Search results
Results from the WOW.Com Content Network
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]
Necrotizing vasculitis, also called systemic necrotizing vasculitis, [1] is a general term for the inflammation of veins and arteries that develops into necrosis and narrows the vessels. [ 2 ] Tumors , medications, allergic reactions , and infectious organisms are some of the recognized triggers for these conditions, even though the precise ...
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 ...
The major tissues affected are nerves and muscles, where irreversible damage starts to occur after 4–6 hours of cessation of blood supply. [4] Skeletal muscle, the major tissue affected, is still relatively resistant to infarction compared to the heart and brain because its ability to rely on anaerobic metabolism by glycogen stored in the cells may supply the muscle tissue long enough for ...
Treatments may include medication, not walking on the affected leg, stretching, and surgery. [1] Most of the time surgery is eventually required and may include core decompression, osteotomy, bone grafts, or joint replacement. [1] About 15,000 cases occur per year in the United States. [4] People 30 to 50 years old are most commonly affected. [3]
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 ]
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.
Chronic inflammation from persistent necrotic debris can cause fibrosis, replacing viable tissue with collagen and scar tissue. [4] The aftermath of necrosis varies depending on the tissue. For instance: In the brain, necrosis often leads to liquefactive necrosis, where tissue becomes soft and liquid-like.