Editing Necrosis (section)

==Pathogenesis==
===Pathways===
Until recently, necrosis was thought to be an unregulated process.<ref name="Kroemer">{{cite journal | vauthors = Kroemer G, Galluzzi L, Vandenabeele P, Abrams J, Alnemri ES, Baehrecke EH, Blagosklonny MV, El-Deiry WS, Golstein P, Green DR, Hengartner M, Knight RA, Kumar S, Lipton SA, Malorni W, Nuñez G, Peter ME, Tschopp J, Yuan J, Piacentini M, Zhivotovsky B, Melino G | display-authors = 6 | title = Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009 | journal = Cell Death and Differentiation | volume = 16 | issue = 1 | pages = 3–11 | date = January 2009 | pmid = 18846107 | pmc = 2744427 | doi = 10.1038/cdd.2008.150 }}</ref> However, there are two broad pathways in which necrosis may occur in an organism.<ref name="Kroemer"/>

The first of these two pathways initially involves [[oncosis]], where swelling of the cells occurs.<ref name="Kroemer"/> Affected cells then proceed to [[blebbing]], and this is followed by [[pyknosis]], in which nuclear shrinkage transpires.<ref name="Kroemer"/> In the final step of this pathway cell nuclei are dissolved into the cytoplasm, which is referred to as [[karyolysis]].<ref name="Kroemer"/>

The second pathway is a secondary form of necrosis that is shown to occur after apoptosis and budding.<ref name="Kroemer"/> In these cellular changes of necrosis, the nucleus breaks into fragments (known as [[karyorrhexis]]).<ref name="Kroemer"/>

===Histopathological changes===
{{Further|Myocardial infarction diagnosis}}
{{Anchor|Pseudopalisade|Cytoplasmic hypereosinophilia}}[[Image:MI_with_contraction_bands_very_high_mag.jpg|thumb|'''[[Karyolysis]]''' (and [[contraction band necrosis]]) in [[myocardial infarction]] (heart attack)]]

The nucleus changes in necrosis and characteristics of this change are determined by the manner in which its DNA breaks down:
* '''[[Karyolysis]]''': the [[chromatin]] of the nucleus fades due to the loss of the DNA by degradation.<ref name="Kumar"/>
* '''[[Karyorrhexis]]''': the shrunken nucleus fragments to complete dispersal.<ref name="Kumar"/>
* '''[[Pyknosis]]''': the nucleus shrinks, and the chromatin condenses.<ref name="Kumar"/>

Other typical cellular changes in necrosis include:
* '''Cytoplasmic hypereosinophilia''' on samples with [[H&E stain]].<ref>{{cite book | chapter = Frozen Section Diagnosis | chapter-url = https://books.google.com/books?id=n8AtBQAAQBAJ&pg=PA320 | page = 320 | archive-url = https://web.archive.org/web/20200804105603/https://books.google.se/books?id=n8AtBQAAQBAJ&pg=PA320 | archive-date=2020-08-04 | vauthors = Marchevsky AM, Balzer B, Abdul-Karim FW |title=Intraoperative Consultation E-Book | series = Foundations in Diagnostic Pathology |year=2014|publisher=Elsevier |isbn=978-0-323-32299-7 |oclc=898153075}}</ref> It is seen as a darker stain of the [[cytoplasm]].
* The '''[[cell membrane]]''' appears discontinuous when viewed with an [[electron microscope]]. This discontinuous membrane is caused by cell blebbing and the loss of [[microvilli]].<ref name="Kumar"/>

On a larger histologic scale, '''pseudopalisades''' (false [[Palisade (pathology)|palisades]]) are hypercellular zones that typically surround necrotic tissue. Pseudopalisading necrosis indicates an aggressive tumor.<ref>{{cite journal | vauthors = Wippold FJ, Lämmle M, Anatelli F, Lennerz J, Perry A | title = Neuropathology for the neuroradiologist: palisades and pseudopalisades | journal = AJNR. American Journal of Neuroradiology | volume = 27 | issue = 10 | pages = 2037–41 | date = 2006 | pmid = 17110662 | pmc = 7977220 }}</ref>

<gallery>
File:4 Bd obs 4 680x512px.tif|'''[[Pyknosis]]''' in a bile infarct
File:Histopathology of cytoplasmic hypereosinophilia in a pituitary adenoma.jpg|'''Cytoplasmic hypereosinophilia''' (seen in left half of image)
File:GBM pseudopalisading necrosis.jpg|'''Pseudopalisading''' seen around necrosis in [[glioblastoma]]
</gallery>