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This is a brief report summarizing topics in ASBMR 2018 held at Montreal, Canada in September 28th to October 1st, 2018. In this report, I would like to introduce several topics from clinical research concerning bone and mineral metabolism other than osteoporosis. One of the topics in this area is the progress of research and development of drugs for rare skeletal diseases, which have been considered to be difficult to treat. Especially, there were many abstracts concerning burosumab, which is a new therapeutic medicine for FGF23-related hypophosphatemic rickets/osteomalacia. In addition, I will focus on the papers concerning muscle, osteocalcin, vitamin D and microbiota.

Bone has several functions such as supporting our body, protecting internal organs and contributing to hematopoiesis. Recently, it has been revealed that bone also works as an endocrine tissue and systemically regulates functions of other organs. It has been reported that fibroblast growth factor 23(FGF23)regulates phosphate metabolism and osteocalcin affect glucose/energy metabolism. In addition, sclerostin, interleukin-11(IL-11)and lipocalin 2 have been also found to be bone-derived humoral factors. Further investigation concerning the network systems among multiple organs via bone-derived hormones may lead to the development of new drugs.

Vitamin D was considered to be one of nutrients which has an important role in the maintenance of calcium and phosphate metabolism. It was then revealed that 1,25-dihydroxyvitamin D metabolized from vitamin D works as a calciotropic hormone. Vitamin D metabolites were further shown to affect cell proliferation and differentiation. In immune system, vitamin D metabolites modulate both innate and adaptive immunity. Epidemiological studies indicated the associations between vitamin D deficiency and various diseases such as autoimmune diseases, allergy, infection and malignancy. In addition, vitamin D supplementation was shown to improve some these diseases.

Fibroblast growth factor 23 (FGF23) is an essential hormone for phosphate metabolism. It has been shown that intravenous administration of some iron formulations including saccharated ferric oxide induces hypophosphatemic osteomalacia with high FGF23 levels. On the other hand, iron deficiency promotes FGF23 and induces hypophosphatemia in patients with autosomal dominant hypophosphatemic rickets (ADHR). While iron and phosphate metabolism is connected, the detailed mechanism of this connection remains to be clarified.