2022 Fiscal Year Final Research Report
Analysis of mechanism for regional osteoporotic changes induced by pathophysiological change of affected tissues associated with refractory pain syndrome
Project/Area Number |
20K09463
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 56020:Orthopedics-related
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Research Institution | Sapporo Medical University |
Principal Investigator |
Iba Kousuke 札幌医科大学, 医学部, 特任教授 (60363686)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 運動器疼痛 / 骨粗鬆症 / 組織損傷 |
Outline of Final Research Achievements |
Consistent with the wound healing process for 14 days, the pain-like behaviors and the expression of bone metabolic markers in the femur of the incised limb of model mice were significantly increased up to 7 days, and then decreased to the same level as those in the control limbs by 14 days after the incisions. Anti-resorptive agents significantly improved the pain-like behaviors in the injured limb associated with the inhibition of bone metabolic markers. A Cox2 inhibitor also significantly improved the pain-like behaviors of the mice, however, had no significant effect on the expression levels of bone metabolic markers. We, therefore, believe that the pathophysiological changes in soft tissue resulting from cutaneous incisions could be related to the induction of bone metabolism.
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Free Research Field |
整形外科、骨粗鬆症、骨代謝疾患、運動器疼痛
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Academic Significance and Societal Importance of the Research Achievements |
ズデック骨委縮や複合性局所疼痛症候群に代表される運動器の難治性疼痛疾患の多くは罹患部位の骨粗鬆化を合併する。また、外傷後や手術後に発生する患肢の骨粗鬆症化は疼痛の誘発や患者の日常生活動作を障害するのみでなく、高齢者においては骨折の危険性を増大させる。これまでは外傷や疾患に伴う非荷重や不動化が骨粗鬆症化の原因と考えられてきた。しかし、今回の研究成果より、運動器の疼痛を引き起こす病的な組織変化自体が骨粗鬆症発生の直接原因の1つとなることを示すことができた。このことは、外傷や疾患に伴う疼痛症状を改善することが、その後に発生する可能性のある骨粗鬆症変化を予防する可能性があることを示唆していると考える。
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