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Caseous necrosis or caseous degeneration [1] (/ ˈ k eɪ s i ə s /) [2] is a unique form of cell death in which the tissue maintains a cheese-like appearance. [3] Unlike with coagulative necrosis, tissue structure is destroyed. Caseous necrosis is enclosed within a granuloma. Caseous necrosis is most notably associated with tuberculoma.
Both dry gangrene and gas gangrene can lead to this type of necrosis. If superimposed infection of dead tissues occurs, then liquefactive necrosis ensues (wet gangrene). [9] Caseous necrosis can be considered a combination of coagulative and liquefactive necrosis, [6] typically caused by mycobacteria (e.g. tuberculosis), fungi and some foreign ...
Caseous necrosis in T.B. is most common site of dystrophic calcification. Liquefactive necrosis in chronic abscesses may get calcified. Fat necrosis following acute pancreatitis or traumatic fat necrosis in breasts results in deposition of calcium soaps. Infarcts may undergo D.C. Thrombi, especially in veins, may produce phleboliths.
A related term, caseation (literally: turning to cheese) refers to a form of necrosis that, to the unaided eye, appears cheese-like ("caseous"), and is typically a feature of the granulomas of tuberculosis. The identification of necrosis in granulomas is important because granulomas with necrosis tend to have infectious causes. [2]
Necrosis is cell death where a cell has been badly damaged through external forces such as trauma or infection and occurs in several different forms. It is the sum of what happens to cells after their deaths. [20] In necrosis, a cell undergoes swelling, followed by uncontrolled rupture of the cell membrane with cell contents being expelled.
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Vitamin D deficiency has also been correlated with an increased risk of Pott’s Disease, particularly spinal TB with caseous necrosis, increasing the risk of necrosis compared to individuals with normal vitamin D levels. A deficiency in vitamin D has been associated with the activation of tuberculosis (TB) for a long time.
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