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

Introduction. NF-kB (nuclear factor kappa beta) is a trascription factor that has an important role in the immune system. It regulates the expression of cytokines, cyclo-oxgenase 2, growth factors. It is a regulator of anti-apoptotic gene expression; it has a role in neo-angiogenesis stimulation and it plays a role during healing of the hand flexor tendonds. We verified if NF-kB is present on the margins of cuff tears and hypothesized that NF-kB might have a role on evolution of cuff tear and on possible mechanisms of cuff healing. Material and methods. Thirty-two consecutive patients with cuff tears were enrolled for this study (average age: 64 years). Tears were classified as small in 7 patients, large in 16 and massive in 9. Samples from anterior and posterior edges of the tear and portion of subacromial bursa were excised during the arthroscopic treatment. Samples of uninjured subscapularis tendon were also excised and used as control. Removed tissues were used for haematoxylin/eosin morphologic evaluation or for immunohisto- chemical analysis. Results. Activated NF-kB increases with the increasing in tear dimension without any differences between anterior and posterior edges, and it is always higher in the bursa. Of the subscapularis sample, only those belonged to patients with massive tears had the activated NF-kB. Inflammatory infiltrate is higher in the anterior edge of massive tears and in the bursa. Neoangiogenesis , . increases with the increasing in the tear dimension and it was particularly observed in the bursa. - •- Conclusions. Activated NF-kB increases with the increasing in the tear dimension ' We hypothesized three possible explanations: over time activated cells increase ( accumulation effect); massive tears are scarcely covered by the bursa, consequently tendon does not receive reparative biochemical stimuli; therefore cells active themselves in order to stimulate inflammation and neoangiogenesis ; activated NF-kB has an anti-apoptotic role on the remained cells.