Kopka Michaela, Monument Michael J, Befus A Dean, Zhang Mei, Hart David A, Salo Paul T, Schneider Prism S, Fan Cun-Yi, Liang Xiangdang, Garven Alexandra, Hildebrand Kevin A
*Department of Surgery, University of Calgary, Calgary, Canada; †Department of Medicine, University of Alberta, Edmonton, Canada; ‡Department of Orthopaedic Surgery, Shanghai Jiao Tong University, Shanghai, China; and §Department of Orthopaedic Surgery, The General Hospital of People's Liberation Army Beijing, Beijing, China.
J Orthop Trauma. 2017 Mar;31(3):e86-e89. doi: 10.1097/BOT.0000000000000747.
Mast cells have been identified as key mediators of posttraumatic joint contracture, and stabilizing medications (ketotifen) have been shown to decrease contracture severity. Serum mast cell tryptase (SMCT) levels are used clinically to monitor mast cell-mediated conditions. The goals of this study were to determine if SMCT levels are elevated in the setting of joint contracture, if they can be decreased in association with ketotifen therapy, and if they correlate with contracture severity.
This study used a previously developed rabbit model in which 39 animals were divided into 4 groups: operatively created joint contracture (ORC, n = 13), operatively created contracture treated with ketotifen at 2 doses (KF0.5, n = 9; KF1.0, n = 9), and healthy rabbits (NC, n = 8). Range of motion measures were performed at 8 weeks after the surgery. Serum samples were collected on postoperative days 1, 3, 5, 7, 21, 35, and 49. SMCT levels were measured using a rabbit-specific enzyme-linked immunosorbent assay.
Levels of SMCT were highest in the operatively created joint contracture group and were significantly greater compared with both ketotifen groups (P < 0.001). Levels were highest at postoperative day 1 with a trend to decrease over time. A positive correlation between SMCT levels and contracture severity was observed in all operative groups (P < 0.05).
Levels of SMCT are elevated in the setting of joint contracture, decreased in association with ketotifen therapy, and positively correlated with contracture severity. This is the first study to establish a relationship between SMCT and joint injury. Measurement of SMCT may be valuable in identifying those at risk of posttraumatic joint contracture.
肥大细胞已被确认为创伤后关节挛缩的关键介质,且已证实稳定药物(酮替芬)可降低挛缩严重程度。血清肥大细胞类胰蛋白酶(SMCT)水平在临床上用于监测肥大细胞介导的疾病。本研究的目的是确定在关节挛缩情况下SMCT水平是否升高,与酮替芬治疗相关时其水平是否可降低,以及它们是否与挛缩严重程度相关。
本研究使用先前建立的兔模型,将39只动物分为4组:手术造成关节挛缩组(ORC,n = 13)、接受两种剂量酮替芬治疗的手术造成挛缩组(KF0.5,n = 9;KF1.0,n = 9)和健康兔组(NC,n = 8)。术后8周进行活动度测量。在术后第1、3、5、7、21、35和49天采集血清样本。使用兔特异性酶联免疫吸附测定法测量SMCT水平。
手术造成关节挛缩组的SMCT水平最高,与两个酮替芬组相比均显著更高(P < 0.001)。术后第1天水平最高,且有随时间下降的趋势。在所有手术组中均观察到SMCT水平与挛缩严重程度呈正相关(P < 0.05)。
在关节挛缩情况下SMCT水平升高,与酮替芬治疗相关时降低,且与挛缩严重程度呈正相关。这是第一项建立SMCT与关节损伤之间关系的研究。测量SMCT可能有助于识别创伤后关节挛缩的高危人群。