Abstract
The effects of postmenopausal osteoporosis for bone defect healing processes have already been reported, but not for senile osteoporosis caused by low-turnover metabolism. Low-Intensity-Pulsed Ultrasound (LIPUS) is known to promote bone defect healing in high-turnover osteoporosis an animal model. The aim of this study was to investigate the effect of LIPUS on the bone-healing process in a low-turnover osteoporosis model using the Senescence-Accelerated Mouse Prone 6 (SAMP6) strain of mice. Twenty-week-old SAMP6 and Senescence-Accelerated Mouse Resistant (SAMR1) mice were used as senile osteoporosis and normal aging models, respectively. Bone defects (diameter, 0.9 mm) were created in the both SAMP6 and SAMR1 femurs. At 7days after surgery, the LIPUS irradiation groups of SAMR1 (R1LG) and SAMP6 (P6LG) were exposed to LIPUS (1.0 MHz, 320 mW, 15 min/day) for 6 days. The non-irradiation groups of SAMR1 (R1CG) and SAMP6 (P6CG) were used as controls. All groups were sacrificed at 14 days after creation of bone defects. Radiological analysis, histological evaluation and immunohistochemical staining for osteocalcin (OC) were performed. From the radiological evaluation, the new bone of defected area in SAMR1 group showed cortical bone-like structure, but that in the SAMP6 group showed trabecular bone-like structures. The increase in bone area in P6LG was greater than that in P6CG according to chronological change analysis using X-ray micro-CT (p < 0.01). Histological analysis revealed outward new bone formation originating in the periosteum in P6LG. Positive reaction for OC was localized on the surface of new bone in P6CG, whereas that in P6LG was observed over the whole region of new bone, from the outer to the bone marrow side. These results showed that LIPUS accelerates healing on low-turnover osteoporosis by promoting bone formation from periosteum and supplementing reduced bone formation from bone marrow.
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