Long bones from the senescence accelerated mouse SAMP6 have increased size but reduced whole-bone strength and resistance to fracture.
The senescence accelerated mouse strain P6 (SAMP6) has emerged as a useful model of senile osteoporosis because it has many features of the disease, including low trabecular bone formation and low areal bone density. We further characterized the SAMP6 model of senile osteoporosis by comparing morphological, mechanical, and densitometric properties of femurs and tibias from SAMP6 mice to those of the control strain (SAMR1) at 4 months and 12 months of age. SAMP6 long bones had increased periosteal width and endosteal area (p < 0.05), resulting in an average increase of 30% in moments of inertia (p < 0.05), but no difference in bone area (p > 0.05) compared with control. Despite their increased moments of inertia, long bones from SAMP6 mice were relatively weak and brittle. Ultimate bending moment was reduced by 25%, and both postyield displacement and energy-to-fracture were reduced by 60% compared with SAMR1 controls (p < 0.001). Average cortical ash fraction was increased slightly from 0.74 in SAMR1 to 0.76 in SAMP6 bones (p < 0.05), indicating that increased mineralization may have contributed to the brittleness of SAMP6 bones. The relative differences we observed--increased endosteal and periosteal dimensions, reduced bending strength, increased brittleness, and increased mineralization--are analogous to changes that occur in the aging human skeleton. Moreover, these features were consistently observed in young (4-month) and old (12-month) animals. These findings extend the previous descriptions of the SAMP6 mouse and identify key mechanical features that further validate its relevance as a unique and functionally relevant model of senile osteoporosis.
Silva
Matthew J
MJ
Department of Orthopaedic Surgery, Barnes-Jewish Hospital at Washington University, St. Louis, Missouri 63110, USA.
Brodt
Michael D
MD
Ettner
Sara L
SL
D019588:Aging, Premature / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*; D000818:Animals; D001696:Biomechanical Phenomena; D015519:Bone Density; D004195:Disease Models, Animal; D005260:Female; D050723:Fractures, Bone / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D010024:Osteoporosis / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*