Necrosis
Introduction
• Necrosis is defined as a localised area of death of tissue
followed by degradation of tissue by hydrolytic enzymes
liberated from dead cells.
• it is invariably accompanied by inflammatory reaction.
• Irreversible cell injury in necrosis of all types is characterised
by 2 major essential changes : i)Cell digestion by lytic
enzymes. ii) Denaturation of proteins. The digestive enzymes
are derived either from the lysosomes of the dead cells
themselves, in which case the digestion is referred to as
autolysis, or from the lysosomes of infiltrating leukocytes,
termed heterolysis.
* Apoptosis is an internally programmed and controlled series
of events causing cell death. It is a vital process that helps
eliminate unwanted cells.
Aetiology
• 1) Poisons: a) Chemical poison includes strong acids and alkalies, drugs,
insecticides, fungicides, and other toxic chemicals. They cause cell death either
by coagulation of proteins or by poisoning the enzymatic systems. b) Toxins of
Pathogenic organisms – the toxins produce by bacteria, fungi, virus, protozoa,
rickettsia may also cause necrosis. c) Plant poison- eg. Mushrooms contain a
toxic glycoside, phallin, which causes renal tubular necrosis. d) Animal poison-
eg Cantharidin from beetles, and bee stings, cause focal necrosis of tissue.
• 2) Disturbances in circulation: a) Ischemia or Loss of blood supply may result in
necrosis and infarction. b) Passive Hypremia. c) General Anemia may result in
necrosis (brain and liver) if the amount of oxygen and nutrient is not sufficient to
maintain cellular metabolism.
• 3) Mechanical injuries cause necrosis when tissues are crushed or when blood
supply is injured or destroyed.
• 4) Thermal changes: Both heat and cold can coagulate protein and cause
necrosis.
• 5) Electric currents produced by lightning or generators may coagulate or char
tissues.
• 6) X ray and nuclear fission substances cause protoplasmic alterations that result
in necrosis.
Pathogenesis of Necrosis
• i)Cell digestion by lytic enzymes
ii) Denaturation of proteins
• Macroscopic appearance:
Areas of necrosis are white, grey, or yellow in colour. Have a cooked meat apperance.
Their borders are sharply demarcated and are usually sorrounded by a red zone of
inflammatory reaction.
• Microscopic appearances:
Cytoplasmic changes:
i) increased eosinophilia of cytoplasm
ii) Glassy homogenous appearance
iii) Cytoplasm is vacuolated, moth eaten
iv) Calcification of dead cells
v) Appearance of myelin figures
vi) Generation of calcium soap
Nuclear changes:
i) Karyolysis: Fading of basophilia of the chromatin due to the action of
DNases of lysosomal origin.
ii) Pyknosis: It is characterized by nuclear shrinkage and increased
basophilia. The DNA condenses into a solid shrunken mass.
iii) karyorrhexis: In this, the pyknotic nucleus undergoes fragmentation.
Types of Necrosis
Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Fibrinoid Necrosis
Coagulative Necrosis
• This is the most common type of necrosis. It is characterise by persistence
of architectural detail of area, but the cellular detail is lost.
• The denaturation of structural and enzymic proteins of the cytoplasm
blocks the proteolysis (dissolution or digestion) of the cell, and thus the
tissue architecture is preserved.
• Coagulative necrosis results most commonly from sudden severe
ischaemia, that is, hypoxic death of cells in such organs as the heart,
kidney, and adrenal gland.
• Infarcts are the best example of coagulative necrosis except brain.
• Morphology
• Grossly, Foci of coagulative necrosis in early stages are pale, firm, and
slighltly swollen. With progression they become more yellowish, softer, and
shrunken.
• Microscopically,
• The hallmark of coagulative necrosis – conversion of normal cells in to
• their ‘tombstones’
Liquefactive Necrosis
• This type of necrosis is characterized by transformation of the tissue into
a liquid mass in which cellular and architectural detail is lost.
• It occurs commonly due to ischaemic injury and bacterial or fungal
infections.
• Liquefactive Necrosis that is caused by neutrophilic leukocyte is called
Pus.
• The common examples are infarct brain and abscess cavity.
• Macroscopically, the tissue in the area of necrosis is liquefied containing
necrotic debris, later a cyst wall is formed; and may be watery, tenacious
or semisolid in consistency. The colour is usually white, yellow, or red.
• Microscopically, no architectural or cellular detail is visible in the area of
necrosis. The entire necrotic mass is surrounded by a zone of acute or
chronic inflammation depending on the length of time necrosis has been
present. Necrotic tissue in the central nervous system does not contain
neutrophils, unless pyogenic bacteria are present.
Caseous Necrosis
• It is characterized by the conversion of dead tissue into a
homogeneous granular mass resembling cheese, and by the
absence of both architectural and cellular detail.
• It combine the features of both Coagulative and liquefactive
necrosis.
• It is encountered mainly with tuberculosis in animals, and
caseous lymphadenitis in sheep. The cheesy appearance in
tuberculosis has been attributed to the capsule of the
tuberculous bacillus Mycobacterium tuberculosis.
Macroscopically, the area of necrosis is a granular amorphous material
resembling cheese.
The mass is dry but creamy in consistency.
It is soft, friable, and white-grey in colour.
Calcium salts are frequently deposited in the dead tissue.
The caseous mass is enclosed within a connective tissue capsule.
Microscopically, the necrosed foci are structureless, eosinophilic, and
contain granular debris.
The surrounding tissue shows characteristic granulomatous inflammatory
reaction consisting of epithelioid cells with interspersed giant cells of
Langhans’ or foreign body type and peripheral mantle of lymphocytes.
Calcification commonly occurs in the necrotic areas, especially in sheep and
cattle.
Fat Necrosis
• Fat necrosis is the death of adipose tissue within the living
individual.
• It is a special form of cell death occurring at two anatomically
different locations but morphologically similar lesions.
• Types: i) Pancreatic fat necrosis
ii) Traumatic fat necrosis
iii) Nutritional fat necrosis
i) Pancreatic fat Necrosis:
Pancreatic enzymes that have leaked out acinar cells and ducts
liquefy the membranes of fat cells in the peritoneum.
lipases split the triglycerides esters contained within fat cells into fatty
acids.
These combines calcium to produce grossly visible chalky white areas (fat
saponification)
Macroscopically, the necrotic fat appears as white or yellowish white, chalky,
firm, opaque masses.
Microscopically, the necrosed fat cells have cloudy appearance (basophilic
calcium deposit), sorrounded by an inflammatory reaction.
ii) Traumatic Fat Necrosis:
It is the death of adipose tissue in an area of mechanical injury.
It commonly occurs in subcutaneous adipose tissue due to mechanical injuries
during working, fighting, or exercising. Examples: in canine from dog bites,
perivaginal fat in cattle from mechanical injury during parturition.
Macroscopically, the pancreatic fat appears as firm, opaque, chalky mass in
the area of injury, surrounded by a zone of acute or chronic inflammatory
reaction.
iii) Nutritional Fat Necrosis :
It is a necrobiotic alteration in fat that is associated with extreme
emaciation and debility.
usually observed in cattle and sheep in tuberculosis and Johne's disease
(paratuberculosis)
Macroscopically, the fat is opaque, chalky white, and usually firm. It may
undergo calcification.
Microscopically,
Fibrinoid Necrosis :
It is characterised by deposition of fibrin-like material which has the staining
properties of fibrin.
It is encountered in various examples of immunologic tissue injury, arterioles
in hypertension, peptic ulcer.
Microscopically, fibrinoid necrosis is identified by brightly eosinophilic, hyaline-
like deposition in the vessel wall.
Necrotic focus is surrounded by nuclear debris of neutrophils (leucocytoclasis).