The Effects of Fibroblast Growth Factor-2 on Rotator Cuff Reconstruction With Acellular Dermal Matrix Grafts

Purpose: Our purpose was to determine whether the local application of fibroblast growth factor (FGF) 2 accelerates regeneration and remodeling of rotator cuff tendon defects reconstructed with acellular dermal matrix (ADM) grafts in rats. Methods: Thirty adult male Sprague-Dawley rats were divided into equal groups undergoing FGF-treated and FGF-untreated repairs. All rats underwent placement of ail ADM graft for the supraspinatus defect (3 x 5 mm). FGF-2 (100 mu g/kg) in a fibrin sealant was applied to both shoulders in the FGF-treated group, whereas only fibrin sealant was applied in untreated group. At 2, 6, and 12 weeks after surgery, 5 rats (10 shoulders) in each group were sacrificed for histologic analysis (3 shoulders) and biomechanical testing (7 shoulders). The controls were 5 unoperated rats (3 histologic and 7 biomechanical control specimens). Results: Unoperated control tendons inserted into the bone by direct insertion; there was a zone of fibrocartilage between the tendon and bone. At 2 weeks, the FGF-treated group had tendon maturing scores similar to those in the untreated group (P>.05). At 6 and 12 weeks, the FGF-treated group had significantly higher scores (P<.05). At 2 weeks, specimens in both the treated and untreated groups exhibited similar strength; the ultimate tensile failure load was 6.0 +/- 4.0 N and 5.8 +/- 2.0 N, respectively (P>.05). At 6 weeks, the FGF-treated specimens were stronger, with an ultimate tensile failure load of 10.2 +/- 3.1 N compared with 7.2 +/- 2.2 N in the untreated group (P=.02). At 12 weeks, the FGF-treated specimens were stronger, with an ultimate tensile failure load of 15.9 +/- 1.6 N compared with 13.2 +/- 2.0 N in the untreated group (P>.0072), and there were no significant differences in strength compared with the controls (17.8 +/- 2.6 N) (P>.05). Conclusions: The remodeling of ADM grafts placed in rat rotator cuff tendon defects was accelerated by the local administration of FGF-2.