Pathology of Necrosis

Necrosis Types

• Liquefactive necrosis: characterized by digestion of dead cells, resulting in a liquid, viscous mass, often seen in abscesses on the skin.
• Caseous necrosis: displays a white, cheese-like appearance of dead cells, commonly associated with tuberculosis in the lung.
• Fibrinoid necrosis: typically seen in immune reactions within blood vessels, often occurring in conditions like Behcet syndrome, which is characterized by systemic vasculitis, oral ulcers, genital ulcers, skin lesions, and ocular lesions.
• Fat necrosis in the mesentery: not a true necrotic pattern, but rather focal areas of fat destruction, often seen in herniated buccal fat pads.

Apoptosis

• Programmed cell death or cellular suicide, tightly regulated to maintain homeostasis.
• Distinct from necrosis, with no significant inflammatory reaction, no loss of cell membrane integrity, and no leakage of cellular contents.
• Apoptosis can coexist with necrosis.

Apoptosis in Normal Processes

• Embryogenesis: cell elimination due to loss of growth factor signaling.
• Normal cell turnover: elimination of cells with short half-lives, and tissue involution due to loss of growth factor stimulation or hormonal changes (e.g., in the endometrium during the menstrual cycle).
• Immune function: decline in leukocytes at the end of inflammation, and elimination of harmful self-reactive lymphocytes.

Pathologic Apoptosis

• DNA damage: activates proapoptotic proteins, often triggered by radiation treatment or cytotoxic drugs.
• Accumulation of misfolded proteins: activates proapoptotic proteins and caspases (cysteine proteases).
• Infections: viral infections, such as adenoviruses, herpesviruses, EBV, and HHV-8, can activate proapoptotic proteins or caspases.
• Killing of infected cells: cytotoxic T lymphocytes (CTLs) activate caspases, leading to apoptosis.