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Critical Reviews™ in Eukaryotic Gene Expression
Facteur d'impact: 2.156 Facteur d'impact sur 5 ans: 2.255 SJR: 0.649 SNIP: 0.599 CiteScore™: 3

ISSN Imprimer: 1045-4403
ISSN En ligne: 2162-6502

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukaryotGeneExpr.v13.i24.140
16 pages

Role of Apoptosis in Glucocorticoid-Induced Osteoporosis and Osteonecrosis

Charalampos Zalavras
Departments of Orthopaedic Surgery, Biochemistry and Molecular Biology, Institute for Genetic Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, CA
Swapnil Shah
Departments of Orthopaedic Surgery, Biochemistry and Molecular Biology, Institute for Genetic Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, CA
Mark J. Birnbaum
Department of Biology, Merrimack College, North Andover, MA
Baruch Frenkel
Institute for Genetic Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033

RÉSUMÉ

Bone disease is a side effect of concern regarding chronic glucocorticoid (GC) administration. Most GC-treated patients exhibit a process of bone loss, frequently leading to osteoporosis, with increased fracture risk, especially in spinal vertebrae. Some GC-treated patients will develop osteonecrosis, a disease with distinct clinical and histopathological features, most often occurring underneath the articular surface of the femoral head. Remarkably, both of these GC-induced bone diseases are associated with osteoblast and osteocyte apoptosis, which is emerging as a potential primary pathogenic mechanism. Here, we review the evidence for osteoblast and osteocyte apoptosis in GC-induced bone disease and highlight current debates: (1) With recent reports describing the antiapoptotic effect of GCs in some in vitro osteoblast models, and with the known adverse effects of GCs on osteoblast cell cycle and differentiation, could the in vivo osteoblast apoptosis be an indirect rather than a direct effect of GCs? (2) What is the pathogenic relationship between GC-induced osteoporosis and osteonecrosis? Could the latter be a mere manifestation of the former? and (3) How does apoptosis fit into the traditional concept of ischemia as a key etiology in osteonecrosis? Regardless of the answers, recent studies with cells, animals, and humans point out bone cell apoptosis as a potential target in the design of treatment for GC-induced bone disease.


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