Connors James C, Hardy Mark A, Kishman Lauren L, Botek Georgeanne G, Verdin Craig J, Rao Nilin M, Kingsley J Derek
Assistant Professor, Division of Foot/Ankle Surgery and Biomechanics, Kent State University College of Podiatric Medicine, Independence, OH.
Division Head and Associate Professor, Division of Foot and Ankle Surgery/Biomechanics, Kent State University College of Podiatric Medicine, Independence, OH.
J Foot Ankle Surg. 2018 Nov-Dec;57(6):1067-1072. doi: 10.1053/j.jfas.2018.03.023.
Charcot neuroarthropathy is a rare but often difficult to manage disease in the neuropathic patient. Early signs such as unremarkable edema, marginal trauma, or minor infection can activate a cascade of bony destruction and lead to gross prominence or deformity, with dire consequences. The exact molecular mechanism is poorly understood. Current theory states that an inflammatory reaction leads to the activation of osteoclasts mediated by specific cytokines. Our study sought to test the genetic expression of certain biomarkers in diabetic patients with and without Charcot neuroarthropathy compared with patients with and without diabetes or neuropathy. A total of 30 patients participated in the study, 17 (57%) males and 13 (43%) females. Peripheral blood samples were drawn, and gene expression was measured using real-time polymerase chain reaction. The expression levels of receptor activator of nuclear factor kappa-B ligand and osteoprotegerin showed no significant increase in the Charcot neuroarthropathy group compared with the healthy control group. We determined that the levels of receptor activator of nuclear factor kappa-B ligand and osteoprotegerin were not significantly increased in Charcot neuroarthropathy patients compared with healthy control patients. These results demonstrate a need for further investigation into alternative molecular pathways to determine the exact mechanism of the disease process.
夏科氏神经关节病是一种在神经性患者中罕见但往往难以管理的疾病。早期迹象，如不明显的水肿、边缘创伤或轻微感染，可引发一系列骨质破坏，导致明显的突出或畸形，后果严重。确切的分子机制尚不清楚。目前的理论认为，炎症反应会导致由特定细胞因子介导的破骨细胞激活。我们的研究旨在测试患有和未患有夏科氏神经关节病的糖尿病患者与患有和未患有糖尿病或神经病变的患者中某些生物标志物的基因表达。共有30名患者参与了该研究，其中17名（57%）为男性，13名（43%）为女性。采集外周血样本，并使用实时聚合酶链反应测量基因表达。与健康对照组相比，夏科氏神经关节病组中核因子κB受体活化因子配体和骨保护素的表达水平没有显著增加。我们确定，与健康对照患者相比，夏科氏神经关节病患者中核因子κB受体活化因子配体和骨保护素的水平没有显著增加。这些结果表明需要进一步研究替代分子途径，以确定疾病过程的确切机制。
