Background: Adhesion formation limits functional recovery after flexor tendon repair. Various growth factors have been implicated in the adhesion scar process. Early growth response factor-1 (EGR-1), a transcription factor associated with synthesis of a variety of key fibrotic growth factors and expression of extracellular matrix genes, has never been identified in a tendon repair model.
Methods: Thirty New Zealand White rabbit forepaws underwent laceration and repair of the middle digit flexor digitorum profundus equivalent in zone II. Sodium morrhuate, a topical sclerosing agent, or phosphate-buffered saline, a standard control, was applied to the repair during closure of the tendon sheath. Tendons were harvested from operated and unoperated forepaws at increasing time intervals (1, 3, 7, 14, and 28 days). Tissues were analyzed by immunohistochemistry and Masson trichrome staining.
Results: Immunohistochemistry demonstrated that EGR-1 is expressed at the site of tendon repair, along the epitenon of the tendon, and in the infiltrate of inflammatory cells in the surrounding sheath-scar matrix. Control, unoperated tendons demonstrated baseline EGR-1 expression within epitenon cells. EGR-1 was maximally expressed on postoperative day 7. Sodium morrhuate and phosphate-buffered saline demonstrated no difference in their ability to augment tendon adhesion scar formation.
Conclusions: : Findings demonstrate the following: (1) EGR-1 expression is increased in the tendon wound environment after flexor tendon laceration repair; (2) normal epitenon cells have low, baseline levels of EGR-1 expression; and (3) sodium morrhuate does not augment scar matrix production more than phosphate-buffered saline. The ideal tendon scar model was not generated.