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缺血性坏死后生长中的股骨头的压痕特性。

Indentation properties of growing femoral head following ischemic necrosis.

作者信息

Pringle Douglas, Koob Thomas J, Kim Harry K W

机构信息

The Center for Research in Skeletal Development and Pediatric Orthopaedics, Shriners Hospitals for Children, 12502 North Pine Drive, Tampa, FL 33612, USA.

出版信息

J Orthop Res. 2004 Jan;22(1):122-30. doi: 10.1016/S0736-0266(03)00135-9.

Abstract

Little is known about the mechanical properties of the growing femoral head as it develops deformity following ischemic injury. The purpose of this study was to determine the indentation stiffness of growing femoral head following ischemic injury and to correlate the changes in stiffness with radiographic and histopathologic changes in the femoral head as it develops deformity. Following the induction of ischemia in 24 piglets, indentation testing of whole femoral heads was performed at 2, 4, and 8 weeks, as well as on femoral heads from eight sham operated animals. At 2 weeks, a 52% reduction of indentation stiffness was observed in the infarcted femoral heads compared to the control heads (p=0.004). The bony epiphyses in infarcted femoral heads were smaller due to growth arrest but they were not deformed. Histologically, no evidence of repair was seen. At 4 and 8 weeks, the indentation stiffness in the infarcted femoral heads was reduced by 75% (p<0.000001) and 72% (p=0.001) respectively compared to the control heads. Variable degree of femoral head deformity and repair was observed at 4 weeks. Severe deformity with extensive revascularization and repair were observed at 8 weeks. Although epiphyseal cartilage was thickened on the infarcted femoral heads only a weak correlation was found between the increase in the cartilage thickness and the decrease in the indentation stiffness (R(2)=0.55). These results indicate that the indentation properties of growing femoral head were significantly affected by ischemic injury, prior to the presence of repair process and deformity. A further decrease in the indentation stiffness was concomitant with repair of the infarcted head. These findings suggest that a reduction in the mechanical properties of the infarcted femoral head include both a cartilage and a bony component, which cannot be differentiated at this point. The study validates early institution of treatments that are aimed at limiting the mechanical loading of the affected hip. The study also suggests that in order to minimize the mechanical compromise of the infarcted femoral head, early institution of treatments aimed at stimulating new bone formation and retarding osteoclastic bone resorption may be beneficial.

摘要

关于生长中的股骨头在缺血性损伤后发生畸形时的力学性能,人们了解甚少。本研究的目的是确定缺血性损伤后生长中的股骨头的压痕硬度,并将硬度变化与股骨头在发生畸形时的影像学和组织病理学变化相关联。在24只仔猪中诱导缺血后,在2周、4周和8周对整个股骨头进行压痕测试,并对8只假手术动物的股骨头进行测试。在2周时,与对照股骨头相比,梗死股骨头的压痕硬度降低了52%(p = 0.004)。梗死股骨头的骨骺因生长停滞而较小,但未变形。组织学上,未见修复迹象。在4周和8周时,与对照股骨头相比,梗死股骨头的压痕硬度分别降低了75%(p < 0.000001)和72%(p = 0.001)。在4周时观察到不同程度的股骨头畸形和修复。在8周时观察到严重畸形并伴有广泛的血管再生和修复。虽然梗死股骨头的骨骺软骨增厚,但软骨厚度增加与压痕硬度降低之间仅发现弱相关性(R(2)=0.55)。这些结果表明,在修复过程和畸形出现之前,缺血性损伤显著影响了生长中股骨头的压痕特性。梗死股骨头压痕硬度的进一步降低与梗死头部的修复同时发生。这些发现表明,梗死股骨头力学性能的降低包括软骨和骨成分,目前无法区分。该研究证实了早期采用旨在限制患髋机械负荷的治疗方法的合理性。该研究还表明,为了使梗死股骨头的力学损伤最小化,早期采用旨在刺激新骨形成和抑制破骨细胞骨吸收的治疗方法可能有益。

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