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This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/E385    most recent 00627.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Scholz-Ahrens, K. E. Articles by Glüer, C.-C. Search for Related Content PubMed PubMed Citation Articles by Scholz-Ahrens, K. E. Articles by Glüer, C.-C.

Glucocorticosteroid-induced osteoporosis in adult primiparous Göttingen miniature pigs: effects on bone mineral and mineral metabolism

¹Institute of Physiology and Biochemistry of Nutrition, Federal Research Centre for Nutrition and Food, Kiel; ²Department of Osteopathology, University Medical Center Hamburg-Eppendorf; ³Medical Physics Research Group, Department of Diagnostic Radiology and ⁴Department of Orthopaedics, University Hospital Schleswig-Holstein, Campus Kiel; and ⁵Department of Oral and Maxillofacial Surgery, Kiel University, Kiel, Germany

Submitted 20 November 2006 ; accepted in final form 24 April 2007

Information on the pathophysiology of glucocorticoid-induced osteoporosis (GIO) is limited, since its clinical picture often reflects a combined effect of glucocorticoids (GC) and the treated systemic disease (i.e., inflammation and immobility). In 50 healthy adult (30-mo-old) primiparous Göttingen minipigs, we studied the short-term (8 mo, n = 30) and long-term (15 mo, n = 10) effect of GC on bone and mineral metabolism longitudinally and cross-sectionally compared with a control group (n = 10). All animals on GC treatment received prednisolone orally at a dose of 1.0 mg·kg body wt^–1·day^–1 for 8 wk and thereafter at 0.5 mg/kg body wt^–1·day^–1. In the short term, GC reduced bone mineral density (BMD) at the lumbar spine by –47.5 ± 5.1 mg/cm³ from baseline (P < 0.001), which was greater (P < 0.05) than the loss [not significant (NS)] in the control group of –11.8 ± 12.6 mg/cm³. Calcium absorption decreased from baseline by –2,488 ± 688 mg/7 days (P < 0.001) compared with –1,380 ± 1,297 mg/7 days (NS) in the control group. Plasma bone alkaline phosphatase (BAP) decreased from baseline by –17.8 ± 2.2 U/l (P < 0.000), which was significantly different (P < 0.05) from the value of the control group of –1.43 ± 4.8 U/l. In the long term, the loss of BMD became more pronounced and bone mineral content (BMC), trabecular thickness, mechanical stability, calcium absorption, 25-hydroxyvitamin D₃, 1,25-dihydroxyvitamin D₃, and parathyroid hormone tended to be lower compared with the control group. There was a negative association between the cumulative dose of GC and BMD, which was associated with impaired osteoblastogenesis. In conclusion, the main outcomes after GC treatment are comparable to symptoms of GC-induced osteoporosis in human subjects. Thus the adult Göttingen miniature pig appears to be a valuable animal model for GC-induced osteoporosis.

bone mineral density; histomorphometry; bone mechanical property; calcium balance; bone marker