopsy samples contained epithelioid granulomas and a nonspecific, amorphous eosinophilic material without focal necrosis, but no bacteria, by using periodic acid-Schiff, Ziehl-Neelsen, and auramine-rhodamine stains.
Microscopically, extensive, severe, transmural, acute and chronic inflammation, ulceration, abscess formation, lymphoid hypertrophy, focal necrosis, and focal peritonitis were present in the terminal ileum, cecum, right colon, and appendix.
Although the intense eosinophilia and focal necrosis are suggestive of a parasitic infection, no parasites have been identified.