The possible role of the transcription factor nuclear factor-κB on evolution of rotator cuff tear and on mechanisms of cuff tendon healing.

BACKGROUND

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.

MATERIALS AND METHODS

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.

RESULTS

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.

CONCLUSIONS

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.