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Necrosis and Apoptosis
Presentor: Dr. Bishal Paudel
1st Year Orthopaedics Resident
Objectives
• To define necrosis and apoptosis
• To explain morphology and mechanism
• To illustrate different types of necrosis
• To discuss briefly about the difference
between necrosis and apoptosis
Cell injury
Reversible vs Irreversible cell injury
Necrosis
• Series of changes that accompany cell death,
largely resulting from the degradative action
of enzymes on lethally injured cells
• characterized by swelling, denaturation and
coagulation of proteins, breakdown of cellular
organelles and cell rupture
• caused by extra-cellular enzymes, liberated
from inflammatory cells
NECROSIS: MORPHOLOGY
Light microscopy (H & E stains)
• Necrotic cells -eosinophilia, glassy
homogeneous appearance
• Cytoplasm- vacuolated
• Myelin figures- whorled phospholipid masses
• Calcified dead cells
• Nuclear changes :
- Karyolysis - gradual fading away of the
basophilic nuclear material, presumably due
to action of DNAses.
- Karyorrhexis - fragmentation of nucleus and
the debris is either phagocytosed by other
cells or just disappears.
- Pyknosis - condensation of nucleus into a deep
basophilic mass. This stage is often followed
by karyorrhexis.
Necrosis: nuclear changes
NORMAL
PYKNOSIS
KARYORHHEXIS
KARYOLYSIS
Necrosis and apoptosis
Types of Necrosis
1) Coagulative necrosis:
- denaturation of cytoplasmic proteins with preservation
of the framework of the coagulated cell
- lschemia/infracts in most tissues (except brain)
• Liquefaction necrosis
- autolysis and heterolysis prevail over protein
denaturation
- necrotic area is soft and filled with fluid with
obliteration of normal architecture
- localized bacterial infection (abscesses) and brain
Caseation necrosis-
- Cellular death with complete loss of architectural
pattern
- Necrotic area is dry, cheesy and friable
- Example: Tuberculosis
• Fat necrosis:
- Enzymatic: acute pancreatitis (saponification of peripancreatic
fat)
- Nonenzymatic: traumatic (eg injury to breast tissue}
• Fibrinoid necrosis:
- Immune vascular reactions (eg, PAN)
- Nonimmune vascular reactions (eg. Hypertensive emergency,
preeclampsia)
• Gangrenous necrosis:
- Distal extremity and GI tract, after chronic ischemia
Apoptosis
• named after the Greek designation for “falling
off”
• Tightly regulated suicide program in which
cells destined to die activate enzymes capable
of degrading the cells own nuclear DNA and
nuclear and cytoplasmic proteins
• Dead cells are rapidly cleared before its
content are leaked out
• Hence does not elicit inflammatory reaction in
the host
Causes of apoptosis
Apoptosis in physiologic situation:
- programmed destruction of cells during embryogenesis, including
implantation, organogenesis, developmental involution, and
metamorphosis
- Involution of hormone-dependent tissues upon hormone withdrawal,
such as endometrial cell breakdown during the menstrual cycle
- Elimination of potentially harmful self-reactive lymphocytes, either
before or after they have completed their maturation
- Death of host cells that have served their useful purpose, such as
neutrophils in an acute inflammatory response
• Apoptosis in pathologic conditions:
- DNA damage. Radiation, cytotoxic anticancer drugs, and
hypoxia
- Accumulation of misfolded proteins- damage caused by free
radicals
- Cell death in certain infections, particularly viral infections, in
which loss of infected cells is largely due to apoptosis-
adenovirus or HIV infection
Morphologic and biochemical changes
in Apoptosis
• Morphology:
- Cell shrinkage : cell is smaller in size; the cytoplasm is
dense and the organelles are more tightly packed
- Chromatin condensation: chromatin aggregates
peripherally, under the nuclear membrane, into dense
masses of various shapes and sizes
- Formation of cytoplasmic blebs and apoptotic bodies
- Phagocytosis of apoptotic cells or cell bodies, usually
by macrophages
Mechanism of Apoptosis
Necrosis and apoptosis
Intrinsic(mitochondrial) pathway
• result of increased mitochondrial permeability and release of
pro-apoptotic molecules (death inducers) into the cytoplasm
Triggered by:
-Loss of survival signal
- DNA damage
-Accumulation of misfolded
proteins
Inhibited by:
- Survival signals- growth factors
Extrinsic death receptor pathway
Responsible for elimination
of self-reactive
lymphocytes and damage
by cytotoxic T lymphocytes
Disorders associated with
Dysregulated Apoptosis
• Defective apoptosis and increased cell survival
- Cancer
- Autoimmune disorders
• Increased apoptosis and excessive cell death
- Neurodegenerative diseases
- Ischemic injury
- Death of virus infected cells
Different between necrosis and apoptosis
Necrosis vs Apoptosis
References
• Robbins Basic Pathology 9th edition
• First Aid 2019
Thank you

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Necrosis and apoptosis

  • 1. Necrosis and Apoptosis Presentor: Dr. Bishal Paudel 1st Year Orthopaedics Resident
  • 2. Objectives • To define necrosis and apoptosis • To explain morphology and mechanism • To illustrate different types of necrosis • To discuss briefly about the difference between necrosis and apoptosis
  • 5. Necrosis • Series of changes that accompany cell death, largely resulting from the degradative action of enzymes on lethally injured cells • characterized by swelling, denaturation and coagulation of proteins, breakdown of cellular organelles and cell rupture • caused by extra-cellular enzymes, liberated from inflammatory cells
  • 6. NECROSIS: MORPHOLOGY Light microscopy (H & E stains) • Necrotic cells -eosinophilia, glassy homogeneous appearance • Cytoplasm- vacuolated • Myelin figures- whorled phospholipid masses • Calcified dead cells
  • 7. • Nuclear changes : - Karyolysis - gradual fading away of the basophilic nuclear material, presumably due to action of DNAses. - Karyorrhexis - fragmentation of nucleus and the debris is either phagocytosed by other cells or just disappears. - Pyknosis - condensation of nucleus into a deep basophilic mass. This stage is often followed by karyorrhexis.
  • 10. Types of Necrosis 1) Coagulative necrosis: - denaturation of cytoplasmic proteins with preservation of the framework of the coagulated cell - lschemia/infracts in most tissues (except brain)
  • 11. • Liquefaction necrosis - autolysis and heterolysis prevail over protein denaturation - necrotic area is soft and filled with fluid with obliteration of normal architecture - localized bacterial infection (abscesses) and brain
  • 12. Caseation necrosis- - Cellular death with complete loss of architectural pattern - Necrotic area is dry, cheesy and friable - Example: Tuberculosis
  • 13. • Fat necrosis: - Enzymatic: acute pancreatitis (saponification of peripancreatic fat) - Nonenzymatic: traumatic (eg injury to breast tissue}
  • 14. • Fibrinoid necrosis: - Immune vascular reactions (eg, PAN) - Nonimmune vascular reactions (eg. Hypertensive emergency, preeclampsia)
  • 15. • Gangrenous necrosis: - Distal extremity and GI tract, after chronic ischemia
  • 16. Apoptosis • named after the Greek designation for “falling off” • Tightly regulated suicide program in which cells destined to die activate enzymes capable of degrading the cells own nuclear DNA and nuclear and cytoplasmic proteins • Dead cells are rapidly cleared before its content are leaked out • Hence does not elicit inflammatory reaction in the host
  • 17. Causes of apoptosis Apoptosis in physiologic situation: - programmed destruction of cells during embryogenesis, including implantation, organogenesis, developmental involution, and metamorphosis - Involution of hormone-dependent tissues upon hormone withdrawal, such as endometrial cell breakdown during the menstrual cycle - Elimination of potentially harmful self-reactive lymphocytes, either before or after they have completed their maturation - Death of host cells that have served their useful purpose, such as neutrophils in an acute inflammatory response
  • 18. • Apoptosis in pathologic conditions: - DNA damage. Radiation, cytotoxic anticancer drugs, and hypoxia - Accumulation of misfolded proteins- damage caused by free radicals - Cell death in certain infections, particularly viral infections, in which loss of infected cells is largely due to apoptosis- adenovirus or HIV infection
  • 19. Morphologic and biochemical changes in Apoptosis • Morphology: - Cell shrinkage : cell is smaller in size; the cytoplasm is dense and the organelles are more tightly packed - Chromatin condensation: chromatin aggregates peripherally, under the nuclear membrane, into dense masses of various shapes and sizes - Formation of cytoplasmic blebs and apoptotic bodies - Phagocytosis of apoptotic cells or cell bodies, usually by macrophages
  • 22. Intrinsic(mitochondrial) pathway • result of increased mitochondrial permeability and release of pro-apoptotic molecules (death inducers) into the cytoplasm Triggered by: -Loss of survival signal - DNA damage -Accumulation of misfolded proteins Inhibited by: - Survival signals- growth factors
  • 23. Extrinsic death receptor pathway Responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes
  • 24. Disorders associated with Dysregulated Apoptosis • Defective apoptosis and increased cell survival - Cancer - Autoimmune disorders • Increased apoptosis and excessive cell death - Neurodegenerative diseases - Ischemic injury - Death of virus infected cells
  • 25. Different between necrosis and apoptosis
  • 27. References • Robbins Basic Pathology 9th edition • First Aid 2019