Necrosis and apoptosis are two terms commonly encountered in clinical and academic pathology. These are complex phenomena of cell death. One is pathological while the other is physiological. It is important to understand the basic differences of these two. This article describes necrosis and apoptosis, their mechanism, and clarifies the difference between the two.
Necrosis may occur directly or after cell degeneration. Early changes are very subtle and appear on electron microscope only after 2 to 3 hours and, in a light microscope, only after 6 hours. Cellular changes can be divided into nuclear changes and cytoplasmic changes. Nuclear material may first clump into dense masses, which stain with basic stains. This is known as “Pyknosis”. Afterwards, these clumps may break up into small particles in a process known as “Karyorrhexis”, or get lysed in a process called “Karyolysis”. Cytoplasmic changes start with the cytoplasm becoming homogenous and stain deeply with acidic stains. This is due to denaturation of cytoplasmic proteins. Special organelles absorb water and swell. Enzymes get released from lysosomes, and the cell breaks down (autolysis). Biochemically all these changes occur in concert with a massive influx of calcium ions. There are many types of necrosis. They are coagulative necrosis, liquefactive necrosis, fat necrosis, caseous necrosis, gummatous necrosis, fibrinoid necrosis, and gangrene.
In coagulative necrosis cells retain the cellular outline for a few days while all the other changes occur. This type of necrosis is seen commonly in solid organs most commonly following poor blood supply. In liquefactive necrosis the cell is lysed completely; thus there is no cellular outline. This is commonly seen in the brain and spinal cord. There are two types of fat necrosis; enzymatic and non-enzymatic fat necrosis. In enzymatic fat necrosis which occurs characteristically in acute pancreatitis, the cell fats get lysed into fatty acids and glycerol by pancreatic lipase and the result forms complexes with calcium. Thus, the appearance is chalky white. Non-enzymatic fat necrosis is mostly seen in subcutaneous tissue, breast and abdomen. Patients with non-enzymatic fat necrosis almost always give a history of trauma. However, trauma is not clearly identified as the definitive cause. Fibrosis closely follows non-enzymatic fat necrosis forming a solid mass sometimes indistinguishable from cancer clinically. Caseous and gummatous necrosis are due to granuloma formation after infections. Fibrinoid necrosis is commonly seen in autoimmune diseases. Gangrene is a widely used term to refer to a clinical condition where extensive tissue necrosis is complicated to varying degrees by secondary bacterial infection. There are three types of gangrene; dry, wet and gas gangrene. Dry gangrene mostly occurs at extremities due to poor blood supply resulting from blockage of arteries. Wet gangrene results from severe bacterial infection superimposed on necrosis. It can occur at extremities as well as in internal organs. Wet gangrene is difficult to demarcate from adjacent healthy tissue; therefore, surgical excision is difficult. Mortality rate in wet gangrene is high. Gas gangrene is due to Clostridium perfringens infection. It is characterized by extensive necrosis and production of gas. There is crepitation on palpation.
Apoptosis is a physiological phenomenon of programmed cell death. When tissues mature and change shape it needs to remove unwanted cells. This is the process where these unwanted cells die off. Apoptosis is a phenomenon coded by genes. The destiny of the cell is coded in its DNA, and it obeys the genetic commands when it is time for the cell to die for the good of the other cells and tissues. Current understanding is that mitochondrial DNA code for apoptosis. Apoptosis is spontaneous, and there is no external agent which causes it. The process is complex and can progress at different rates in different tissues.
Necrosis vs Apoptosis
• Necrosis is a type of cell death due to an external causative agent while apoptosis is an internal predetermined process of cell death.
• Protective mechanisms and drugs administered to fight off the causative agent may prevent necrosis while nothing can prevent apoptosis.
Also, read the Difference Between Gangrene and Necrosis