Effect of intermittent treatment with human parathyroid hormone 1–34 in SAMP6 senescence-accelerated mice

Abstract

We examined trabecular and cortical bone in the senescence-accelerated mouse prone 6 (SAMP6) murine model of senile osteoporosis after treatment with human PTH 1-34. Sixteen-week-old female SAMP6 mice were assigned to control and PTH groups. PTH (20 microg/kg) was administered sc 3 times a week for 12 weeks. The control mouse strain, senescence-accelerated mouse resistant 1 (SAMR1), was used for comparison. The femoral metaphysis and diaphysis were used to measure bone mineral density (BMD), analyze the trabecular and the cortical structure by micro-computed tomography, and for conducting the bone strength test. PTH significantly attenuated the loss of BMD, improved the trabecular bone microstructure, and increased the bone strength in the femoral metaphysis. We did not find any differences in the bone strength of the femoral diaphysis after PTH treatment, although the cortical bone volume and cortical thickness were improved. Although the cortical thickness increased, the cortical bone density decreased, likely because of the increase of cortical porosity in the distal metaphysis after administration of PTH.

Black bear parathyroid hormone has greater anabolic effects on trabecular bone in dystrophin-deficient mice than in wild type mice

“…This is similar to studies with PTH in other mouse models, which show approximately a 10% increase in cortical bone ultimate force with PTH [50, 51]. Our study showed a comparable increase in femoral ultimate force of approximately 8%, though the difference was not significant.…”

Treatment of osteoporosis in a mouse model of Duchenne muscular dystrophy using black bear parathyroid hormone

“…Cortical bone did not display the marked changes with bbPTH treatment that were observed in trabecular bone. This is similar to studies with PTH in other mouse models, which show approximately a 10% increase in cortical bone ultimate force with PTH (Washimi, et al, 2010, Zhou, et al, 2003. Our study showed a comparable increase in femoral ultimate force of approximately 8%, though the difference was not significant, and no change was detected in stress or modulus of toughness.…”

“…As expected, bbPTH improved many skeletal outcomes in wild type mice as compared to vehicle-treated wild type mice, consistent with literature administering PTH analogs to healthy mice (Washimi, et al, 2010, Lippuner, et al, 2004, Frost, 1999, Kanis, et al, 1994, Lane and Yao, 2010. bbPTH treated mice showed improvements in force to failure, and moments of inertia, indicating an improved cortical structure consistent with increased strength.…”

Effect of vitamin K2 on the development of stress-induced osteopenia in a growing senescence-accelerated mouse prone 6 strain

“…SAMP strains are categorized into 11 groups according to the senile diseases that they develop naturally, such as senile amyloidosis (SAMP1, 2, 7 and 11), temporomandibular disorders (SAMP3), senile osteoporosis (SAMP6), learning and memory impairments (SAMP8 and 10) and cataract (SAMP9) (15)(16)(17). The SAMP6 strain presents decreasing BMD from the age of 16 weeks, and has a lifespan of ~32 weeks (18). In order to assess the effects of various drugs affecting BMD, additional approaches to reduce BMD must be taken in the SAMP6 strain.…”