Department of Orthopaedics and Traumatology, University of Rome Sapienza, Piazzale Aldo Moro 5, Rome, Italy.
J Shoulder Elbow Surg. 2013 May;22(5):673-80. doi: 10.1016/j.jse.2012.06.005. Epub 2012 Sep 7.
We verified if the nuclear factor-κB (NF-κB) was present on the margins of rotator cuff tears (RCTs). Because NF-κB regulates apoptosis and stimulates neoangiogenesis, we hypothesized that NF-κB has a role in the evolution of RCT and in possible mechanisms of RCT healing.
Samples from tear margins, subacromial bursa, and healthy subscapular tendons were excised during arthroscopic treatment of patients with posterosuperior RCT. Sections were cut and stained with hematoxylin and eosin for morphologic evaluation and used for immunohistochemical analysis with NF-κB p65 antibody.
The presence of NF-κB in the RCT margins and subacromial bursa increases with increasing tear size. NF-κB is also present in the subscapularis tendon of patients with large and massive RCT. Analogously, we observed that neoangiogenesis grows with increasing RCT size and is always present in the subscapularis tendon independently from RCT size. Statistical analysis indicates that NF-κB and neoangiogenesis are correlated, regardless of the dimension of the RCT.
This is the first study that identifies the association between activated NF-κB and RCT. Activated NF-κB on the margins of RCT increases with increasing tear size. We hypothesized a series of possible causes responsible for NF-κB activation; however, we believe that activation is due to tissue hypoxia. Activated p65 directly stimulates neoangiogenesis, but the same factors that regulate NF-κB activation might also act as neoangiogenesis inductors.
我们验证了核因子-κB（NF-κB）是否存在于肩袖撕裂（RCT）的边缘。由于 NF-κB 调节细胞凋亡并刺激新生血管形成，我们假设 NF-κB 在 RCT 的演变及其可能的 RCT 愈合机制中起作用。
在关节镜治疗后上 RCT 患者期间，从撕裂边缘、肩峰下囊和健康肩胛下肌腱中切除标本。用苏木精和伊红染色进行形态学评估，并使用 NF-κB p65 抗体进行免疫组织化学分析。
随着撕裂尺寸的增加，RCT 边缘和肩峰下囊的 NF-κB 存在增加。NF-κB 也存在于大 RCT 和巨大 RCT 患者的肩胛下肌腱中。类似地，我们观察到随着 RCT 尺寸的增加，新生血管形成增加，并且无论 RCT 尺寸如何，它始终存在于肩胛下肌腱中。统计分析表明，NF-κB 和新生血管形成之间存在相关性，无论 RCT 的大小如何。
这是第一项确定激活的 NF-κB 与 RCT 之间关联的研究。RCT 边缘的激活 NF-κB 随着撕裂尺寸的增加而增加。我们假设了一系列可能导致 NF-κB 激活的原因；然而，我们认为激活是由于组织缺氧引起的。激活的 p65 直接刺激新生血管形成，但调节 NF-κB 激活的相同因素也可能作为新生血管形成诱导剂。
