Analysis of molecular mechanism of systemic bone metabolism abnormality in systemic autoimmune diseases

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K21329
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Metabolomics; Orthopaedic surgery
• Research Institution: Saitama Medical University
• Principal Investigator: Yokota Kazuhiro 埼玉医科大学, 医学部, 講師 (20406440)
• Research Collaborator: MIMUA Toshihide 埼玉医科大学, 医学部, 教授 ; AIZAKI Yoshimi 埼玉医科大学, 医学部, 助手
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 自己免疫性疾患 / 関節リウマチ / 全身性骨代謝異常 / 骨粗鬆症 / 破骨細胞 / 破骨細胞様細胞 / 炎症性サイトカイン / 抗環状シトルリン化ペプチド抗体

Outline of Final Research Achievements

It is well known that systemic autoimmune disease potentiates osteoporosis but the underlying mechanism is not known. In the current study, we revealed that differentiation potential of bone-resorbing cells, i.e., osteoclasts and osteoclast-like cells derived from the peripheral blood of patients with rheumatoid arthritis (RA), was significantly higher than that of healthy volunteers (both, n=6). In addition, we confirmed that the differentiation potential of bone-resorbing cells was most closely associated with the titer of the anti-cyclic citrullinated peptide antibody (ACPA). Furthermore, in RA patients with high ACPA titer (n=4, more than 40 U/mL), systemic bone mineral density was significantly lower than in RA patients with low ACPA titer (n=4, less than 40 U/mL）. From the above, ACPA titer might be a new predictive factor of osteoporosis in patients with systemic autoimmune disease, such as RA.

Free Research Field

骨免疫学