Objectives: Scientific databases index numerous references related to the treatment of Kienböck's disease; yet little is known about the nature of the disease and its pathognomonic features. This study provides a cross-sectional analysis of the pattern and extent of osteonecrosis in a large cohort and a longitudinal analysis to determine the spontaneous disease progression in single patients who have not had surgical management until fragmentation of the lunate.
Methods: In a prospective case series, the pattern and extent of osteonecrosis were correlated with the duration of symptoms in all patients with Kienböck's disease confirmed using high-resolution 3-T magnetic resonance imaging (MRI) and ultra-thin section computed tomographic (CT) scan since 2009. Furthermore, a retrospective consecutive case series study was conducted to determine the rate of spontaneous evolution in all consecutive patients treated conservatively in our university hospital since 1990.
Results: Among the 35 consecutive patients with Kienböck's disease diagnosed in high-resolution 3-T MRI and ultra-thin section CT, 46% (16/35) presented degeneration of lunate cartilage on CT scan in the first 12 months following the onset of symptoms. Median wrist pain duration of patients presenting a fracture of the lunate was 14 months. Thirty-one percent (11/35) of the patients had arthritis of the lunate, yet no fractures at the time of examination. Of 106 consecutive patients with Kienböck's disease and complete records, who did not have surgical intervention until fragmentation of the lunate, three cases were identified with well-documented spontaneous courses from apparently intact lunate morphology until fragmentation within 6 months.
Conclusions: Kienböck's disease progresses substantially faster than previously described and, contrary to current classifications, the articular cartilage of the lunate degenerates in early stages.
Level Of Evidence: Diagnostic accuracy, Level IV.
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http://dx.doi.org/10.1016/j.bjps.2014.05.037 | DOI Listing |
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Department of Global Health, Medicine and Welfare, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki City, Nagasaki Prefecture 852-8523, Japan.
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The endothelium is the gatekeeper of vessel health, and its dysfunction is pivotal in driving atherogenesis. Here, we present a protocol to replicate endothelial-macrophage crosstalk during atherogenesis, called the "atherogenesis-on-chip" model, based on the Emulate dual-channel perfusion system. We describe a model for studying endothelial-macrophage interactions during atherogenesis in human aortic endothelial cells and human macrophages using qPCR and secretome analysis, fluorescence microscopy, and flow cytometry.
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Divison of Molecular and Vascular Biology, IRDA, Kumamoto University, Kumamoto 860-0811, Japan. Electronic address:
Angiogenesis begins as endothelial cells migrate, forming a sprouting tip and subsequent growth-rich stalk cells. Here, we present a protocol for transcriptomic and epigenomic analyses of tip-like cells in cultured endothelial cells. We describe steps for stimulating human umbilical vein endothelial cells (HUVECs) with vascular endothelial cell growth factor (VEGF) to generate tip-like cells.
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