骨粗しょう症の分子機構

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  • Molecular Mechanism Underlying Osteoporosis
  • セイカツ シュウカンビョウ シリーズ コツソショウショウ ノ ブンシ キコウ

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Recently, great advances have been made in both the basic pathophysiology and clinical management of osteoporosis. Osteoporosis is caused by an imbalance between osteoclastic bone resorption and osteoblastic bone formation. Osteoblasts, arising from mesenchymal stem cell, form bones and regulate osteoclast formation. Osteoclasts are derived from hematopoietic stem cells. Bone-resorbing molecules act on osteoblasts to induce RANKL (receptor activator of NF-κB ligand) on the osteoblast surface. RANKL, in turn, binds to its receptor RANK on an osteoclast precursor to enhance osteoclast differentiation. Osteoporosis most often affects postmenopausal women. Estrogen deficiency induces enhanced bone resorption, which is mainly due to the action of bone-resorbing cytokines, such as IL-1, IL-6 and TNF-α. Nutritional factors also contribute to the development of osteoporosis. The deficiency in calcium and vitamin D leads to secondary hyperparathyroidism and enhanced bone resorption. Recently, vitamin K deficiency and vitamin A excess are known to be the risk factors for osteoporotic fracture. For the past several years, many large-scale clinical trials have revealed that potent antiresorptive drugs such as bisphosphonates significantly increase bone mineral density and markedly decrease the incidence of fragility fracture. Based on these advances, the osteoporosis from the viewpont of nutrition should be explored in more detail.

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