Necrosis

Necrosis usually follows overwhelming injury — ischaemia, toxins, infection, trauma — that depletes ATP and damages membranes. Cells and organelles swell (oncosis), plasma and lysosomal membranes rupture, enzymes digest the cell, and its contents leak out, provoking acute inflammation. Cytoplasm becomes intensely eosinophilic; the nucleus shows pyknosis, karyorrhexis and finally karyolysis (fading as DNA is degraded). Leaked intracellular proteins are measured clinically as markers of injury: troponins (myocardium), transaminases ALT/AST (liver), creatine kinase (muscle), lipase (pancreas).

Morphological patterns: coagulative — the commonest; architecture preserved for days because proteins denature (infarcts of heart, kidney, spleen); liquefactive — enzymatic digestion to a liquid (brain infarcts, abscesses); caseous — cheese-like, friable, within granulomas (tuberculosis, some fungi); fat necrosis — release of lipases (acute pancreatitis) with saponification (chalky calcium soaps), or trauma to breast fat; fibrinoid — immune complexes and fibrin in vessel walls (vasculitis, malignant hypertension); gangrenous — clinical term for necrosis of a limb or bowel, dry (coagulative) or wet (with superimposed infection, liquefactive).

Some necrosis is regulated: necroptosis (RIPK1–RIPK3–MLKL, caspase-independent) and pyroptosis (caspase-1 activation in inflammasomes, gasdermin D pores, IL-1β release) are inflammatory programmed deaths important in infection.