Bone Marrow - Necrosis




comment:
Bone marrow necrosis is characterized by cytoplasmic vacuolization, indistinct cell borders, nuclear pyknosis, karyolysis, and karyorrhexis ( Figure 1




There are several known causes of bone marrow necrosis. It may occur as a direct result of compound administration (e.g.,cyclophosphamide) or may be secondary to severe infectious disease states (e.g., septicemia) or tissue ischemia caused by vascular injury, thrombosis, or vascular occlusion. Specific causes of the latter include neoplasia (e.g., tumor emboli, vascular occlusion), disseminated intravascular coagulation (thrombosis), and exposure to endotoxin (vascular injury). Necrosis caused by an obstruction of the blood supply (infarct) generally has well-delineated borders microscopically as a distinguishing feature ( Figure 3


In a rat study to evaluate the effects of feed restriction on common toxicologic parameters, severe diet restriction (75%reduction) of only two weeks resulted in bone marrow necrosis and degeneration. Specific observations included vacuolated or necrotic-appearing stromal cells, necrosis of hematopoietic cells, remaining hematopoietic tissue <25% of concurrent controls, focal areas of hemorrhage, and readily observed emperipolesis of neutrophils within the megakaryocytes.
recommendation:
Necrosis should always be recorded and graded, and the distribution should be described in the pathology narrative. Regarding necrosis and inflammation, primary or secondary inflammatory processes must be distinguished: a primary process should be recorded separately, while a secondary process need only be recorded or described if warranted by its severity. Gross morphologic descriptors, such as “coagulative” and “caseous,” should not be used for histologic description of necrotic lesions. When a thrombus is seen or is perceived to be the cause of the necrosis, it may be described and interpreted as ischemic necrosis/infarct in the narrative and the thrombus, if present, recorded separately.references:
Bain BJ, Clark DM, Lampert IA, Wilkins BS. 2001. Bone Marrow Pathology, 3rd ed. Blackwell, Ames, IA, 90-140. Abstract: http://onlinelibrary.wiley.com/book/10.1002/9780470757130
Levin S, Semler D, Ruben Z. 1993. Effects of two weeks of feed restriction on some common toxicologic parameters in Sprague-Dawley rats. Toxicol Pathol 21:1-14. Abstract: http://www.ncbi.nlm.nih.gov/pubmed/8378702
MacKenzie WF, Eustis SL. 1990. Bone marrow. In: Pathology of the Fischer Rat: Reference and Atlas (Boorman GA, Eustis SL, Elwell MR, Montgomery CA, Mackenzie WF, eds). Academic Press, San Diego, 315-337. Abstract: http://www.ncbi.nlm.nih.gov/nlmcatalog/9002563
Rebar AH. 1993. General responses of the bone marrow to injury. Toxicol Pathol 21:118-129. Full Text: http://tpx.sagepub.com/content/21/2/118.full.pdf
Travlos GS. 2006. Histopathology of the bone marrow. Toxicol Pathol 34:566-598. Abstract: http://tpx.sagepub.com/content/34/5/566.abstract
Weiss DJ. 2010. Myelonecrosis and acute inflammation. In: Schalm’s Veterinary Hematology, 5th ed (Weiss DJ, Wardrop KJ, eds). Wiley-Blackwell, Ames, IA, 106-111. Abstract: http://vet.sagepub.com/content/40/2/223.1
Web page last updated on: June 19, 2014