The effects of low bone mineral density associated with abnormal bone metabolism on the progression of scoliosis

2021 Fiscal Year Final Research Report

• Project/Area Number: 20K22734
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0802:Biomedical structure and function and related fields
• Research Institution: Kanazawa University
• Principal Investigator: Yokogawa Noriaki 金沢大学, 医薬保健学総合研究科, 特任助教 (90623645)
• Project Period (FY): 2020-09-11 – 2022-03-31
• Keywords: 側弯症 / マウス / LAT1 / アミノ酸トランスポーター / 骨密度 / 軟骨 / 成長板

Outline of Final Research Achievements

Through the longitudinal observation of scoliosis mice with chondrocyte-specific inactivation of Slc7a5, the gene encoding the essential amino acid transporter L-type amino acid transporter 1 (LAT1), we examined whether the development and progression of scoliosis is similar to that of idiopathic scoliosis, and whether reduced mineral bone density is a cause of scoliosis progression. LAT1-inactivated mice were characterized as having features similar to early-onset idiopathic scoliosis, and bone mineral density loss was observed to occur secondary to the onset and progression of scoliosis, suggesting that bone mineral density loss in idiopathic scoliosis is a consequence of scoliosis progression.

Free Research Field

整形外科

Academic Significance and Societal Importance of the Research Achievements

特発性側弯症において骨密度低下と側弯進行は密接に関連していると考えられてきたが、臨床的な研究には限界があり、骨密度低下が側弯進行の原因かあるいは結果かはこれまで不明のままであった。L-type amino acid transporter 1を軟骨細胞特異的に不活化することによって得られた、特発性側弯症と類似した特徴をもつマウスの経時的な観察においては、側弯症の進行がほぼ終了した後に骨密度の低下が起こっており、骨密度の低下は側弯進行の「原因」ではなく「結果」であることが示唆された。