Section 9 Four Types of Necrosis

When cells undergo necrosis, the resulting tissue damage ahs a characteristic appearance that depends on the cause and location of the injury.  There are four main types of necrosis, each name for what the affected tissue looks like.

1. Liquefaction Necrosis

In liquefaction necrosis, dead cells liquefy into a soupy, fluid-filled mass.  This occurs because lytic enzymes release from the lysosomes of dying cells break down proteins and other cellular components.  Liquefaction necrosis most commonly results from infection and follows this progression:

• Cells die and release hydrolytic enzymes that digest surrounding tissue.
• Macrophages arrive and release cytokines to recruit additional white blood cells, including neutrophils (also phagocytes), to the area.
• Phagocytes engulf debris and if present, the infecting agent (e.g., bacteria, virus, fungi).
• If the bacteria resist phagocytosis, the infection persists and may require antibiotics.  (Viral and fungal infections require antiviral and antifungal medications respectively).
• A fluid-filled space or abscess may form, particularly in closed tissue such as beneath the skin (e.g., from a splinter carrying bacteria).  Treatment may include lancing the abscess to release fluid and deliver antibiotic therapy.
  • If the wound is open, the battle between bacteria and phagocytes may produce pus – a protein-rich fluid containing dead cells and cell debris.

2. Coagulative Necrosis

Coagulative necrosis is the most common type and typically results from ischemia (in any organ other than the brain).   During ischemia, cells switch to anaerobic metabolism, generating large amounts of lactic acid.  This acidic environment denatures proteins – including the lytic enzymes that otherwise liquefy the tissue.  As a result, the dead tissue takes on a firm, pale yellow, cheese-like appearance.

Because the lytic enzymes are themselves denatured, the tissue is not dissolved into soup – it retains its structural outline (at least temporarily) while the cells within are dead.  This is commonly seen in ischemic kidney tissue and in the heart following a myocardial infarction (heart attack).

Some bacterial infections can cause coagulative necrosis rather than liquefactive necrosis, particularly when bacterial toxins induce ischemia.  Similarly viral infections can also induce coagulative necrosis when they cause severe hypoxia in tissues.

3. Caseous Necrosis

Caseous necrosis is caused by particular types of infection rather than ischemia.  Instead of dying as a result of hypoxia, cell death is induced by specific bacteria and fungal infections and the ensuing response by white blood cells.

The most common example is tuberculosis (TB) – a serious respiratory disease caused by the bacterium Mycobacterium tuberculosis and spread by respiratory droplets.  Certain fungal respiratory infections (e.g., histoplasmosis, cryptococcosis, and coccidioidomycosis) can also result in caseous necrosis.

In these respiratory infections, the killing of lung cells attracts white blood cells, including macrophages to the area.  The macrophages promptly wall off the infected area and release digestive chemicals causing the affected cells to disintegrate.  The dead tissue has a cheese-like appearance, a necrotic zone that becomes enclosed within a granuloma (an aggregation of macrophages).  When fully walled off (often with a rim of calcium), this is called a Ghon focus.  The contained tissue has a soft, crumbly, cheese-like appearance, hence the name ‘caseous’ (from the Latin word for cheese).

The danger of TB lies in its ability to persist in latency.  Live bacteria can remain viable inside the Ghon focus for years or even decades.  If the person later becomes immunocompromised (due to aging, HIV, or another illness), the bacteria, can reactivate causing progressive lung destruction, form expanding cavities, and even spread through the bloodstream to other organ.

4. Fat Necrosis

Fat necrosis is rare and occurs specifically in fatty tissues such as the pancreas or breast tissue.  When cells in these tissues die, lipase (an enzyme that breaks down triglycerides) is released.  Lipase cleaves triglycerides into glycerol and fatty acid chains.  The freed fatty acids then bind to calcium, forming a chalky, soap-like residue.  This white, chalky deposit is the hallmark of fat necrosis.