Abstract
Parathyroid hormone (PTH) analogs have a powerful anabolic effect on bone and are used in the treatment of patients with severe osteoporosis. However, there are limitations to how long they can be safely administered. Withdrawal of PTH results in the cancelation of its effects, necessitating subsequent treatment to maintain the bone quantity and quality. This study assessed the effects of Eldecalcitol (ELD), an active vitamin D3 derivative, after PTH in estrogen-deficient osteoporotic rats. Six-month-old female rats were ovariectomized, and PTH administration was started 7 weeks later. After 4 weeks of PTH treatment, the animals were divided into three groups and either continued to receive PTH (PTH–PTH), or were switched to ELD (PTH–ELD) or vehicle (PTH–Veh) for an additional 4 weeks. In the femur, increased BMD by 4 weeks treatment of PTH was significantly reduced in PTH–Veh but not in PTH–PTH and PTH–ELD. The same tendency was observed in the lumbar vertebrae. MicroCT imaging and histomorphometry analysis revealed that the favorable bone structure changes by PTH administration were also maintained in the femurs and tibias of the PTH–PTH and PTH–ELD groups. Increased bone strength by 4-week treatment of PTH in lumber also maintained in PTH–ELD. Furthermore, minimodeling was observed in the PTH–ELD group. These results demonstrate that treatment with ELD sequentially following PTH prevented the bone quantity and strength reduction that accompanies PTH withdrawal in estrogen-deficient rats.
Highlights
Osteoporosis is a skeletal disorder characterized by a reduction in bone strength and an increase in bone fracture risk
The parathyroid hormone (PTH) analogs PTH1-34 and PTH1-84 are currently the only approved agents categorized as anabolic agents [1]
bone mineral density (BMD) of the lumbar spine (L2–L4) and femur at time point ‘Pre’ (7 weeks after ovariectomy or sham operation), at Wk 4, and at Wk 8 were measured using dual-energy X-ray absorptiometry (Fig. 1)
Summary
Osteoporosis is a skeletal disorder characterized by a reduction in bone strength and an increase in bone fracture risk. The goal of osteoporosis treatment is to reduce bone fracture risk by preventing loss of bone quantity or quality. Drugs for the treatment of osteoporosis fall into two major classes, anti-bone-resorptive agents and anabolic agents. There are several types of anti-resorptive treatments such as selective estrogen receptor modulators (SERMs), bisphosphonates, and active vitamin D analogs. The parathyroid hormone (PTH) analogs PTH1-34 and PTH1-84 are currently the only approved agents categorized as anabolic agents [1]. PTH stimulates bone formation by increasing osteoblast numbers via osteoblastogenesis [2], thereby increasing the bone mineral density (BMD) of the spine and reducing the risk of vertebral fractures in postmenopausal women with prevalent vertebral fractures [3].
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