Department of Plastic and Aesthetic Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, #79 Qingchun Road, Hangzhou, 310003, Zhejiang Province, China.
Department of Orthopedics, The First Affiliated Hospital, College of Medicine, Zhejiang University, #79 Qingchun Road, Hangzhou, 310003, Zhejiang Province, China.
J Orthop Surg Res. 2021 May 5;16(1):293. doi: 10.1186/s13018-021-02445-y.
Peritendinous adhesion is among the common complications after tendon injury. Numerous studies have been carried out to prevent its formation, including modifications of surgical procedures, postoperative cares, application of medicines, etc. This study dynamically monitored fluctuations of inflammation, state of oxidative stress, and histopathologic changes around injured tendon to provide theoretical basis for further exploration in mechanisms of peritendinous adhesion formation.
Eighteen mature Sprague-Dawley male rats were randomly allocated into 6 equal groups. Compared with control and sham group, every rat's right hind Achilles tendon in experimental groups was cut and repaired by the modified Kessler technique. Besides control and sham group, samples of tendon margin and serum were collected at different time points after the surgery. Content of TNF-α, IL-1β, and TGF-β were assayed in harvested serum. Reactive oxygen species (ROS) were detected, expression levels of related genes (IL-1β, IL-6, SOD1, SOD2, COL1, HIF1A) were quantified by qPCR, and various histopathological evaluations were performed.
Indicators (TNF-α, IL-1β, TGF-β1, ROS) were noticed to have a similar trend of significant rising 24 h after the surgery except TGF-β which was rising 72 h later. So were the expression trends of IL-1β, IL-6, SOD1, SOD2, and COL1. HIF1A, inversely correlated with SOD2, showed the progressive relief of regional tissue hypoxia. Histological evaluation showed the same tendency that fibrosis and inflammation were getting serious 48 h later after the surgery.
Inflammation, oxidative stress in injured tendon resulted from acute trauma, would be getting intense in 24 h. Peritendinous adhesion emerges and aggravates after 48 h. Thus, prompt efficient measures are advised to be taken after the injury as soon as possible.
腱周粘连是肌腱损伤后的常见并发症之一。为了预防其形成，已经进行了大量的研究，包括手术方式的改进、术后护理、药物应用等。本研究动态监测了损伤肌腱周围炎症、氧化应激状态和组织病理学变化的波动，为进一步探索腱周粘连形成机制提供了理论依据。
将 18 只成熟的 SD 雄性大鼠随机分为 6 组。与对照组和假手术组相比，实验组每只大鼠的右后跟腱均采用改良 Kessler 技术进行切割和修复。除对照组和假手术组外，术后不同时间点采集肌腱边缘和血清样本。采集的血清中测定 TNF-α、IL-1β 和 TGF-β 的含量。检测活性氧（ROS），通过 qPCR 定量检测相关基因（IL-1β、IL-6、SOD1、SOD2、COL1、HIF1A）的表达水平，并进行各种组织病理学评估。
术后 24 小时，除 TGF-β 外，其他指标（TNF-α、IL-1β、TGF-β1、ROS）均呈明显升高趋势，IL-1β、IL-6、SOD1、SOD2、COL1 的表达趋势也相似。与 SOD2 呈负相关的 HIF1A 显示局部组织缺氧程度逐渐缓解。组织学评价显示，术后 48 小时，纤维化和炎症程度加重。
急性创伤引起的损伤肌腱内炎症、氧化应激在 24 小时内会加剧。腱周粘连在 48 小时后出现并加重。因此，建议在受伤后尽快采取及时有效的措施。
