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髋关节骨关节炎终末期患者股骨头下软骨下骨微损伤的积累。

Accumulation of microdamage in subchondral bone at the femoral head in patients with end-stage osteoarthritis of the hip.

机构信息

Department of Orthopaedic Surgery, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa, 761-0793, Japan.

Department of Anatomy and Neurobiology, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa, 761-0793, Japan.

出版信息

J Bone Miner Metab. 2019 Sep;37(5):880-885. doi: 10.1007/s00774-019-00988-z. Epub 2019 Jan 30.

Abstract

In end-stage osteoarthritis (OA) of the hip, the effect of bone metabolism with and without cartilage is unclear. In this study, we aimed to investigate histomorphology and microdamage in the subchondral bone of the femoral head in areas with and without articular cartilage in patients with end-stage OA. Nineteen femoral heads were evaluated in 10 women who underwent total hip arthroplasty for OA and in nine cadaveric controls (CNT). Chondral thickness and subchondral bone plate thickness (SBP.Th) were measured in 5-mm-wide areas where cartilage was lost (area A) or preserved (area B) in OA and in corresponding areas in the load-bearing portion of the femoral head in the CNT. Histomorphometry and microdamage in 5 × 5-mm areas of cancellous bone were assessed. SBP.Th and bone volume were significantly greater in area A than in area B or in the CNT. Osteoid volume was significantly greater in area A than in area B or in the CNT. There was no significant difference in eroded surface between area A and CNT. Microcrack density was significantly greater in area A than in area B or in the CNT. Although accumulation of microdamage was caused by concentration of stress on the subchondral bone in the cartilage loss area in end-stage OA, remodeling for microdamage repairing mechanism was not enhanced. It was considered that the subchondral cancellous bone volume was increased because of modeling, not remodeling, by stress concentration due to articular cartilage loss.

摘要

在髋关节终末期骨关节炎(OA)中,伴有或不伴有软骨的骨代谢的影响尚不清楚。在这项研究中,我们旨在研究终末期 OA 患者股骨头软骨下骨的骨形态发生和微损伤。在接受全髋关节置换术治疗 OA 的 10 名女性和 9 名尸体对照(CNT)中,评估了 19 个股骨头。在 OA 中,在软骨缺失(区域 A)或保留(区域 B)的 5-mm 宽区域测量软骨厚度和软骨下骨板厚度(SBP.Th),并在 CNT 的股骨头负重部分的相应区域测量。评估松质骨 5×5-mm 区域的组织形态计量学和微损伤。与区域 B 或 CNT 相比,区域 A 的 SBP.Th 和骨体积明显更大。与区域 B 或 CNT 相比,区域 A 的类骨质体积明显更大。区域 A 和 CNT 之间的侵蚀表面没有显著差异。与区域 B 或 CNT 相比,区域 A 的微裂纹密度明显更大。尽管在终末期 OA 中,软骨缺失区域的骨下骨集中应力导致微损伤的积累,但微损伤修复机制的重塑并未增强。由于关节软骨丧失导致的应力集中,被认为是模型而不是重塑导致了骨下松质骨体积的增加。

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