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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0552v1 201/3/321    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bitto, A. Articles by Squadrito, F. Search for Related Content PubMed PubMed Citation Articles by Bitto, A. Articles by Squadrito, F.

A Bitto, Messina, Italy
F Polito, Messina, Italy
B Burnett, Scottsdale, United States
R Levy, Scottsdale, United States
V Di Stefano, Messina, Italy
M Armbruster, Scottsdale, United States
H Marini, Messina, Italy
L Minutoli, Messina, Italy
D Altavilla, Messina, Italy
F Squadrito, Dep of Clinical and Experimental Medicine and Pharmacology, University of Messina, Messina, 98123, Italy

Correspondence: Francesco Squadrito, Email: francesco.squadrito{at}unime.it

Glucocorticoid-induced osteoporosis (GIO) is the most important secondary cause of bone loss. Clinical evidence suggests a role for genistein aglycone in the prevention of osteoporosis. We investigated whether genistein could prevent GIO as well as the development of osteonecrosis in the femoral head using an experimental rat model. A total of 28 female Sprague-Dawley rats were used in the study. GIO and osteonecrosis were induced by daily subcutaneous injections of 30 mg/kg of methylprednisolone (MP; n=7). Another group of animals (MP + GEN; n=7) concomitantly received methylprednisolone (30 mg/kg/sc) and genistein aglycone (5 mg/kg/ip) for 60 days. Control animals were administered daily with vehicle (VEH) or genistein (GEN; 5 mg/kg/ip) only. At the beginning and end of the treatment, animals were examined for bone mineral density (BMD) and bone mineral content (BMC). After sacrifice, serum was collected to determine bone-alkaline phosphatase (b-ALP), carboxy-terminal collagen crosslink (CTX) and osteoprotegerin (OPG) levels. Femurs were removed and tested for breaking strength and bone histology analyzed for structural quality of the femoral neck. Genistein aglycone prevented bone loss as measured by BMD and BMC. Moreover, genistein significantly increased the bone formation markers b-ALP and OPG, reduced the bone resorption marker CTX and statistically maintained comparable strength versus the VEH only group. Finally, histological scoring revealed a protective effect of genistein on bone structure statistically comparable to the VEH control animals. Results suggest that the genistein aglycone might be a preventive treatment for GIO and complications of osteonecrosis with long-term glucocorticoid treatment.