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Isolation of Mesenchymal Stem Cells from Human Alveolar Periosteum and Effects of Vitamin D on Osteogenic Activity of Periosteum-derived Cells
Published on: May 4, 2018
[Updates on rickets and osteomalacia: vitamin D deficiency : its pathophysiology and treatment]
1Third Department of Medicine, Teikyo University Chiba Medical Center, Japan.
Abstract:
Vitamin D deficiency is a common cause of rickets/osteomalacia. Milder decrease in vitamin D store, vitamin D insufficiency, does not lead to clinical rickets/osoteomalacia but could result in mineralization defect and an increased fracture risk. Vitamin D store is easily assessed by serum 25 (OH) D concentration : less than 20 ng/mL is generally considered vitamin D deficiency whereas between 20 and 30 ng/mL vitamin D insufficiency. In the management of bone and mineral disorders including rickets/osteomalacia, it is a common practice in many countries to measure serum 25 (OH) D, and if deficiency/insufficiency is present, which would be corrected by native vitamin D. However, in Japan, serum 25 (OH) D is not routinely measured because it is not covered by national health insurance policy, thus vitamin D deficiency/insufficiency is often overlooked and even misdiagnosed. There has been no native vitamin D that can be prescribed in Japan, thus patients with vitamin D deficiency/insufficiency have been prescribed active instead of native vitamin D. These circumstances must be changed to increase the awareness of vitamin D deficiency/insufficiency.
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