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Necrosis comes from the Greek word "necros" which means “dead”. This is the premature or unexpected death of the cell and, eventually, of living tissues which may be caused by external factors such as infection, trauma or toxins.


Comparison of cell deaths


Necrobiosis is programmed cell death. It happens to an individual or group of cells that is at the end of their life span. This process happens unnoticed by the body as the dead cells is continually replaced by the same cell type during cell mitosis and meiosis. It does not cause any disruption to the body's normal function because cell function goes uninterrupted. Actually, this happens in adults as a part of normal cell turnover. Examples of this process are the keratinization of the skin and the replacement of red blood cells from the bone marrow.


Apoptosis is another form of cell death where removal happens one cell at a time. These cells are programmed to remove lyses on its own. It sends chemical signals to the immune system to send phagocytes to locate and engulf dead cells for excretion.

Apptosis does not disrupt the cell's normal function and will happen unnoticed. This process happens as embryonic morphogenesis, metamorphosis, mature tissue homeostasis, involution of adult tissue and cell death from radiation, chemotherapy, or cell-mediated immunity.


Necrosis is cell death that happens after injury. Degeneration of cells may develop as necrosis if injury continues. If the body's adaptive responses could no longer cope and the condition becomes irreversible, cell death will occur. But unlike the former models of cell death described above, this has a pathological process and a sequel.

Morphologic markers

Necrosis has the following characteristics:

  • It is always pathologic.
  • Involves layers of cells.
  • It is energy independent.
  • Cell inflammation and mitochondrial destruction often leads to depletion of energy levels.
  • Homeostasis is not maintained.
  • Although the nuclei is destroyed, there is no DNA cleaving.
  • Cell membrane structure is destroyed.
  • The necrotic cell will release its intracellular contents and trigger an inflammatory sequence.
  • Dead cells will be ingested by neutrophils and macrophages.


Treatment for necrosis involves a two-way process.

The first step often involves treating the underlying cause of necrosis. After the cause of necrosis has been managed, the necrotic tissue will remain in the body. A standard protocol for necrotic tissue is surgical removal of the dead tissue. This will depend on how much damage has been done - from small patches of skin to limbs that need to be amputated.

Other doctors resort to chemical debridement through enzymes which gently scour the dead tissues to gradual reveal recovering tissues.

Another but highly select option, is the use of maggots. These eat up the dead tissues and reveal living tissue underneath.


Necrosis may be classified according to how much tissue or cells are preserved.

  • Coagulative necrosis. In this type of necrosis, cell and tissue framework are preserved. When viewed from the microscope, integral cell parts such as nucleus, cytoplasm, and cellular outlines and arrangement are still intact. This is difficult to detect unless when the affected area is large and subtle changes in the tissue is obvious. This happens from acute conditions such as short-lived exposure to toxins or sudden loss of blood supply.
  • Liquefactive necrosis. This is also known as lytic necrosis. This type of necrosis involves enzymes that quickly dissolves the cell. This is observed in bacterial infections where pus is present. Pus is evidence of this type of necrosis.

Meanwhile, special forms of necrosis include the following:

  • Fat necrosis. This may happen because of intense trauma (traumatic fat necrosis) or due to an enzyme that splits fat into fatty acid and glycerol (enzymatic fat necrosis).
  • Zenker necrosis. Also known as Zenker degradation which is the disappearance of muscle striations after necrosis happens.
  • Caseation necrosis. Existence of crumbly, cheesy or pasty amorphous substance in the necrotic area which is often seen in tuberculous lesions.
  • Fibrinoid necrosis. Presence of acellular homogenous protein that looks like fibrin which accumulates in connective tissues and walls of blood vessels.
  • Gangrenous necrosis. This is tissue death due to cut off blood supply which putrefied due to infection of saprophytic bacteria. It may be classified as wet or dry.
  • Infarct. It is a type of coagulative necrosis that comes from lack of blood supply.


Necrosis can be recognized by three indicators as manifested microscopically.

  • Changes in the nucleus.
    • Swelling and aggregation of chromatin.
    • Reduction of chromatin and deflation of the nucleus.
    • The nucleus breaks up.
    • The enzyme deoxyribonuclease dissolves the nucleus.
  • Changes in cytoplasmic staining.
    • Stains positive with vital dyes which reflect abnormal leakiness of the cell membrane.
    • Cytoplasm becomes opaque because of protein denaturation.
    • Abnormally high presence of eosinophils that are attracted to the acidic dyes.
  • Ultrastructural changes that happens in a sequence.
    • Gradual and constant loss of chromatin in the nucleus.
    • Central rupture of the nuclear membrane.
    • Breakdown of the cell membrane.
    • Clumping within the mitochondria.

When viewed by the naked eye, the following characteristics will be present:

  • Pallor of the tissue
  • Soft, crumbly tissues that have no strength
  • Well-defined demarcation of healthy from dead tissue

Local incidence

Pinoys are no strangers to necrosis, although many will interchange it with gangrene.

A publicized botched up enhancement on a celebrity with silicone oil had everybody watching what necrotic tissue looks like and re-thinking about the costs of cosmetic surgery.

During the surge of Ondoy in 2009 where snakes came out of nowhere, the Department of Health readied their anti-venom and informed the public about the local signs of snake bite which includes necrosis.