Necrosis (in Greek Νεκρός = Dead) is the name given to unprogrammed death of cells and living tissue. It is less orderly than apoptosis, which are part of programmed cell death. In contrast with apoptosis, cleanup of cell debris by phagocytes of the immune system is generally more difficult, as the disorderly death generally does not send "eat-me" cell signals which tell nearby phagocytes to engulf the dying cell. This lack of signalling makes it harder for the immune system to locate and recycle dead cells which have died through necrosis than if the cell had undergone apoptosis.

There are many causes of necrosis including injury, infection, cancer, infarction, invenomation and inflammation. Severe damage to one essential system in the cell leads to secondary damage to other systems, a so-called "cascade of effects". Necrosis is caused by special enzymes that are released by lysosomes which are capable of digesting cell components or the entire cell itself. The injuries received by the cell may compromise the lysosome membrane, or may set off an unorganized chain reaction which causes the release in enzymes. Unlike in apoptosis, cells that die by necrosis may release harmful chemicals that damage other cells. Biopsy material necrosis is halted by fixation or freezing.

Morphologic patterns

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There are seven distinctive morphologic patterns of necrosis:

• Coagulative necrosis – typically seen in hypoxic environments (e.g. myocardial infarction, infarct of the spleen). Cell outlines remain after cell death and can be observed by light microscopy.
• Liquefactive necrosis – is associated with cellular destruction and pus formation (e.g. pneumonia)
• Gummatous necrosis – is restricted to necrosis involving spirochaetal infections (e.g. syphilis)
• Haemorrhagic necrosis – is due to blockage of the venous drainage of an organ or tissue and occurs in testicular torsion.
• Caseous necrosis – is a mix of coagulative necrosis and liquefactive necrosis (e.g. tuberculosis)
• Fatty necrosis – results from the action of lipases on fatty tissues (e.g. acute pancreatitis, breast tissue necrosis)
• Fibrinoid necrosis – caused by immune-mediated vascular damage. It is marked by deposition of fibrin-like proteinaceous material in arterial walls, which appears smudgy and acidophilic on light microscopy.

Histological Features

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Several histological features convey the gradual, irreversible transformation into necrosis from sub-lethal damage. The following sequential structural changes can be observed under a light microscope:

• An Eosinophilic Cytoplasm

• Pyknosis

• Karyorrhexis

• Karyolysis

• Eventually complete karyolysis is attained. The dead cell appears as an anucleate and eosinophilic mass.

Arachnogenic necrosis

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Spider bites are cited as causing necrosis in some areas. These claims are widely disputed, but experts say the possibility is still there. Examples include:

• Brown recluse spiders in the midwestern United States
• White-tailed spiders in Australia

See also

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• Peripheral vascular disease
• Aseptic bone necrosis
• Gangrene
• Ischemic cascade
• Necrotoxins are toxins that cause necrosis
• Cystic medial necrosis

Death | Cell biology

Nekróza | Nekrose | Necrosis | Nécrose | Nekroso | Necrosi | Nekrozė | Nekrózis | Necrose | Nekroza | Necrose | Некроз | Nekros