2021 Fiscal Year Final Research Report
Relationship between thinning of articular cartilage due to endochondral ossification and osteoarthritis
| Project/Area Number |
19K18465
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56020:Orthopedics-related
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| Research Institution | Tottori University |
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Principal Investigator |
NAGIRA Keita 鳥取大学, 医学部附属病院, 助教 (00759516)
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | 変形性関節症 / 内軟骨性骨化（軟骨内骨化） / 軟骨下骨板 / 血管新生 / 軟骨下骨 / 非脱灰標本 |
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| Outline of Final Research Achievements |
The subchondral bone plate (Subcho.BP) in non-decalcified specimens was divided into two layers of osteocyte and non-osteocyte region. We evaluated detailed mechanism of changing osteochondral unit in focusing Subcho.BP divided into two layer in two rat models of osteoarthritis (OA).
In the age-related OA model, the thickening of Subcho.BP thickness was earlier than cartilage surface damage. Subchondral bone OA scores also increased earlier than cartilage OA scores. Strong correlation with the thickness of non-osteocyte layer and radiological sclerosis. On the other hand, in the surgical OA model, cartilage surface damage and increased apoptosis of chondrocytes preceded and followed by thickening of the Subcho.BP. These changes were accompanied by increasing angiogenesis in Subch.BP, which was suppressed by endochondral ossification inhibitors. Thus, the endochondral ossification of articular cartilage may continue to progress, suggesting an association with osteosclerosis in OA.
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| Free Research Field |
整形外科
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| Academic Significance and Societal Importance of the Research Achievements |
病態未解明な変形性関節症（OA）の関節軟骨変性・菲薄化機序において、元来、関節軟骨は関節内部からの血液の供給がないため、軟骨内骨化シグナルが生じても骨化することなく軟骨の変性・破壊だけで終わってしまうと考えられていた。
しかし、本研究では軟骨下骨からの血管進入（新生）により、関節軟骨においても軟骨内骨化が進行し、OAの骨硬化は関節軟骨の軟骨内骨化によって生じている可能性が示唆された。以上より、軟骨内骨化の抑制がOAに対する新たな治療標的となりOAの進行を予防する新規治療の開発が期待でき、本研究の学術的・社会的意義は大きい。
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