Tears of the tendon-bone interface are common, particularly in the rotator cuff, affecting 22% of the general population, and >50% of those over 60 years old. These injuries show poor healing even after surgical repair, and as such, augmentation with tissue-engineered grafts has been suggested for improved outcomes. Here, we evaluate a novel collagen scaffold, with an organised lamellar structure and desirable mechanical properties, identified to be a potentially clinically viable tendon tissue augment.
In vitro, immune response was assessed by measuring expression of pro-inflammatory cytokines in human monocyte (THP-1) cells cultured with collagen scaffolds for 24 or 48 hours. alamarBlue® and fluorescent staining were used to determine if the scaffolds could sustain primary tenocyte cell growth over a 7-day period. In vivo, the supraspinatus was excised from the humerus of 23 sexually mature Sprague-Dawley rats. The tendon was either repaired using sutures alone, or sutures augmented with scaffolds. Biomechanical properties including elasticity and load to failure, were assessed using an Instron device at 12 weeks post-repair. H&E stained tendon sections were graded for collagen fibre density and orientation, healing at bone-tendon interface, vascularity, and presence of inflammatory cells.
In vitro, scaffolds did not increase the expression of pro-inflammatory cytokines (IL-1β, TNF-α, IL-8) compared with either untreated controls or cells exposed to surgical sutures. alamarBlue® and fluorescent staining confirmed adherence and growth of cells on scaffolds. In vivo, scaffold augmentation increased elasticity of the repaired tendon-bone interface, but slightly lowered ultimate load to failure. There were no visible structural differences between groups.
Further work is underway to better characterise cell response to the scaffold, and to fully determine its potential for improved healing outcomes in vivo. However, results here suggest that the scaffold is cytocompatible, with potential to augment tendon-bone healing without inducing adverse immune response.