Cell Death: Necrosis vs. Apoptosis
1. Introduction
Cell death is a fundamental biological process, essential in development, tissue homeostasis, and
pathology. Two major forms are distinguished: Necrosis (uncontrolled, pathological) and
Apoptosis (controlled, programmed). Key differences lie in energy dependence, membrane
integrity, and inflammatory response.
2. Necrosis
Definition & Features
Uncontrolled cell death due to irreversible injury. Always pathological.
Pathological Basis
Triggered by hypoxia, ischemia, toxins, infections, or trauma.
Mechanism
Energy-independent (passive). Failure of ATP production leads to ion imbalance, osmotic
swelling, loss of membrane integrity, and cell lysis, releasing enzymes.
Morphological Changes
• Cell swelling (oncosis).
• Loss of membrane integrity.
• Nuclear changes: Pyknosis (condensation), Karyorrhexis (fragmentation), Karyolysis
(dissolution).
, Types of Necrosis
• Coagulative: Ischemia in solid organs (heart, kidney).
• Liquefactive: Brain infarct, abscess.
• Caseous: TB granulomas (cheesy appearance).
• Fat necrosis: Acute pancreatitis.
• Fibrinoid: Immune-mediated vascular injury.
• Gangrenous: Limb ischemia (dry/wet).
Consequences
Cell contents are released, causing damage to surrounding tissue. Always associated with
inflammation.
3. Apoptosis
Definition & Features
Programmed cell death (genetic, energy-dependent). Physiological but may also occur in disease.
Physiological Roles
• Embryogenesis (e.g., digit separation).
• Elimination of self-reactive T-cells.
• Hormone-dependent involution (e.g., endometrium).
• Cell turnover in tissues (e.g., intestinal lining).
Mechanism
Energy-dependent (active) and controlled by caspases (cysteine proteases). Two major pathways:
Intrinsic (mitochondrial: cytochrome c release → caspase-9) and Extrinsic (death receptor: Fas
ligand/TNF receptor → caspase-8).
1. Introduction
Cell death is a fundamental biological process, essential in development, tissue homeostasis, and
pathology. Two major forms are distinguished: Necrosis (uncontrolled, pathological) and
Apoptosis (controlled, programmed). Key differences lie in energy dependence, membrane
integrity, and inflammatory response.
2. Necrosis
Definition & Features
Uncontrolled cell death due to irreversible injury. Always pathological.
Pathological Basis
Triggered by hypoxia, ischemia, toxins, infections, or trauma.
Mechanism
Energy-independent (passive). Failure of ATP production leads to ion imbalance, osmotic
swelling, loss of membrane integrity, and cell lysis, releasing enzymes.
Morphological Changes
• Cell swelling (oncosis).
• Loss of membrane integrity.
• Nuclear changes: Pyknosis (condensation), Karyorrhexis (fragmentation), Karyolysis
(dissolution).
, Types of Necrosis
• Coagulative: Ischemia in solid organs (heart, kidney).
• Liquefactive: Brain infarct, abscess.
• Caseous: TB granulomas (cheesy appearance).
• Fat necrosis: Acute pancreatitis.
• Fibrinoid: Immune-mediated vascular injury.
• Gangrenous: Limb ischemia (dry/wet).
Consequences
Cell contents are released, causing damage to surrounding tissue. Always associated with
inflammation.
3. Apoptosis
Definition & Features
Programmed cell death (genetic, energy-dependent). Physiological but may also occur in disease.
Physiological Roles
• Embryogenesis (e.g., digit separation).
• Elimination of self-reactive T-cells.
• Hormone-dependent involution (e.g., endometrium).
• Cell turnover in tissues (e.g., intestinal lining).
Mechanism
Energy-dependent (active) and controlled by caspases (cysteine proteases). Two major pathways:
Intrinsic (mitochondrial: cytochrome c release → caspase-9) and Extrinsic (death receptor: Fas
ligand/TNF receptor → caspase-8).
