3 and 1.0 g) [40], while 8 week-old growing mice exhibited a positive response in trabecular and cortical bone [38] and [39]. Investigations of WBV as a treatment for osteoporosis have shown

a positive impact on ovariectomized rats with greatest increase in bone mass at high frequencies [34], [41] and [43] while other investigation reported only an impact on cortical bone AZD8055 cell line [42] or no substantial impact [45]. These variable results suggest a more complex involvement of the hormonal system in the mechano-sensitivity of bone to WBV. Interestingly, a positive osteogenic response to “limb vibration” in the absence of weight-bearing has been observed, suggesting an additional mechano-transduction pathway than pure selleck chemicals bone strain [9] and [46]. Previous WBV studies on both patients and

animals indicate that vibration is most effective in young growing bone and low density bone. Therefore WBV treatment may offer a promising route to non-invasively stimulate bone formation in OI children. The objectives of the present study were to investigate the effects of WBV on the cortical and trabecular bone formation in growing mice suffering a severe form of osteogenesis imperfecta (oim mice). All animal experiments followed the British Home office and institutional guidance (project license 70/6852). 24 Homozygous wild type (B6C3Fe-a/a-+/+) and 24 homozygous oim (B6C3Fe-a/a-oim/oim) female mice were bred. Due to a procollagen α2 gene AMP deaminase recessive mutation, homozygous oim mice produce abnormal homotrimeric collagen type I (Col1-(α1)3) which results in a phenotype mimicking the human type III osteogenesis imperfecta (small body weight, skeletal deformities and brittle bones) [47].

Starting at 3 weeks of age (just after weaning), 12 mice from each genotype group (vibrated groups: Wild vib and oim vib) were placed into a custom built WBV transparent plastic cage for 15 min per day, 5 days in a week during 5 weeks. The cage was vibrated vertically at a frequency of 45 Hz and a peak acceleration of ± 0.3 g. This vibration regimen was demonstrated to be osteogenic on young growing mice [38] and [39]. The vibration cage had 8 slots (10 ∗ 10 cm each so that 8 mice could vibrate simultaneously) and was mounted on a linear electromagnetic actuator (LAL95-015-70F linear actuator and LAC-1 controller, SMAC Europe Ltd., UK). The linear actuator provided a sinusoidal vertical movement and was force-controlled by a custom made LabVIEW program (NI Corporation Ltd., USA) via a laptop computer and a digital acquisition card (NI USB-6211 multifunction DAQ, NI Corporation Ltd., USA). The actuator was powered by a generator (HY3005D-2, Rapid Electronics Ltd., UK). The acceleration was monitored via an accelerometer (DE-ACCM3D, Dimension Engineering LTD, USA) fixed in the middle of the vibrating cage and the force of the actuator was operator-tuned to obtain a maximum peak acceleration of ± 0.3 g.