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Necrosis
 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.
 Various agents such as hypoxia, chemical and
physical agents, microbial agents,
immunological injury, etc
 Two essential changes characterise
irreversible cell injury in necrosis of all types
◦ Cell digestion by lytic enzymes
◦ Denaturation of proteins
For more : Visit www.dentaltutor.in
Morphologically, there are five
types of necrosis
 Cogulative
 Liquefaction
 Caseous
 Fat
 Fibrinoid
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 It’s a form of tissue necrosis in which the
component cells are dead but the basic tissue
architecture is preserved for at least several
days.
 The affected tissues take on a firm texture
 Presumably the injury denatures not only
structural proteins but also enzymes and so
blocks the proteolysis of the dead cells
◦ as a result, eosinophilic, anucleate cells may persist
for days or weeks
◦ Ultimately, the necrotic cells are removed by
phagocytosis of the cellular debris.
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 Most common type of
necrosis
 Mostly from sudden
cessation of blood flow
(ischaemia)
 Less often from bacterial
and chemical agents.
 It’s characteristic of
infarcts (areas of ischemic
necrosis) in all solid
organs except the brain.
 The organs commonly
affected are the heart,
kidney, and spleen
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Coagulative necrosis of the left
ventricular wall
 Gross
◦ foci of coagulative necrosis in the early stage are pale,
firm, and slightly swollen.
◦ With progression, they become more yellowish, softer,
and shrunken.
 Microscopically
◦ the hallmark of coagulative necrosis - the conversion of
normal cells into their ‘tombstones’
 outlines of the cells are retained so that the cell type but
their cytoplasmic and nuclear details are lost.
◦ The necrosed cells are swollen and appear more
eosinophilic than the normal, along with nuclear changes
described above.
◦ But cell digestion and liquefaction fail to occur
◦ Eventually, the necrosed focus is infiltrated by
inflammatory cells
◦ And the dead cells are phagocytosed leaving granular
debris and fragments of cells
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For more : Visit www.dentaltutor.in
Infarct Kidney
The affected area on right shows cells with intensely eosinophilic
cytoplasm of tubular cells but the outlines of tubules are still
maintained.
The nuclei show granular debris.
The interface between viable and non-viable area shows nonspecific
chronic inflammation and proliferating vessels
 Due to ischaemic injury and bacterial or fungal
infections
 degradation of tissue by the action of powerful
hydrolytic enzyme.
 The common examples are infarct brain
and abscess cavity.
 Whatever the pathogenesis, liquefaction
completely digests the dead cells, resulting in
transformation of the tissue into a liquid viscous
mass.
 If the process was initiated by acute
inflammation, the material is frequently creamy
yellow and is called pus
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For more : Visit www.dentaltutor.in
 Gross
◦ The affected area is soft with liquefied centre
containing necrotic debris.
◦ Later, a cyst wall is formed.
 Microscopically,
◦ the cystic space contains necrotic cell debris and
macrophages filled with phagocytosed material.
◦ The cyst wall is formed by proliferating capillaries,
inflammatory cells, and gliosis (proliferating glial
cells) in the case of brain
◦ proliferating fibroblasts in the case of abscess
cavity
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For more : Visit www.dentaltutor.in
Liquefactive necrosis brain
The necrosed area on right side of the field
shows a cystic space containing cell debris,
while the surrounding zone shows granulation
tissue and gliosis.
 found in the centre of foci
of tuberculous infections.
 It combines features of
both coagulative and
liquefactive necrosis.
 term "caseous" (cheese-
like) is derived from the
friable yellow-white
appearance of the area of
necrosis
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 Grossly
◦ foci of caseous necrosis,
◦ as the name implies, resemble dry cheese and are soft,
granular and yellowish.
◦ This appearance is partly attributed to the histotoxic effects of
lipopolysaccharides present in the capsule of the tubercle
bacilli, Mycobacterium tuberculosis.
 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.
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Caseous necrosis lymph node
There is eosinophilic, amorphous, granular material, while the periphery
shows granulomatous inflammation.
 Refers to focal areas of fat destruction
◦ Acute pancreatic necrosis,
◦ traumatic fat necrosis commonly in breasts
 Pancreatic enzymes that have leaked out of
acinar cells and ducts
◦ liquefy the membranes of fat cells in the peritoneum.
◦ lipases split the triglyceride esters contained within fat
cells to fatty acid.
◦ These combines calcium to produce grossly visible
chalky white areas (fat saponification)
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For more : Visit www.dentaltutor.in
Fat necrosis in acute pancreatitis.
The areas of white chalky deposits represent foci of fat
necrosis with calcium soap formation (saponification) at sites
of lipid breakdown in the mesentery.
 Grossly
◦ fat necrosis appears as
yellowish-white and firm
deposits.
◦ Formation of calcium soaps
imparts the necrosed foci
firmer and chalky white
appearance.
 Microscopically
◦ the necrosed fat cells have
cloudy appearance
◦ surrounded by an
inflammatory reaction.
For more : Visit www.dentaltutor.in
Formation of calcium
soaps is identified in
the tissue sections as
amorphous, granular
and basophilic material
 Characterised by deposition of fibrin-like
material which has the staining properties of
fibrin.
 It is encountered in various examples of
immunologic tissue injury
◦ immune complex vasculitis,
◦ autoimmune diseases,
◦ Arthus reaction
 Arterioles in hypertension, peptic ulcer
For more : Visit www.dentaltutor.in
For more : Visit www.dentaltutor.in
Fibrinoid necrosis in an artery in a patient with polyarteritis nodosa.
The wall of the artery shows a circumferential bright pink area of
necrosis with protein deposition and inflammation (dark nuclei of
neutrophils).
 Microscopically
◦ identified by brightly
eosinophilic, hyaline-like
deposition in the vessel
wall.
◦ Necrotic focus is
surrounded by nuclear
debris of neutrophils
(leucocytoclasis)
◦ Local haemorrhage may
occur due to rupture of the
blood vessel.
For more : Visit www.dentaltutor.in
Fibrinoid necrosis in autoimmune
vasculitis. The vessel wall shows
brightly pink amorphous material
and nuclear fragments of necrosed
neutrophils
 Robbinson's basic pathology 8 ed
 Harsh Mohan - Textbook of Pathology 6th Ed.
 Color atlas of pathology
For more : Visit www.dentaltutor.in
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https://www.facebook.com/notesdental
http://www.slideshare.net/DeepakKumarGupta2
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Necrosis

  • 2.  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.  Various agents such as hypoxia, chemical and physical agents, microbial agents, immunological injury, etc  Two essential changes characterise irreversible cell injury in necrosis of all types ◦ Cell digestion by lytic enzymes ◦ Denaturation of proteins For more : Visit www.dentaltutor.in
  • 3. Morphologically, there are five types of necrosis  Cogulative  Liquefaction  Caseous  Fat  Fibrinoid For more : Visit www.dentaltutor.in
  • 4.  It’s a form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved for at least several days.  The affected tissues take on a firm texture  Presumably the injury denatures not only structural proteins but also enzymes and so blocks the proteolysis of the dead cells ◦ as a result, eosinophilic, anucleate cells may persist for days or weeks ◦ Ultimately, the necrotic cells are removed by phagocytosis of the cellular debris. For more : Visit www.dentaltutor.in
  • 5.  Most common type of necrosis  Mostly from sudden cessation of blood flow (ischaemia)  Less often from bacterial and chemical agents.  It’s characteristic of infarcts (areas of ischemic necrosis) in all solid organs except the brain.  The organs commonly affected are the heart, kidney, and spleen For more : Visit www.dentaltutor.in Coagulative necrosis of the left ventricular wall
  • 6.  Gross ◦ foci of coagulative necrosis in the early stage are pale, firm, and slightly swollen. ◦ With progression, they become more yellowish, softer, and shrunken.  Microscopically ◦ the hallmark of coagulative necrosis - the conversion of normal cells into their ‘tombstones’  outlines of the cells are retained so that the cell type but their cytoplasmic and nuclear details are lost. ◦ The necrosed cells are swollen and appear more eosinophilic than the normal, along with nuclear changes described above. ◦ But cell digestion and liquefaction fail to occur ◦ Eventually, the necrosed focus is infiltrated by inflammatory cells ◦ And the dead cells are phagocytosed leaving granular debris and fragments of cells For more : Visit www.dentaltutor.in
  • 7. For more : Visit www.dentaltutor.in Infarct Kidney The affected area on right shows cells with intensely eosinophilic cytoplasm of tubular cells but the outlines of tubules are still maintained. The nuclei show granular debris. The interface between viable and non-viable area shows nonspecific chronic inflammation and proliferating vessels
  • 8.  Due to ischaemic injury and bacterial or fungal infections  degradation of tissue by the action of powerful hydrolytic enzyme.  The common examples are infarct brain and abscess cavity.  Whatever the pathogenesis, liquefaction completely digests the dead cells, resulting in transformation of the tissue into a liquid viscous mass.  If the process was initiated by acute inflammation, the material is frequently creamy yellow and is called pus For more : Visit www.dentaltutor.in
  • 9. For more : Visit www.dentaltutor.in
  • 10.  Gross ◦ The affected area is soft with liquefied centre containing necrotic debris. ◦ Later, a cyst wall is formed.  Microscopically, ◦ the cystic space contains necrotic cell debris and macrophages filled with phagocytosed material. ◦ The cyst wall is formed by proliferating capillaries, inflammatory cells, and gliosis (proliferating glial cells) in the case of brain ◦ proliferating fibroblasts in the case of abscess cavity For more : Visit www.dentaltutor.in
  • 11. For more : Visit www.dentaltutor.in Liquefactive necrosis brain The necrosed area on right side of the field shows a cystic space containing cell debris, while the surrounding zone shows granulation tissue and gliosis.
  • 12.  found in the centre of foci of tuberculous infections.  It combines features of both coagulative and liquefactive necrosis.  term "caseous" (cheese- like) is derived from the friable yellow-white appearance of the area of necrosis For more : Visit www.dentaltutor.in
  • 13. For more : Visit www.dentaltutor.in
  • 14.  Grossly ◦ foci of caseous necrosis, ◦ as the name implies, resemble dry cheese and are soft, granular and yellowish. ◦ This appearance is partly attributed to the histotoxic effects of lipopolysaccharides present in the capsule of the tubercle bacilli, Mycobacterium tuberculosis.  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. For more : Visit www.dentaltutor.in
  • 15. For more : Visit www.dentaltutor.in Caseous necrosis lymph node There is eosinophilic, amorphous, granular material, while the periphery shows granulomatous inflammation.
  • 16.  Refers to focal areas of fat destruction ◦ Acute pancreatic necrosis, ◦ traumatic fat necrosis commonly in breasts  Pancreatic enzymes that have leaked out of acinar cells and ducts ◦ liquefy the membranes of fat cells in the peritoneum. ◦ lipases split the triglyceride esters contained within fat cells to fatty acid. ◦ These combines calcium to produce grossly visible chalky white areas (fat saponification) For more : Visit www.dentaltutor.in
  • 17. For more : Visit www.dentaltutor.in Fat necrosis in acute pancreatitis. The areas of white chalky deposits represent foci of fat necrosis with calcium soap formation (saponification) at sites of lipid breakdown in the mesentery.
  • 18.  Grossly ◦ fat necrosis appears as yellowish-white and firm deposits. ◦ Formation of calcium soaps imparts the necrosed foci firmer and chalky white appearance.  Microscopically ◦ the necrosed fat cells have cloudy appearance ◦ surrounded by an inflammatory reaction. For more : Visit www.dentaltutor.in Formation of calcium soaps is identified in the tissue sections as amorphous, granular and basophilic material
  • 19.  Characterised by deposition of fibrin-like material which has the staining properties of fibrin.  It is encountered in various examples of immunologic tissue injury ◦ immune complex vasculitis, ◦ autoimmune diseases, ◦ Arthus reaction  Arterioles in hypertension, peptic ulcer For more : Visit www.dentaltutor.in
  • 20. For more : Visit www.dentaltutor.in Fibrinoid necrosis in an artery in a patient with polyarteritis nodosa. The wall of the artery shows a circumferential bright pink area of necrosis with protein deposition and inflammation (dark nuclei of neutrophils).
  • 21.  Microscopically ◦ identified by brightly eosinophilic, hyaline-like deposition in the vessel wall. ◦ Necrotic focus is surrounded by nuclear debris of neutrophils (leucocytoclasis) ◦ Local haemorrhage may occur due to rupture of the blood vessel. For more : Visit www.dentaltutor.in Fibrinoid necrosis in autoimmune vasculitis. The vessel wall shows brightly pink amorphous material and nuclear fragments of necrosed neutrophils
  • 22.  Robbinson's basic pathology 8 ed  Harsh Mohan - Textbook of Pathology 6th Ed.  Color atlas of pathology For more : Visit www.dentaltutor.in
  • 23. Like, share and comment on https://www.facebook.com/notesdental http://www.slideshare.net/DeepakKumarGupta2 For more : Visit www.dentaltutor.in