Cell injury, apoptosis and necrosis !
- Process
A damaged cell can recover, die in an orderly way (apoptosis) or die in a messy, inflammatory way (necrosis).
Updated 2026-11-01
See it in 3D: Liver
What it is
Faced with an insult (lack of oxygen, toxins, infection), a cell first shows reversible changes; if the damage persists, it dies. Apoptosis is programmed, orderly death without inflammation; necrosis is accidental death with burst membranes and inflammation. The pattern of necrosis points to the cause.
Key facts
- Coagulative necrosis: the outlines of cells remain but nuclei are lost; typical of myocardial and renal infarcts.
- Liquefactive necrosis: the tissue turns liquid; typical of brain infarcts and abscesses.
- Caseous necrosis: amorphous granular «cheese-like» material inside granulomas; typical of tuberculosis.
- Fat necrosis: lipases release fatty acids that bind calcium (saponification); typical of acute pancreatitis.
- Fibrinoid necrosis: bright pink deposits in vessel walls in vasculitis and malignant hypertension.
Step by step
- Insult: hypoxia, toxins, radiation, microbes or immune attack.
- Reversible injury: the sodium pump fails, water enters, the cell swells and blebs; fatty change may appear.
- If the damage goes on: membranes are injured, calcium floods in and lysosomes burst.
- Intrinsic apoptosis: BAX/BAK proteins release cytochrome c from the mitochondrion; BCL-2 prevents it.
- Extrinsic pathway: Fas ligand or TNF activates death receptors and caspase 8.
- Executioner caspases break the cell into apoptotic bodies that macrophages eat without inflammation.
Apoptosis versus necrosis
| Feature | Apoptosis | Necrosis |
|---|---|---|
| Extent | Single cells | Groups of cells, areas of tissue |
| Cell size | Shrinks | Swells |
| Nucleus | Pyknosis and karyorrhexis; apoptotic bodies | Pyknosis, karyorrhexis and karyolysis |
| Membrane | Intact; blebs that break off | Ruptured; contents spill into the tissue |
| Inflammation | No | Yes |
| Examples | Embryonic development, hormone withdrawal, cytotoxic T cells, Councilman bodies in hepatitis | Infarct, abscess, tuberculosis, pancreatitis |
In the lab
- On H&E an apoptotic cell is small, with very eosinophilic cytoplasm and a dense or fragmented nucleus, sometimes with a clear halo around it.
- In a recent myocardial infarct the fibres look more eosinophilic and lose their nuclei, and neutrophils arrive within the first days.
Test yourself
Think of the answer, then tap the question to see it.
Which type of necrosis is seen in a brain infarct?
Liquefactive necrosis, because brain tissue has few structural proteins and many enzymes.
Which released mitochondrial protein triggers the intrinsic pathway of apoptosis?
Cytochrome c, which builds the apoptosome and activates caspase 9.
Which type of necrosis is typical of tuberculosis?
Caseous necrosis: granular, eosinophilic, amorphous material in the centre of the granuloma.
Why does apoptosis not cause inflammation?
The membrane stays intact and apoptotic bodies are eaten before their contents leak out.
See it in 3D
The structures of Durgical's 3D anatomy where it is found.
Related
- Organelles: nucleus, ER, Golgi, mitochondria, lysosomes, peroxisomes
- Cell adaptations: hypertrophy, hyperplasia, atrophy, metaplasia
- Cell cycle, mitosis and meiosis
- Wound healing: phases and scar
Related conditions
- Myocardial Infarction (Heart Attack)
- Ischaemic stroke
- Pulmonary tuberculosis
- Acute pancreatitis
- Viral hepatitis
Microorganisms
Educational content on normal microscopic structure and its clinical relevance; no substitute for studying slides or for a health professional's advice.
Sources: 4.6 Tissue Injury and Aging (OpenStax (Rice University), 2022); What Is Cancer? (National Cancer Institute, 2021).
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Representative model, for educational purposes only.