抄録
Recent investigations on osteoporosis have led to a better understanding of the pathology and treatment of the disease. However, the decline in sex hormones that typically accompanies aging makes it difficult to separately investigate the complex factors that cause the disease in humans. Various animal-based studies have demonstrated the pathology of senile osteoporosis (SO) and postmenopausal osteoporosis (PO), but a number of uncertainties remain as to the pathology behind the occurrence of both conditions. In the present study, we prepared ovariectomized senescence-accelerated mouse-prone 6 (SAMP6) mice and investigated the site specificity of trabecular structural properties in alveolar and tibial bone. The experimental animals were the SAMP6 mice (n = 10), while SAM-resistant/1 (SAMR1) mice (n = 10) served as controls. All mice were ovariectomized at 16 weeks of age and sacrificed at Week 17 and 20. The tibia and mandible bone samples were extracted and scanned using micro-computed tomography and subjected to bone morphometry. The results showed that trabecular bone was significantly thinner in the ovariectomized SAMP6 mice than in the ovariectomized SAMR1 mice at 17 weeks, but at 20 weeks, there were no significant differences in the tibial bone. In terms of alveolar bone, there were no significant differences in bone morphometry findings at week 17 but bone volume fraction and trabecular bone pattern factor values were significantly lower in the ovariectomized SAMP6 mice than in the ovariectomized SAMR1 mice at 20 weeks. The results therefore suggest that single onset of either PO or SO has little impact on alveolar bone but complex SO/PO onset causes severe alveolar bone resorption.
