Glucocorticoid (GC)-induced osteoporosis (GIO) occurs in patients undergoing therapeutic intervention for inflammatory disorders such as rheumatoid arthritis and lupus. The effect of long-term GC administration on bone turnover was investigated in two frequently used mouse strains; C57BL/6 and CD1 in order to assess the influence of genetic background.
GIO was induced in 12 weeks old female C57BL/6 and CD1 mice by s.c. insertion of long-term (60 days) release prednisolone or placebo pellets. Animal care and experimental procedures were approved and conducted in accordance with the Home Office Animals Act of 1986 (UK).
Biomechanical properties of the long bones as assessed by three point bent testing revealed that femoral elasticity and strength significantly decreased in CD1 mice receiving CG, whereas C57BL/6 mice showed no differences between placebo and prednisolone treatment.
Bone turnover was assessed by microcomputer tomography (micro-CT). Contrary to C57BL/6 mice, prednisolone treated CD1 mice developed osteoporosis and presented reduced trabecular bone volume and trabecular number. Serum carboxy-terminal telopeptide of type I collagen (CTX-I) measured by ELISA validated the effects of GC on 12 weeks old CD1 mice that had significant bone degradation, whereas bone turnover was not affected by long term GC administration in 12 weeks old C57BL/6 mice.
While administration of long term release prednisolone pellets provides a robust GIO animal model in 12 weeks old CD1 mouse strain, 12 weeks old C57BL/6 mice were not susceptible to GIO due to long term prednisolone administration. This study indicates that for the induction of experimental GIO, the mouse strain choice should be carefully evaluated.
17 May 2014 - 20 May 2014