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Liquefactive necrosis (or colliquative necrosis) is a type of necrosis which results in a transformation of the tissue into a liquid viscous mass. [1] Often it is associated with focal bacterial or fungal infections, and can also manifest as one of the symptoms of an internal chemical burn . [ 2 ]
Acute inflammation of the lung (usually in response to pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings. [15] Heat and redness are due to increased blood flow at body core temperature to the inflamed site. Swelling is caused by accumulation of fluid.
Research into hormones and wound healing has shown estrogen to speed wound healing in elderly humans and in animals that have had their ovaries removed, possibly by preventing excess neutrophils from entering the wound and releasing elastase. [26] Thus the use of estrogen is a future possibility for treating chronic wounds.
Timing is important to wound healing. Critically, the timing of wound re-epithelialization can decide the outcome of the healing. [11] If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months; [12] [13] If the epithelization of a wounded area is fast, the healing will result in regeneration.
The lack of oxygen (hypoxia) causes cell death in a localized area which is perfused by blood vessels failing to deliver primarily oxygen, but also other important nutrients. While ischemia in most tissues of the body will cause coagulative necrosis, in the central nervous system ischemia causes liquefactive necrosis , as there is very little ...
A proinflammatory cytokine causes hyperinflammation, the leading cause of lung tissue destruction in cystic fibrosis. [12] With such a strong inflammatory response and an elevated number of immune cells, lungs of cystic fibrosis patients cannot clear the bacteria and become more susceptible to infections.
Necrosis can be activated by components of the immune system, such as the complement system; bacterial toxins; activated natural killer cells; and peritoneal macrophages. [1] Pathogen-induced necrosis programs in cells with immunological barriers (intestinal mucosa) may alleviate invasion of pathogens through surfaces affected by inflammation. [1]
Inflammation is essential to protect against viral and bacterial infection, as well as noxious stimuli. It is an integral part of the healing process, though prolonged inflammation can be detrimental. The network dynamics of inflammation change with age, and factors such as genes, lifestyle, and environment contribute to these changes. [5]