Effects of mild hyperbaric oxygen on osteoporosis induced by hindlimb unloading in rats
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ORIGINAL ARTICLE
Effects of mild hyperbaric oxygen on osteoporosis induced by hindlimb unloading in rats Ai Takemura1,5 · Paola Divieti Pajevic2 · Tatsuro Egawa3 · Rika Teshigawara4 · Tatsuya Hayashi3 · Akihiko Ishihara1 Received: 20 August 2019 / Accepted: 20 March 2020 © The Japanese Society Bone and Mineral Research and Springer Japan KK, part of Springer Nature 2020
Abstract Introduction Disuse-induced bone loss is caused by a suppression of osteoblastic bone formation and an increase in osteoclastic bone resorption. There are few data available for the effects of environmental conditions, i.e., atmospheric pressure and/or oxygen concentration, on osteoporosis. This study examined the effects of mild hyperbaric oxygen at 1317 hPa with 40% oxygen on unloading-induced osteoporosis. Materials and methods Eighteen 8-week old male Wistar rats were randomly divided into three groups: the control for 21 days without unloading and mild hyperbaric oxygen (NOR, n = 6), the unloading for 21 days and recovery for 10 days without mild hyperbaric oxygen (HU + NOR, n = 6), and the unloading for 21 days and recovery for 10 days with mild hyperbaric oxygen (HU + MHO, n = 6). Results The cortical thickness and trabecular bone surface area were decreased in the HU + NOR group compared to the NOR group. There were no differences between the NOR and HU + MHO groups. Osteoclast surface area and Sclerostin (Sost) mRNA expression levels were decreased in the HU + MHO group compared to the HU + NOR group. These results suggested that the loss of the cortical and trabecular bone is inhibited by mild hyperbaric oxygen, because of an inhibition of osteoclasts and enhancement of bone formation with decreased Sost expression. Conclusions We conclude that exposure to mild hyperbaric oxygen partially protects from the osteoporosis induced by hindlimb unloading. Keywords Hindlimb unloading · Osteoporosis · Mild hyperbaric oxygen · Oxidative metabolism · Bone loss
Introduction
* Ai Takemura takemura.ai.46c@kyoto‑u.jp 1
Laboratory of Cell Biology and Life Science, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto 606‑8501, Japan
2
Department of Translational Dental Medicine, Boston University Goldman School of Dental Medicine, Boston, MA 02118, USA
3
Laboratory of Sports and Exercise Medicine, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto 606‑8501, Japan
4
Laboratory of Developmental Epigenome, Graduate School of Medicine, Kyoto University, Kyoto 606‑8507, Japan
5
Present Address: Department of Sports Research, Japan Institute of Sport Sciences, Tokyo 115‑0056, Japan
Osteoporosis is a disease characterized by loss of bone mass that leads to fragility fractures risk [1, 2], and is caused by a combination of multiple factors, including genetic factors, hormonal status, physical activity, and/or life style [3, 4]. Bone size and shape adapt to environmental stimuli, such as mechanical loading, unloading, and prolonged bed rest [5–9]. Osteocytes are bone cells th
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