Morphological and mechanical properties of caudal vertebrae in the SAMP6 mouse model of senile osteoporosis.
The senescence-accelerated mouse, strain P6 (SAMP6), is a model of senile osteoporosis with relatively low bone mineral density (BMD), low rates of bone formation and reduced long-bone bending strength. Seeking to extend previous descriptions of the SAMP6 skeletal phenotype, we assessed the morphological and mechanical properties of vertebrae from SAM mice at 4 and 12 months of age. We hypothesized that, relative to SAMR1 controls, vertebrae from SAMP6 mice have: (1) less trabecular bone, (2) increased endosteal and periosteal bone size and (3) decreased whole-bone strength. Caudal vertebrae from adult female mice (SAMR1 and SAMP6; 4 and 12 months; n = 10-11 per group) were evaluated by micro-computed tomography and mechanical compression testing. SAMP6 vertebrae had 33% less trabecular bone volume in cephalad and caudal end regions than SAMR1 (P < 0.001) due to significant reductions in both trabecular number (P = 0.002) and thickness (P < 0.001). In contrast to previous findings in SAMP6 long bones, SAMP6 vertebrae showed no evidence of increased overall bone dimensions compared to SAMR1, and in fact had smaller total bone area (TA) and endosteal area (EA) at 12 months of age. Whereas SAMR1 vertebrae showed signs of age-related expansion from 4 to 12 months, SAMP6 vertebral dimensions did not change with age. Mechanical properties of SAMP6 vertebrae were not significantly different than SAMR1 vertebrae (stiffness, yield force, ultimate force, displacement at ultimate force, energy to ultimate force; P > 0.05), another finding in contrast to previous results in SAMP6 long bones. In summary, reduced vertebral trabecular bone volume is another feature of the SAMP6 mice with relevance to senile osteoporosis. However, age-related bone expansion and reduced whole-bone strength were not evident in SAMP6 vertebrae, indicating that while the SAMP6 mouse has many features relevant to senile osteoporosis in humans, not all features are observed or detectable at all skeletal sites.
Silva
Matthew J
MJ
Orthopaedic Research Laboratories, Department of Orthopaedic Surgery, Barnes-Jewish Hospital at Washington University, St. Louis, MO 63110, USA. silvam@wustl.edu
Brodt
Michael D
MD
Uthgenannt
Brian A
BA
D000818:Animals; D015519:Bone Density; D004195:Disease Models, Animal; D005260:Female; D051379:Mice; D010024:Osteoporosis / Q000503:physiopathology*; D013131:Spine / Q000033:anatomy & histology* / Q000502:physiology*