Irreversible cell damage leads invariably to cell death as a result of interactions with noxious stimuli. Infectious agents, oxygen deprivation or hypoxia, and extreme environmental factors such as heat, radiation, or exposure to ultraviolet irradiation are all included in these noxious stimuli. The subsequent death is referred to as necrosis, commonly distinct from the other significant consequence of permanent damage, referred to as apoptosis cell death. Apoptosis is a cell death that is programmed or structured and may be physiological or pathological. Additional knowledge is beyond the scope of this chapter about this type of cell death. A pathological process is almost always associated with necrosis as a form of cell death. 

They show two main types of microscopes or macroscopic appearance as cells die from necrosis. The first is liquefactive necrosis, also referred to as colliquative necrosis, characterized by a partial or total breakdown of dead tissue and liquid, viscous mass transformation. The tissue and cellular profile degradation occur in liquefactive necrosis within hours. Coagulative necrosis, the other significant pattern, is distinguished, in contrast to liquefactive necrosis, by the preservation of typical necrotic tissue architecture for several days after cell death. 

The slimy, liquid-like essence of tissues undergoing liquefactive necrosis results in liquefaction. In part, this morphological appearance is due to the activities of hydrolytic enzymes that cause cellular organelles to dissolve in a cell undergoing necrosis. Liquefaction enzymes are derived either from bacterial hydrolytic enzymes or from lysosomal hydrolytic enzymes.

Types of necrosis :

Six types of necrosis are identified based on the morphological patterns associated with cell death.

a. Liquefactive necrosis

b. coagulative necrosis

c. Caseous Necrosis

d. Fat Necrosis

e. Gangrenous Necrosis

f. Fibrinoid necrosis

  1. Liquefactive necrosis :

The necrosis pattern that is seen with infections. The pattern is also seen in the brain following ischemic injury. The release of digestive enzymes and neutrophil constituents causes liquefaction in infections, although there is a poor understanding of the cause of liquefactive necrosis following ischemic injury in the brain.

Gross Appearance: Due to pus formation, the tissue is in a liquid state and sometimes creamy yellow. 

  • Coagulative necrosis :

Occurs in any organ in the body but the brain; this is the default necrosis trend associated with ischemia or hypoxia. 

Gross Appearance: tissue is solid, and for days after cell death, architecture is preserved. 

  • Caseous necrosis :

A rare form of tuberculosis-related cell death. 

Gross appearance: white, fluffy, cheesy-looking material (case-looking).

A granuloma is known as the entire structure formed in response to tuberculosis. 

  • Fat necrosis :

Acute inflammation affecting tissues with multiple adipocytes, such as the pancreas and breast tissue, causes fat necrosis. Digestive enzymes that break down lipids to produce free fatty acids are released by damaged cells. 

Gross Appearance: Whitish deposits as a consequence of calcium soap formation. 

  • Gangrenous Necrosis : 

Medical usage in the description of lower limb ischemic necrosis (sometimes upper limbs or digits). 

Gross appearance: varying degrees of putrefaction on black skin. 

  • Fibrinoid necrosis :

Vascular damage (autoimmunity, immune complex deposition, infections (viruses, spirochetes, rickettsiae)) is a pattern associated with this. 

Gross Appearance: Not necessarily grossly discernible. 

All of these reflect morphological patterns, grossly, and microscopically evident. Typically, fibrinoid necrosis is evident only microscopically. In the following paragraphs, we examine the characteristic gross and microscopic effects of liquefactive necrosis.

Difference between Apoptosis and Necrosis:

DefinitionProgrammed cell deathPremature cell death
Process Occurs through shrinkage of cytoplasm, followed by chromatin condensationOccurs through swelling of cytoplasm along with mitochondria followed by cell lysis
Cause Naturally occurring physiological processThe pathological process, caused by external agents such as toxins, trauma, and infections.
Membrane integrityPlasma membrane blebbing is observed without losing integrityThe membrane integrity is loosened.
ChromatinAggregation of chromatinNo structural changes in chromatin
OrganellesMitochondria become leaky often by forming membrane pores, while lysosomes kept their integrity. Organelles still function even after cell death.Lysosomes become leaky, while mitochondria kept their integrity. Organelles are disintegrated by swelling and do not function after cell death.
Vesicle formationMembrane-bound vesicles called apoptotic bodies fragments the cell into small bodiesNo vesicle formation. Complete cell lysis occurs and releases contents into the extracellular fluid.
RegulationTightly regulated by its activation pathway of enzymesUnregulated process
CaspaseCaspase dependent pathwayCaspase independent pathway
Energy requirementThe active process occurs at 40cThe inactive process does not occur at 40c
Digestion of DNANon-random mono and oligonucleosomal length fragmentation of DNA and show band pattern in Agarose gel electrophoresis.DNA in the cell is randomly digested and shows a smear in Agarose gel electrophoresis.
Timing of DNA digestionPrelytic DNA fragmentation.Postlytic DNA digestion.
OccurrenceThe localized process involves destroying individual cellsAffects contiguous cell groups
PhagocytosisEither by phagocytes or adjacent cellsBy phagocytes
SymptomsNeither inflammation nor tissue damageA significant inflammatory response is generated. May cause tissue damage
InfluenceOften beneficial, but abnormal activity may lead to diseases.Always harmful. If necrosis is untreated- it may be fatal.
FunctionInvolved in regulation of the number of cells in multicellular organisms. Involved in tissue damage and induction of the immune system, defending the body from pathogens as well.

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