Abstract
Alendronate (Aln) has been the first-line drug for osteogenesis imperfecta (OI), while the comparable efficacy of Aln and strontium ranelate (SrR) remains unclear. This study is aimed at comparing the effects of SrR and Aln treatment in a mouse model of OI. Three-week-old oim/oim and wt/wt female mice were treated with SrR (1800 mg/kg/day), Aln (0.21 mg/kg/week), or vehicle (Veh) for 11 weeks. After the treatment, the average number of fractures sustained per mouse was significantly reduced in both SrR- and Aln-treated oim/oim mice. The effect was comparable between these two agents. Both SrR and Aln significantly increased trabecular bone mineral density, bone histomorphometric parameters (bone volume, trabecular number, and cortical thickness and area), and biomechanical parameters (maximum load and stiffness) as compared with the Veh group. Both treatments reduced bone resorption parameters, with Aln demonstrating a stronger inhibitory effect than SrR. In contrast to its inhibitory effect on bone resorption, SrR maintained bone formation. Aln, however, also suppressed bone formation coupled with an inhibitory effect on bone resorption. The results of this study indicate that SrR has comparable effects with Aln on reducing fractures and improving bone mass and strength. In clinical practice, SrR may be considered an option for patients with OI when other medications are not suitable or have evident contraindications.
Highlights
Osteogenesis imperfecta (OI) is a genetic disorder in connective tissues characterized by increased bone fragility
Analysis of mouse body weight revealed that the Veh-treated oim/oim mice were significantly smaller than the Veh-treated wt/wt mice at both 3 and 14 weeks (Figure 1(a))
There were no significant differences in weight gain among the Veh, strontium ranelate (SrR), or Aln groups for either wt/wt or oim/oim genotype for the duration of the study (Figure 1(a))
Summary
Osteogenesis imperfecta (OI) is a genetic disorder in connective tissues characterized by increased bone fragility. There has been no curative treatment for OI. Bisphosphonate (BP), which inhibits osteoclastmediated bone resorption by inhibiting farnesyl diphosphate synthetase, has been the standard treatment for OI and demonstrated effectiveness in increasing bone mineral density (BMD), reducing pain, and decreasing fracture [3,4,5]. This type of medication may result in undesirable outcomes, such as impairment in bone healing and modeling, damage to bone cells, and accumulation of microdamage in the bone [6, 7]. An increasing number of studies have searched for other promising agents such as strontium ranelate (SrR) [10]
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