Interestingly, the bone volume was increased in the TGF-ß2 treated animals [ 30].
Consistent with this data, Bikle et al. have demonstrated that trabecular bone volume was increased by 23% and 88%, respectively, in male and female IGF-I KO mice compared to wild-type mice.
It is of interest that the studies by Day and colleagues also indicate that, although the bone volume is increased in specimens of subchondral bone from human subjects with early OA, there is a decrease in the elastic tissue modulus [ 8], similar to the effects of osteoporosis on bone mechanical properties.
Trabecular and cortical bone volumes were increased by ZA, with no change in the cortical/trabecular volume ratio.
Other studies demonstrated larger callus formation after nerve resection [ 7, 66] and corroborate the observation that bone union is faster and fracture callus volume is increased in patients with head injuries involving coma without clarifying whether this is neuronal, mediated as a direct consequence of the head injury or metabolical, or biochemical as an indirect consequence [ 1].
Our sales volume was increasing steadily.
Whole body BMD, BMC, and trabecular bone volume were lower, while medullary area was increased in PIO rats compared to controls.
Bone volume was significanty increased due to the presence of human full-length adiponectin.
Thus, Thra1 PV /+ mice have an increase in bone mineral content despite the reduction in tissue mineralization density because their trabecular and cortical bone volume is substantially increased.
The trabecular bone volume was significantly increased by alendronate administration in both wild-type and MLII mice, and microcompression studies showed that the reduced biomechanical stability of ML II vertebral bodies was normalized by alendronate treatment (Fig 10B).
