Avascular bone necrosis
Avascular bone necrosis (synonyms: aseptic bone necrosis, subchondral avascular necrosis[1]) is a term describing bone necrosis of a non-infectious origin (hence aseptic), accompanied by bone ischemia (hence avascular). In Anglo-Saxon literature, the abbreviation AVN (AVascular Necrosis) is used.
Etiopathogenesis[edit | edit source]
In the pathogenesis of the disease, a disorder of the microcirculation of the bone marrow and bone is used. The causes of microcirculation disorders can be divided into:
- Known causes
- Probable causes
- Idiopathic bone necrosis
Known causes[edit | edit source]
- Fracture (mechanical compression of blood vessels).
- decompression sickness (occlusion of blood vessels with bubbles).
Probable causes[edit | edit source]
- metabolic diseases and diseases that increase blood coagulation – sickle cell anemia (occlusion of blood vessels by rigid erythrocytes), diabetes mellitus, disorders of lipid metabolism. pancreatitis, tumors, gout,
- systemic lupus erythematosus,
- iatrogenic – as a complication of corticoid administration, forced reduction of fractures and dislocations, dialysis,
- alcoholism,
- smoking.
Idiopathic bone necrosis[edit | edit source]
These are often necrosis in very young boys.
The above list is far from complete, there are even several mnemonics for very long lists of causes - STARS, PLASTIC RAGS, ASEPTIC.[2].
Avascular bone necrosis most often affects convex articular surfaces - in these places there is no collateralization and the terminal arteries are fragile. The reduced vascularization of the yellow (vs. red) bone marrow further contributes to susceptibility. In the case of idiopathic necrosis, the exact pathophysiology is not clear, usually neither thrombosis nor coagulopathy[1] is demonstrated.
Eponyms[edit | edit source]
Below is a very abbreviated list of avascular necrosis eponyms [3].
- Morbus Legg-Calvé-Perthes – femoral head.
- Morbus Osgood-Schlatter – fragmentation of the tuberositas tibiae.
- Morbus Friedrich – medial edge of the clavicle.
- Morbus Köhler I − os naviculare pedis.
- Morbus Kienböck – os lunatum.
- Morbus Sever - calcaneus.
- Morbus Freiberg - 2nd, 3rd, and 4th. metatarsus.
- Morbus Panner - capitulum humeri.
- Morbus Ahlback - medial condyle of the femur.
- Morbus Blount - medial part of the proximal tibial metaphysis.
- Morbus Sindig-Larsen-Johansson – patella.
- Morbus Pierson – Symphysis (Pubic symphysis).
- Morbus Haas – humeral head.
Display[edit | edit source]
As a result of a blood supply disorder (ischemia), bone resorption and calcification can be recognized on a plain image within 6-8 weeks, manifesting as inhomogeneities in a bone infarction.
Links[edit | edit source]
Related Articles[edit | edit source]
Used Literature[edit | edit source]
- SOSNA, A – VAVŘÍK, P – KRBEC, M. Základy ortopedie. 1. edition. Triton, 2001. 175 pp. ISBN 80-7254-202-8.
Reference[edit | edit source]
- ↑ a b CRISTINA, Fondi – FRANCHI, Alessandro. Definition of bone necrosis by the pathologist [online]. ©2007. [cit. 2016-11-19]. <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781178/>.
- ↑ GAILLARD, Frank. Avascular necrosis causes (mnemonic) [online]. [cit. 2016-11-19]. <https://radiopaedia.org/articles/avascular-necrosis-causes-mnemonic>.
- ↑ GAILLARD, Frank. Avascular necrosis [online]. [cit. 2016-11-19]. <https://radiopaedia.org/articles/avascular-necrosis>.
