Editing Necrosis (section)

==Classification==

Structural signs that indicate irreversible cell injury and the progression of necrosis include dense clumping and progressive disruption of [[gene]]tic material, and disruption to membranes of cells and [[organelles]].<ref name="Craft">{{cite book |vauthors=Craft J, Gordon C, Tiziani A, Huether SE, McCance KL, Brashers VL | title = Understanding pathophysiology | year = 2010 | publisher = Elsevier Australia | location = Chatswood, N.S.W. | isbn = 978-0-7295-3951-7 |oclc=994801732}}</ref>

===Morphological patterns===

There are six distinctive morphological patterns of necrosis:<ref name="Kumar">{{cite book|vauthors=Kumar V, Abbas AK, Aster JC, Fausto N | title = Robbins and Cotran pathologic basis of disease | year = 2010 | publisher = Saunders/Elsevier | location = Philadelphia, PA | isbn = 978-1-4160-3121-5 | pages = 12–41 | edition = 8th |oclc=1409188915}}</ref>

# [[Coagulative necrosis]] is characterized by the formation of a gelatinous (gel-like) substance in dead tissues in which the architecture of the tissue is maintained,<ref name="Kumar"/> and can be observed by light microscopy. Coagulation occurs as a result of protein [[Denaturation (biochemistry)|denaturation]], causing [[albumin]] to transform into a firm and opaque state.<ref name="Craft"/> This pattern of necrosis is typically seen in [[Hypoxia (medical)|hypoxic]] (low-oxygen) environments, such as [[infarction]]. Coagulative necrosis occurs primarily in tissues such as the kidney, heart and adrenal glands.<ref name="Craft"/> Severe [[ischemia]] most commonly causes necrosis of this form.<ref name="McConnell">{{cite book | author = McConnell TH | title = The nature of disease: pathology for the health professions | year = 2007 | publisher = Lippincott Williams & Wilkins | location = Baltimore, Mar. | isbn = 978-0-7817-5317-3 |oclc=71139383}}</ref>
# [[Liquefactive necrosis]] (or colliquative necrosis), in contrast to coagulative necrosis, is characterized by the digestion of dead cells to form a viscous liquid mass.<ref name="Kumar"/> This is typical of bacterial, or sometimes fungal, infections because of their ability to stimulate an inflammatory response. The necrotic liquid mass is frequently creamy yellow due to the presence of dead [[leukocyte]]s and is commonly known as [[pus]].<ref name="Kumar"/> [[Hypoxia (medical)|Hypoxic]] [[Infarction|infarcts]] in the brain presents as this type of necrosis, because the brain contains little connective tissue but high amounts of digestive enzymes and lipids, and cells therefore can be readily digested by their own enzymes.<ref name="Craft"/>
# [[Gangrenous necrosis]] can be considered a type of coagulative necrosis that resembles mummified tissue. It is characteristic of ischemia of lower limb and the gastrointestinal tracts. 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).<ref>{{cite book| author = Sattar | title = Fundamentals of Pathology | year = 2015 | publisher = Pathoma LLC | location = Chicago, IL | isbn = 978-0-9832246-2-4| pages = 5 | edition = 2015th |oclc=1301972970}}</ref>
# [[Caseous necrosis]] can be considered a combination of coagulative and liquefactive necrosis,<ref name="Craft"/> typically caused by [[mycobacteria]] (e.g. [[tuberculosis]]), fungi and some foreign substances. The necrotic tissue appears as white and [[friable]], like clumped cheese. Dead cells disintegrate but are not completely digested, leaving granular particles.<ref name="Craft"/> Microscopic examination shows [[amorphous]] granular debris enclosed within a distinctive inflammatory border.<ref name="Kumar"/> Some [[granuloma]]s contain this pattern of necrosis.<ref name="Stevens">{{cite book|vauthors=Stevens A, Lowe JS, Young B, Deakin PJ | title = Wheater's basic histopathology: a colour atlas and text |year = 2002 | publisher = Churchill Livingstone | location = Edinburgh | isbn = 978-0-443-07001-3 | edition = 4th |oclc=606877653}}</ref>
# [[Fat necrosis]] is specialized necrosis of fat tissue,<ref name="Stevens"/> resulting from the action of activated [[lipase]]s on fatty tissues such as the [[pancreas]]. In the pancreas it leads to acute [[pancreatitis]], a condition where the [[pancreatic enzymes]] leak out into the [[peritoneum|peritoneal]] cavity, and liquefy the membrane by splitting the [[triglyceride]] esters into [[fatty acids]] through fat [[saponification]].<ref name="Kumar"/> Calcium, magnesium or sodium may bind to these lesions to produce a chalky-white substance.<ref name="Craft"/> The calcium deposits are microscopically distinctive and may be large enough to be visible on radiographic examinations.<ref name="McConnell"/> To the naked eye, calcium deposits appear as gritty white flecks.<ref name="McConnell"/>
# [[Fibrinoid necrosis]] is a special form of necrosis usually caused by immune-mediated vascular damage. It is marked by complexes of [[antigen]] and [[antibodies]], referred to as [[immune complex]]es deposited within [[artery|arterial]] walls<ref name="Kumar"/> together with [[fibrin]].<ref name="Kumar"/>

===Other clinical classifications of necrosis===

# There are also very specific forms of necrosis such as [[gangrene]] (term used in clinical practices for limbs which have had severe hypoxia), [[gummatous]] necrosis (due to [[spirochaete|spirochaetal]] infections) and hemorrhagic necrosis (due to the blockage of venous drainage of an organ or tissue).{{citation needed|date=May 2023}}
# Myonecrosis is the death of individual muscle fibres due to injury, hypoxia, or infection. Common causes include spontaneous diabetic myonecrosis (a.k.a. diabetic muscle infarction) and clostridial myonecrosis (a.k.a. [[gas gangrene]]).<ref>{{Cite web |title=Medical Definition of Myonecrosis; Doctor Written |url=https://www.rxlist.com/myonecrosis/definition.htm |access-date=2023-06-09 |website=RxList |language=en}}</ref>
# Some [[spider bite]]s may lead to necrosis. In the United States, only spider bites from the [[brown recluse spider]] (genus [[Loxosceles]]) reliably progress to necrosis. In other countries, spiders of the same genus, such as the [[Chilean recluse]] in South America, are also known to cause necrosis. Claims that [[yellow sac spider]]s and [[hobo spider]]s possess necrotic [[venom]] have not been substantiated.{{citation needed|date=May 2023}}
# In blind mole rats (genus ''[[Spalax]]''), the process of necrosis replaces the role of the systematic [[apoptosis]] normally used in many organisms. Low oxygen conditions, such as those common in blind mole rats' burrows, usually cause cells to undergo apoptosis. In adaptation to higher tendency of cell death, blind mole rats evolved a mutation in the [[tumor suppressor]] protein [[p53]] (which is also used in humans) to prevent cells from undergoing apoptosis. Human cancer patients have similar mutations, and blind mole rats were thought to be more susceptible to cancer because their cells cannot undergo apoptosis. However, after a specific amount of time (within 3 days according to a study conducted at the University of Rochester), the cells in blind mole rats release [[interferon-beta]] (which the immune system normally uses to counter viruses) in response to over-proliferation of cells caused by the suppression of apoptosis. In this case, the interferon-beta triggers cells to undergo necrosis, and this mechanism also kills cancer cells in blind mole rats. Because of tumor suppression mechanisms such as this, blind mole rats and other [[spalacid]]s are resistant to cancer.<ref>{{cite web| vauthors = Saey TH |title=Cancer cells self-destruct in blind mole rats|url=http://www.sciencenews.org/view/generic/id/346267/description/Cancer_cells_self-destruct_in_blind_mole_rats|website=[[Science News]]|publisher=[[Society for Science and the Public]]|access-date=27 November 2012|date=5 November 2012|archive-date=19 June 2013|archive-url=https://web.archive.org/web/20130619171046/http://www.sciencenews.org/view/generic/id/346267/description/Cancer_cells_self-destruct_in_blind_mole_rats|url-status=live}}</ref><ref name="pmid23129611">{{cite journal | vauthors = Gorbunova V, Hine C, Tian X, Ablaeva J, Gudkov AV, Nevo E, Seluanov A | title = Cancer resistance in the blind mole rat is mediated by concerted necrotic cell death mechanism | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 47 | pages = 19392–6 | date = November 2012 | pmid = 23129611 | pmc = 3511137 | doi = 10.1073/pnas.1217211109 | doi-access = free | bibcode = 2012PNAS..10919392G }}</ref>