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Cited by 428

The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.

Glucocorticoid-induced osteonecrosis

Open access
Weinstein, Robert S.·2012·Endocrine

Abstract

Awareness of the need for prevention of glucocorticoid-induced fractures is growing, but glucocorticoid administration is often overlooked as the most common cause of nontraumatic osteonecrosis. Glucocorticoid-induced osteonecrosis develops in 9–40% of patients receiving long-term therapy although it may also occur with short-term exposure to high doses, after intra-articular injection, and without glucocorticoid-induced osteoporosis. The name, osteonecrosis, is misleading because the primary histopathological lesion is osteocyte apoptosis. Apoptotic osteocytes persist because they are anatomically unavailable for phagocytosis and, with glucocorticoid excess, decreased bone remodeling retards their replacement. Glucocorticoid-induced osteocyte apoptosis, a cumulative and unrepairable defect, uniquely disrupts the mechanosensory function of the osteocyte–lacunar–canalicular system and thus starts the inexorable sequence of events leading to collapse of the femoral head. Current evidence indicates that bisphosphonates may rapidly reduce pain, increase ambulation, and delay joint collapse in patients with osteonecrosis.

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Metadata

Authors
Weinstein, R. S.
Venue
Endocrine
Published
2011-12-15
Volume
41
Issue
2
Pages
183-190
ISSN
  • 0969-711X (ISSN-L)
  • 1355-008X
  • 1559-0100
OpenAlex
W1967302620
Cited by
428
References
32
FWCI
13.76
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Glucocorticoid-induced osteonecrosis. https://app.cochat.ai/papers/10.1007/s12020-011-9580-0
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Weinstein, R. S. (2012). Glucocorticoid-induced osteonecrosis. Endocrine. https://doi.org/10.1007/s12020-011-9580-0

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